Aneurysmal subarachnoid hemorrhage (SAH) is a stroke subtype that affects, preponderantly, young adults. This condition carries a mortality of approximately 30-50% and a rate of permanent neurological disability of 30%. In addition, a substantial number of patients with an apparent good outcome suffer from residual neurocognitive impairment which, though subtle, prevents them from returning to work and having a normal life. Based on these data, it has been estimated that SAH is responsible for almost a quarter of all the years lost because of stroke. The calcium channel blocker nimodipine remains the only pharmacological treatment for SAH. This drug, however, has limited effectiveness and its use in clinical practice may be limited due to hypotension. Therefore, novel and effective treatments for this condition are desperately needed. The outcome in SAH has been associated with early brain injury, vasospasm, and delayed cerebral ischemia. Mechanistically, these processes are characterized by micro- and macro-vascular dysfunction, microthrombi formation, blood-brain barrier (BBB) dysregulation, brain edema, and neural-cell survival. Soon after SAH, there is a robust inflammatory response characterized by pyrexia, leukocytosis, and upregulation of adhesion molecules and cytokines in the periphery and in the CNS. Observational studies have shown that patients with more severe inflammatory responses experience worse outcomes after SAH. At the molecular level, different proinflammatory intracellular signaling pathways, including mitogen-activated protein-kinase and nuclear factor kappa-β, are activated in cerebral vessels after experimental SAH and their inhibition has been shown to decrease the occurrence of vasospasm. In addition, clinical and preclinical data have linked cytokine upregulation (interleukins [IL]-1B, IL-6 and IL-8, tumor necrosis factor-α, and monocyte chemoattractant protein-1), enhanced expression of adhesion molecules (selectins, integrins, and ICAM), and neutrophil activation to vasospasm of large cerebral arteries, microvascular dysregulation, and cell death. Moreover, immune cells regulate hemostasis and secrete active proteases, including matrix metalloproteinase 9, which promote microthrombosis and induce blood brain barrier dysfunction, respectively. In this context, it has been suggested that an enhanced inflammatory burden might contribute to brain injury in SAH through numerous downstream mechanisms. On the other hand, growing evidence demonstrates that neuroinflammation may influence the proliferation and migration of progenitor cells that participate of synaptic plasticity, neurogenesis, and neurorepair.

Offering up-to-date coverage of everything from historical and international perspectives to basic science and today's clinical practice, Miller's Anesthesia, 10th Edition, remains the #1 reference and trusted learning resource for practitioners and trainees in this complex field. Dr. Michael Gropper leads a team of expert editors and contributing authors who provide current information on the technical, scientific, and clinical issues you face each day—whether you're managing a challenging patient care situation, preparing for the boards, or studying for recertification. - Addresses timely topics alongside foundational basic science for an in-depth and comprehensive understanding of the field. - Contains thoroughly up-to-date content, including two new chapters: The Immune System: Implications for Anesthetic Management and Emergency Preparedness in Healthcare. - Provides new content in key areas such as sustainability, global health equity, the effect of anesthetics on immune function, anesthesia for special populations, coverage of infectious diseases including COVID-19, and occupational exposure and safety. - Offers state-of-the-art coverage of anesthetic drugs, guidelines for anesthetic practice and patient safety, new techniques, step-by-step instructions for patient management, the unique needs of pediatric patients, and much more—all highlighted by more than 1,200 full-color illustrations (300 new to this edition) for enhanced visual clarity. - Includes 40+ video clips demonstrating patient positioning, ultrasound, echocardiograms, and other imaging, and anesthetic procedures in real time.

This textbook addresses the classical use of Transcranial Doppler (TCD) and Transcranial Color-Coded Duplex Sonography (TCCS), focusing on the usefulness of neurological monitoring beyond classical acute brain injuries present in the daily intensive care medical practice. It encompasses a wide range of critical pathologies where neurological impact is part of clinical evolution, offering practical approaches for managing, application and interpretation of neurosonology to assist the physician to making real-time individualized decisions at bedside. It is an academic guide developed and edited by international experts being a very useful resource in daily practice for intensivists, neurologists, neurosurgeons and other specialists involving in critical care.

With advances in medicine and medical innovation, the face of neurosurgery has changed dramatically. A new era of surgeons values the need to undertake research in everyday practice and actively participate in the clinic and laboratory in order to improve patient prognosis. Highlighting the principles of basic neuroscience and its application to neurosurgical disease, this book breaks down neurological conditions into current academic themes and advances. The book is split into two sections, with the first covering basic and computational neuroscience including neuroanatomy, synaptic transmission and the growing use of artificial intelligence. The second section concentrates on specific conditions, such as gliomas, spinal tumors, and peripheral nerve injury. Outlining the clinical and pathophysiological principles of neurological conditions, this valuable book describes key animal models, helping clinicians design and conduct appropriate research projects to further knowledge and improve prognosis.

