Brain Edema: From Molecular Mechanisms to Clinical Practice. This item is unavailable.Brain Edema: From Molecular Mechanisms to Clinical Practice

Brain Edema: From Molecular Mechanisms to Clinical Practice brings together the most widely recognized experts in experimental and clinical brain edema research to review the current knowledge gathered on the molecular and cellular pathophysiology and clinical management of brain edema. This timely book also discusses future directions of research and treatment.

Brain edema is an integral and acutely life-threatening part of the pathophysiology of multiple cerebral and non-cerebral disorders, including traumatic brain injury, cerebral ischemia, brain tumors, cardiac arrest, altitude sickness and liver failure. Affecting millions worldwide, research over the past few years has shown that a plethora of complex molecular and cellular mechanisms contribute to this pathological accumulation of water in the brain parenchyma.

In parallel, the development of new neuroimaging tools has provided a new way to examine how edema develops longitudinally and in real time, both in pre-clinical models and in patients. Despite intense research over the past few decades, therapeutic options are still limited and sometimes not effective.

• Presents a comprehensive understanding of the molecular mechanisms involved in edema formation and resolution
• Discusses the specific role of edema development in several pathologies, including traumatic brain injury, stroke, brain tumors, cardiac arrest, and liver failure
• Proposes a new classification of edema based on molecular processes
• Discusses clinical management of new clinical trials coming from pre-clinical studies
• Addresses the possible link between edema formation, other molecular and cellular processes, including inflammation and neuroinflammation

Dr. Jérôme Badaut received his PhD degree in 1999 in Neuroscience at University of Paris VI (France) after his training in the cerebrovascular field performed under supervision of Prof Lasbennes in the CNRS laboratory of Dr Jacques Seylaz. After a postdoctoral fellowship at University of Lausanne in Prof P.J. Magistretti and Prof L. Regli laboratories, he grew a strong interest on the roles of the astrocytes in neurovascular unit after stroke. He set an international expertise on the role of the astrocytic water channels in edema processes after brain injuries and also in other functions such as brain energy metabolism, when he was group leader in Neurosurgery departments at Lausanne and then Geneva (Switzerland). Then, he started to inquiry the role of neurovascular unit in pediatric traumatic brain injury when he held position of assistant professor in departments of pediatrics and physiology of the school of medicine in Loma Linda University (CA, USA). Dr Badaut is now tenured research officer at The National Center for Scientific Research (CNRS, France) in “Institut des Neurosciences Cognitives d’Aquitaine” (INCIA, UMR5287 CNRS-University of Bordeaux). He is leading the Brain Molecular Imaging group, a multidisciplinary team working on the development of new biomarkers in the field of brain injuries with for focus traumatic brain injury and neurovascular dysfunction.

Dr. Plesnila studied medicine in Regensburg and Munich, Germany, and spend the first few years of his scientific carrier working on the molecular mechanisms of astrocytic cell swelling in the laboratory of Axel Baethmann at the Institute for Surgical Research, Munich, Germany. After a post-doctoral fellowship at Harvard Medical School, he expanded his research interests to traumatic brain injury and cerebral ischemia in vivo. After research professorships at the Department of Neurosurgery in the University of Munich and at the Royal College of Surgeons in Ireland (RCSI), Dr. Plesnila’s laboratory for experimental stroke research is presently located at the Institute for Stroke and Dementia Research (ISD) at the University of Munich Medical Center. His research focus is the role of cerebral vessels including the blood-brain barrier and inflammation after brain damage.