This book contains articles presented at the 12th International Conference on Cerebral Vasospasm, held in Lucerne, Switzerland, in July 2013. The included papers represent a balanced cross-section of the enormous progress achieved in basic and clinical research on aneurysmal subarachnoid hemorrhage and its sequelae, including early neurovascular events and delayed cerebral vasospasm. The section on basic research covers a broad range of aspects, with a special focus on animal models for the study of acute events after experimental subarachnoid hemorrhage. The section on clinical topics encompasses imaging and endovascular management, surgical innovations and techniques, management and monitoring in neurocritical care, the status of clinical trials, and factors involved in aneurysm formation. This edition is of interest not only for basic researchers but also for clinicians who wish to apply state-of-the-art knowledge to the research and management of this devastating condition.

The book contains 48 articles presented at the 11th International Conference on Cerebral Vasospasm held in Cincinnati, Ohio, USA, in July 2011. This collection of papers represents a cross-section of the enormous progress that has been made towards a thorough understanding and effective treatment of neurovascular events following aneurysmal subarachnoid hemorrhage, including cerebral vasospasm. It is of interest to clinicians who wish to apply state-of-the-art knowledge to their management of this devastating condition and to basic scientists wishing to expand their understanding of cerebrovascular and neural pathophysiology related to subarachnoid hemorrhage.

This book highlights the latest developments in acute and delayed neurovascular injury studies including delayed cerebral vasospasm, early brain injury, micro-circulation compromise, spreading cortical depolarization, neuroinflammation, and long-term cognitive dysfunctions after subarachnoid hemorrhage. About 32 chapters cover original presentations from the 14th international conference on neurovascular events after subarachnoid hemorrhage, held in Los Angeles in October 2017. Neurosurgeons, neurologists, and neuro-ICU practitioners discuss clinical observations, new pilot treatments, clinical trials, academic and industrial interactions, including surgical and endovascular approaches, brain injury monitoring, new developments in brain imaging, ICU management, early brain injury scales and management, counter cortical depolarization management and anti-inflammation management. In addition, animal models used to study acute and delayed neurovascular events, the basic mechanisms of vascular, neuronal, and CSF physiology, new experimental treatment strategies, new frontiers in the treatment of neurovascular injuries, and new research directions are discussed.

The contributions in this book were presented at the fifth European-Japanese Joint Conference for Stroke Surgery, held in July 2010 in Duesseldorf, Germany. The topics treated are the management of cerebral and ventricular hemorrhage, extra-intracranial bypass surgery, surgical and endovascular treatment of cervical and intracranial arterial occlusive disease, and embolization and microsurgery of AVM and dural AV-fistulas.

Bryce Weir is a high-profile, respected neurologist. Dr. Macdonald is a colleague of Dr. Weir's and is a "rising star" in the field of neurology.This book is the first to cover all aspects of cerebral vasospasm in depth. It takes the reader from the first descriptions of this puzzling and deadly phenomenon to the latest laboratory evidence explaining its pathophysiology. Packed with clinical pearls, it is a must for neurosurgeons, interventional radiologists, neurologists, and neuropathologists. Key Features* Examines the current understanding of vascular smooth muscle physiology* Provides in-depth overviews of symptoms and treatments* Written by acknowledged experts on the subject* Vividly illustrated with beautiful photographs and diagrams* Cites over 4,000 key papers on vasospasms* Presents key data in an easy-to-use format

