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Author:   Helen E. Scharfman ,  Paul S. Buckmaster, DVM, Ph.D.
Publisher:   Springer
Imprint:   Springer
Edition:   Softcover reprint of the original 1st ed. 2014
Volume:   813
Dimensions:   Width: 17.80cm , Height: 1.90cm , Length: 25.40cm
Weight:   0.938kg
ISBN:  

9789402407891

ISBN 10:   9402407898
Pages:   339
Publication Date:   23 August 2016
Audience:   Professional and scholarly ,  Professional & Vocational
Format:   Paperback
Publisher's Status:   Active
Availability:   Manufactured on demand  
We will order this item for you from a manufactured on demand supplier.

Table of Contents

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 againstrational 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?.

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