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Issues in clinical epileptology: a view from the bench / edited by Helen E. Scharfman, Paul S. Buckmaster.

Colaborador(es): Tipo de material: TextoTextoSeries Advances in Experimental Medicine and Biology ; 813Editor: Dordrecht : Springer Netherlands : Springer, 2014Descripción: xxi, 339 páginas : 50 ilustraciones, 29 ilustraciones en colorTipo de contenido:
  • texto
Tipo de medio:
  • computadora
Tipo de portador:
  • recurso en línea
ISBN:
  • 9789401789141
Formatos físicos adicionales: Edición impresa:: Sin títuloClasificación LoC:
  • RC346-429.2
Recursos en línea:
Contenidos:
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?.
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Springer eBooks

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?.

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