This book focuses on subarachnoid hemorrhage (SAH), describing in detail the neurophysiology, anatomy, epidemiology, grading, anesthesia management, coiling and interventional treatment of this dangerous disease. Written by leading international experts, it highlights the state-of-the-art techniques for the diagnosis and treatment (non-surgical and surgical) of SAH and the clinical variations. It also examines the reliability of the new techniques versus the standard clinical methods to predict problems related to SAH and its recent diagnosis and management. The book starts with a brief discussion of the epidemiology of SAH, cerebral circulation, anatomy of brain blood vessels and neurophysiology related to this fatal disease. Then, in the following chapters it covers grading of subarachnoid hemorrhage, anesthesia management of SAH, treatment, subarachnoid hemorrhage coiling and radiological intervention. Lastly, it explores surgical treatment of intracranial aneurysms in more detail, and addresses complications, critical care management and headache in SAH, traumatic SAH and prognosis. Featuring numerous images, tables, schema, illustrations and videos, the book is intended for junior and senior anesthesiologists, neuroscientists, intervention radiologists, intensivists and neurosurgeons.

Deficits within the brain microcirculation contribute to poor patient outcome following aneurysmal subarachnoid hemorrhage (SAH). However, the underlying pathophysiology is not well understood. Intra-cerebral (parenchymal) arterioles are encased by specialized glial processes, called astrocyte endfeet. Ca2+ signals in the endfeet, driven by the ongoing pattern of neuronal activity, regulate parenchymal arteriolar diameter and thereby influence local cerebral blood flow. In the healthy brain, this phenomenon, called neurovascular coupling (NVC), matches focal increases in neuronal activity with local arteriolar dilation. This ensures adequate delivery of oxygen and other nutrients to areas of the brain with increased metabolic demand. Recently, we demonstrated inversion of NVC from vasodilation to vasoconstriction in brain slices obtained from SAH model animals. This pathological change, which would restrict blood flow to active brain regions, was accompanied by an increase in the amplitude of spontaneous Ca2+ events in astrocyte endfeet. It is possible that the emergence of higher amplitude endfoot Ca2+ events shifts the polarity of NVC after SAH by elevating levels of vasoactive agents (e.g. K+ ions) within the perivascular space. In the first aim of this dissertation we tested whether altered endfoot Ca2+ signaling underlies the inversion of NVC after SAH. Brain injury is often associated with increased levels of extracellular purine nucleotides (e.g. ATP). A recent study found that ATP levels in the cerebrospinal fluid of aneurysmal SAH patients were roughly 400-fold higher than that of non-SAH controls. Astrocytes express a variety of purinergic (P2) receptors that, when activated, could trigger a spike in intra-cellular Ca2+. It is possible that enhanced signaling via astrocyte P2 receptors underlies the change in endfoot Ca2+ signaling after SAH. In the second aim of this dissertation we determined the role of purinergic signaling in the generation of high-amplitude spontaneous endfoot Ca2+ events after SAH. Parenchymal arteriolar diameter and endfoot Ca2+ dynamics were recorded simultaneously in fluo-4-loaded rat brain slices using combined infrared-differential interference contrast and multi-photon fluorescence microscopy. We report that SAH led to a time-dependent emergence of spontaneous endfoot high-amplitude Ca2+ signals (eHACSs) that were only present in brain slices exhibiting inversion of NVC. Depletion of intracellular Ca2+ stores abolished spontaneous endfoot Ca2+ signals, including eHACSs, and restored arteriolar dilation in SAH brain slices to two downstream elements in the NVC signaling cascade, (1) increased endfoot Ca2+ and (2) elevated extracellular K+. We next tested the role of purinergic signaling in the generation of SAH-induced eHACSs by recording endfoot activity before and after treatment with the broad-spectrum purinergic receptor antagonist, suramin. Remarkably, suramin selectively abolished eHACSs and restored vasodilatory NVC in SAH brain slices. Desensitization of Ca2+-permeable ionotropic purinergic (P2X) receptors had no effect on eHACSs after SAH. However, eHACSs were selectively blocked using a cocktail of inhibitors targeting Gq-coupled purinergic (P2Y) receptors. Collectively, our results support a model in which SAH leads to an emergence of P2Y receptor-mediated eHACSs that cause inversion of NVC. Further, we identify the FDA-approved drug, suramin, as a potential therapy to be used in the treatment of aneurysmal SAH.