Aneurysmal subarachnoid hemorrhage (aSAH) still represents a significant cause of morbidity and mortality around the world and its outcome can be dramatically impacted by early and expert care. SAH treatment comprises early neurosurgical or endovascular treatment of the ruptured aneurysm, strategies to reduce further neurological injury, and managing systemic complications. In fact, management of aSAH is a multidisciplinary issue and the current state of knowledge is in rapid evolution. Nevertheless, the guidelines are not up to date. The last American aSAH guidelines were issued in 2012 and covered literature up until May 2010, and in 2013 members of the Guidelines Committee of the European Stroke Organization reviewed them from a European standpoint. Since then, considerable advances have been made in diagnostic methods, surgical and endovascular techniques, and clinical management paradigms. Subarachnoid hemorrhage is still a relevant health problem and, although its incidence varies among populations, a quarter of patients affected by aSAH die and approximately half of survivors are left with some persistent neurological deficit. Taking into account the fact that the prognosis of aSAH patients is affected by multiple factors and that some of them can be influenced by therapeutic strategies and management procedures, we believe that there is a need to reassess which interventions provide the greatest benefit to patients.

Mechanisms of brain-immune interactions became a cutting-edge topic in systemic neurosciences over the past years. Acute lesions of the brain parenchyma, particularly, induce a profound and highly complex neuroinflammatory reaction with similar mechanistic properties between differing disease paradigms like ischemic stroke, intracerebral hemorrhage (ICH) and traumatic brain injury (TBI). Resident microglial cells sense tissue damage and initiate inflammation, activation of the endothelial brain-immune interface promotes recruitment of systemic immune cells to the brain and systemic humoral immune mediators (e.g. complements and cytokines) enter the brain through the damaged blood-brain barrier. These cellular and humoral constituents of the neuroinflammatory reaction to brain injury contribute substantially to secondary brain damage and neurodegeneration. Diverse inflammatory cascades such as pro-inflammatory cytokine secretion of invading leukocytes and direct cell-cell-contact cytotoxicity between lymphocytes and neurons have been demonstrated to mediate the inflammatory ‘collateral damage’ in models of acute brain injury. Besides mediating neuronal cell loss and degeneration, secondary inflammatory mechanisms also contribute to functional modulation of neurons and the impact of post-lesional neuroinflammation can even be detected on the behavioral level. The contribution of several specific immune cell subpopulations to the complex orchestration of secondary neuroinflammation has been revealed just recently. However, the differential vulnerability of specific neuronal cell types and the molecular mechanisms of inflammatory neurodegeneration are still elusive. Furthermore, we are only on the verge of characterizing the control of long-term recovery and neuronal plasticity after brain damage by inflammatory pathways. Yet, a more detailed but also comprehensive understanding of the multifaceted interaction of these two supersystems is of direct translational relevance. Immunotherapeutic strategies currently shift to the center of translational research in acute CNS lesion since all clinical trials investigating direct neuroprotective therapies failed. To advance our knowledge on brain-immune communications after brain damage an interdisciplinary approach covered by cellular neuroscience as well as neuroimmunology, brain imaging and behavioral sciences is crucial to thoroughly depict the intricate mechanisms.

This book offers valuable guidance to neurointensivists, other neurocritical care staff, and those desiring to develop a neurocritical care unit via a thorough discussion of neurological emergencies and neurocritical care unit organization. This comprehensive volume begins with a review of acute neurological emergencies as managed clinically in the neurocritical care unit. Topics include acute cerebrovascular, neurological, and neurosurgical disorders. The unique aspect of this book is its description of the organization of the neurocritical care unit. We focus on how other services in the hospital interact with and assist neurocritical care operations, telemedicine/telestroke, and neurocritical care personnel and their roles. A review of expected outcomes of neurocritical care conditions is also included. Neurointensivists, neurocritical care unit staff leadership, hospital administrators, and those interested in developing a neurocritical care unit will find Neurointensive Care Unit: Clinical Practice and Organization to be an invaluable guide.

The process of inflammation, which causes the swelling and redness around a wound, is a vital part of the body's system for fighting off infections. When the body is hurt, the immune system produces chemical signals telling cells to multiply without dying, allowing skin to close over a gash, for example. Other chemicals spur the growth of new blood vessels to feed the recovering tissue. Scientists have linked inflammation to cancer and recently to heart disease in several ways. Doctors suspect that long-term inflammation or infection is involved in up to 20 per cent of cancers, including those of the oesophagus, colon, skin, stomach, liver, bladder, breast and some kinds of lymphoma. C-reactive protein (CRP) is one of the acute phase proteins that increase during systemic inflammation. It's been suggested that testing CRP levels in the blood may be a new way to assess cardiovascular disease risk. A high sensitivity assay for CRP test (hs-CRP) is now widely available. This new book presents recent leading-edge research from around the world.