This updated second edition of Acute Ischemic Stroke: Imaging and Intervention provides a comprehensive account of the state of the art in the diagnosis and treatment of acute ischemic stroke. The basic format of the first edition has been retained, with sections on fundamentals such as pathophysiology and causes, imaging techniques and interventions. However, each chapter has been revised to reflect the important recent progress in advanced neuroimaging and the use of interventional tools. In addition, a new chapter is included on the classification instruments for ischemic stroke and their use in predicting outcomes and therapeutic triage. All of the authors are internationally recognized experts and members of the interdisciplinary stroke team at the Massachusetts General Hospital and Harvard Medical School. The text is supported by numerous informative illustrations, and ease of reference is ensured through the inclusion of suitable tables. This book will serve as a unique source of up-to-date information for neurologists, emergency physicians, radiologists and other health care providers who care for the patient with acute ischemic stroke.

A distinction between primary and secondary brain damage of vari ous origin, particularly in acute lesions, such as head injury and ische mia is not entirely new. The concept is of practical significance, be cause it is the foremost intention of all clinical efforts to prevent, or at least attenuate the development of secondary sequelae. Primary dam age to nervous elements usually cannot be influenced by treatment. Its prevention is the objective of prophylactic measures. The current volume gathered prominent scientists and clinicians from various fields to pro vide a competent introduction and survey of the various aspects involved in secondary brain damage. It was attempted to provide criteria for the distinction between the primary and secondary phenomena on a morpho logical and functional level, on the basis of the kinetics involved and, most importantly, regarding the different specific manifestations, such as disturbances of microcirculation, aspects of the blood-brain barrier, and of cellular structure and function at a molecular level. Although it was not expected that a grand unifying hypothesis will be reached recon cilable with the many, occasionally opposing views on such a complex subject, nevertheless, the present volume attains an appropriate result. It can best be described as a mosaic of many different pieces which only as an ensemble reflect the current state of the art.

Highlighting concepts of brain ischemia, this book looks at the molecular mechanisms of its development leading to brain tissue changes and describes strategies of neuroprotective therapy. Coverage includes cellular reactions in response to acute focal brain ischemia, microglial activation and local inflammation in focal brain ischemia, programmed cell death, primary and secondary neuroprotection, gangliosides, and modern therapeutic approaches to acute focal brain ischemia. The authors are neurologists affiliated with the Russian State Medical University. Annotation (c)2003 Book News, Inc., Portland, OR (booknews.com).

This second edition presents core clinical neuroanesthesia and neurointensive care knowledge in a practical, user-friendly format.

Accessible handbook covering the investigation, diagnosis and management of transient ischemic attacks and minor strokes.

Brain Hypoxia and Ischemia explores the various aspects of cell death and survival that are crucial for understanding the basic mechanisms underlying brain hypoxia and ischemia. Chapters focus on a panorama of issues including the role of ion channels/transporters, mitochondria and apoptotic mechanisms, the roles of glutamate/NMDA, mechanisms in penumbral cells and the importance of intermittent hypoxia and gene regulation under these stressful conditions. The volume explores findings from both mammalian and invertebrate model systems and their applicability to human systems and diseases. Careful consideration is also given to differences in hypoxia and ischemia across development. This volume aims to increase the understanding of these mechanisms and to stimulate research on better diagnosis and treatment of diseases that afflict the brain and potentially other organs when O2 levels are dysregulated. Brain Hypoxia and Ischemia is designed for neuroscientists, clinicians and medical/graduate students for use in both basic research and clinical practice.

This e-book will review special features of the cerebral circulation and how they contribute to the physiology of the brain. It describes structural and functional properties of the cerebral circulation that are unique to the brain, an organ with high metabolic demands and the need for tight water and ion homeostasis. Autoregulation is pronounced in the brain, with myogenic, metabolic and neurogenic mechanisms contributing to maintain relatively constant blood flow during both increases and decreases in pressure. In addition, unlike peripheral organs where the majority of vascular resistance resides in small arteries and arterioles, large extracranial and intracranial arteries contribute significantly to vascular resistance in the brain. The prominent role of large arteries in cerebrovascular resistance helps maintain blood flow and protect downstream vessels during changes in perfusion pressure. The cerebral endothelium is also unique in that its barrier properties are in some way more like epithelium than endothelium in the periphery. The cerebral endothelium, known as the blood-brain barrier, has specialized tight junctions that do not allow ions to pass freely and has very low hydraulic conductivity and transcellular transport. This special configuration modifies Starling's forces in the brain microcirculation such that ions retained in the vascular lumen oppose water movement due to hydrostatic pressure. Tight water regulation is necessary in the brain because it has limited capacity for expansion within the skull. Increased intracranial pressure due to vasogenic edema can cause severe neurologic complications and death.