Issues in Clinical Epileptology: A View from the Bench

This book is dedicated to Dr. Philip A. Schwartzkroin.  The book has a novel format because it is not intended to be a set of reviews. Instead, it is an effort to explore important topics in the epilepsy research field. Because articles are written by leaders in the field who have years of experienc...

Πλήρης περιγραφή

Λεπτομέρειες βιβλιογραφικής εγγραφής
Συγγραφή απο Οργανισμό/Αρχή: SpringerLink (Online service)
Άλλοι συγγραφείς: Scharfman, Helen E. (Επιμελητής έκδοσης), Buckmaster, Paul S. (Επιμελητής έκδοσης)
Μορφή: Ηλεκτρονική πηγή Ηλ. βιβλίο
Γλώσσα:English
Έκδοση: Dordrecht : Springer Netherlands : Imprint: Springer, 2014.
Σειρά:Advances in Experimental Medicine and Biology, 813
Θέματα:
Διαθέσιμο Online:Full Text via HEAL-Link
Πίνακας περιεχομένων:
  • Preface
  • Foreword
  • Part I Seizures, epileptiform activities and regional localization
  • How can we identify ictal and interictal abnormal activity?- How can we translate “epileptiform” activity in vitro into something that is clinically relevant?- What is the importance of abnormal “background” activity in seizure generation?- What is a seizure focus?- What is a seizure network? Very fast oscillations at the interface between normal and epileptic brain
  •  What is a seizure network? Long-range network consequences of focal seizures
  • Is there any such thing as “generalized” epilepsy?- Part II Synaptic plasticity
  • Are there really “epileptogenic” mechanisms or only corruptions of “normal” plasticity?- When and how do seizures kill neurons - and is cell death relevant to epileptogenesis?- How is homeostatic plasticity important in epilepsy?- Is plasticity of GABA ergic mechanisms relevant to epileptogenesis?- Do structural changes in GABA neurons give rise to the epileptic state?- Does mossy fiber sprouting give rise to the epileptic state?- Does brain inflammation mediate pathological outcomes in epilepsy?- Are changes in synaptic function that underlie hyperexcitability responsible for seizure activity?- Does epilepsy cause a reversion to immature function?- Are alterations in transmitter receptor and ion channel expression responsible for the epilepsies?- Part III Models and methods
  • How do we assess the clinical relevance of models of mesial temporal lobe epilepsy?-  How do we make models that are useful in understanding partial epilepsies?- What non-neuronal mechanisms should be studied to understand epileptic seizures?- What epilepsy comorbidities are important to model in the laboratory? Clinical perspectives
  • Understanding epilepsy comorbidities: how can animal models help?- What new modeling approaches will help us identify promising drug treatments?- What are the arguments for and against rational therapy for epilepsy?- How can advances in epilepsy genetics lead to better treatments and cures?- How might novel technologies such as optogenetics lead to better treatments in epilepsy?.