Kooperativer Bibliotheksverbund

UID:

Format: 1 online resource (xvi, 213 pages) : , digital, PDF file(s).

ISBN: 1-107-15793-5 , 1-280-91693-1 , 9786610916931 , 0-511-29012-8 , 0-511-32117-1 , 0-511-28952-9 , 0-511-28820-4 , 0-511-54510-X , 0-511-28888-3

Series Statement: Cambridge pocket clinicians

Content: You have just encountered a possible stroke patient. You ask yourself, what should I do first? How do I know it is a stroke? Is it too late to reverse the damage? How do I do the right things in the right order? This book will help you answer these critical questions. It provides practical advice on the care of stroke patients in a range of acute settings. As new and effective treatments become available, and designated stroke centers are created, this guidebook will help inform the healthcare professionals responsible for delivering care. The content is arranged in chronological order, covering the things to consider in assessing and treating the patient in the emergency department, the stroke unit, and then on transfer to a rehabilitation facility. All types of stroke are covered. A comprehensive set of appendices contain useful reference information including dosing algorithms, conversion factors and stroke scales.

Note: Title from publisher's bibliographic system (viewed on 05 Oct 2015). , Preface -- , List of abbreviations -- , Stroke in the emergency department -- , Is this a stroke? -- , What type of stroke? -- , What to do first -- , Airway -- breathing -- circulation (ABCs) -- , What was the time of onset? -- , How bad are the symptoms now? -- , Do a non-contrast head CT -- , If the CT shows no blood, try to get the artery open -- , Recommended diagnostic evaluation -- , Ischemic stroke -- , Definition -- , Etiology -- , Diagnosis -- , The four components of ischemic stroke care -- , Acute therapy and optimization of neurological status -- , Etiological work-up for secondary prevention -- , Prevention of neurological deterioration or medical complications -- , Stroke recovery and rehabilitation -- , Ischemic stroke outcome -- , General timeline -- , TPA protocol -- , TPA indications -- , Strong contraindications -- , Relative contraindications -- , Procedure -- , Dose -- , Sample post-TPA orders -- , Risks vs. benefits of TPA -- , Unproven therapies. , Subarachnoid hemorrhage (SAH) -- , Definition -- , Epidemiology -- , Presentation -- , Diagnosis -- , Ruptured aneurysms : management -- , Prognosis -- , Admission sequence -- , Unruptured aneurysms -- , Organization of stroke care -- , Timely care -- , Stroke units -- , Stroke centers -- , Stroke teams -- , Rehabilitation -- , Secondary stroke prevention -- , Prevention of medical complications -- , Multidisciplinary rehabilitation team -- , Discharge planning -- , Appendix 1 : Numbers and calculations -- , Appendix 2 : IV TPA dosing chart -- , Appendix 3 : Sample admission orders -- , Appendix 4 : Sample discharge summary -- , Appendix 5 : Stroke radiology -- , Appendix 6 : Transcranial doppler ultrasound (TCD) -- , Appendix 7 : Heparin protocol -- , Appendix 8 : Insulin protocol -- , Appendix 9 : Medical complications -- , Appendix 10 : Brainstem syndromes -- , Appendix 11 : Cerebral arterial anatomy -- , Appendix 12 : Stroke in the young and less common stroke diagnoses -- , Appendix 13 : Brain death criteria -- , Appendix 14 : Neurological scales -- , Recommended reading -- , References. , Neurological deterioration in acute ischemic stroke -- , Probable causes -- , Initial evaluation of patients with neurologic deterioration -- , Stroke enlargement -- , Drop in perfusion pressure -- , Recurrent stroke -- , Cerebral edema and mass effect -- , Hemorrhagic transformation -- , Metabolic disturbance -- , Seizure -- , Symptom fluctuations without a good cause -- , The uncooperative patient -- , Ischemic stroke prevention : why we do the things we do -- , Investigations -- , Ischemic stroke prevention : general measures -- , Atrial fibrillation (A fib) -- , Carotid stenosis -- , Acute carotid occlusion -- , Lacunar strokes -- , Cervical arterial dissection -- , Patent foramen ovale -- , Transient ischemic attack (TIA) -- , Definition -- , Etiology -- , Presentation -- , Differential diagnosis -- , Clinical approach to a patient with suspected TIA -- , Prognosis after TIA -- , Intracerebral hemorrhage (ICH) -- , Definition -- , Etiology -- , Presentation -- , Diagnosis and evaluation -- , Management -- , English

Additional Edition: ISBN 0-521-67494-8

Language: English

URL: Volltext

URL: https://doi.org/10.1017/CBO9780511545108

UID:

Format: 1 online resource (xvii, 294 pages) : , digital, PDF file(s).

Edition: Third edition.

ISBN: 1-108-61711-5 , 1-108-75982-3

Series Statement: Cambridge medicine

Content: You have just encountered a possible stroke patient. You ask yourself: what should I do first? How do I know it is a stroke? Is it too late to reverse the damage? This book provides integral assistance in answering these critical questions. All content is arranged in chronological order, covering all considerations in assessing and treating patients in the emergency room, stroke unit, and rehabilitation facilities. This new edition offers readers the latest information on stroke treatment, and features brand new chapters on stroke radiology, endovascular therapy, the uncommon causes of stroke, cerebral venous thrombosis, stroke prevention, and the transition to outpatient care. The comprehensive set of appendices contains useful reference information, including dosage algorithms, conversion factors, and stroke scales.

Note: Preceded by Acute stroke care : a manual from the University of Texas-Houston Stroke Team / Ken Uchino, Jennifer K. Pary, James C. Grotta. 2nd ed. 2011. , Title from publisher's bibliographic system (viewed on 28 Oct 2019). , Stroke in the emergency department -- What to do first -- Ischemic stroke -- Stroke radiology -- Intravenous thrombolysis -- Endovascular therapy (ET) -- Neurological deterioration in acute ischemic stroke -- Ischemic stroke etiology and secondary prevention -- Transient ischemic attack (TIA) -- Less common causes of stroke -- Cerebral venous sinus thrombosis -- Intracerebral hemorrhage (ICH) -- Subarachnoid hemorrhage (SAH) -- Organization of stroke care -- Stroke rehabilitation -- Transition to outpatient stroke care.

Additional Edition: ISBN 1-108-73132-5

Language: English

URL: https://doi.org/10.1017/9781108759823

URL: https://doi.org/10.1017/9781108759823

UID:

Format: 1 online resource : , illustrations (chiefly color)

Edition: Seventh edition

ISBN: 0-323-69425-X

Content: Authored by the world's foremost stroke experts, this classic text brings you fully up to date with current research findings and management approaches for cerebrovascular disease. Stroke: Pathophysiology, Diagnosis, and Management, 7th Edition, covers every aspect of this fast-moving field, and is an ideal resource for stroke specialists, general neurologists, and other medical professionals with an interest in stroke. You'll find expert clinical guidance, comprehensive pathophysiology coverage, data from recent trials, advances in diagnostic tests, full-color CT images, pathology slides, and much more, for a complete picture of today's stroke medicine. Helps you recognize the clinical manifestations of stroke, use the latest laboratory and imaging studies to arrive at a diagnosis, and generate an effective medical and surgical treatment plan. Keeps you abreast of the overwhelming volume of studies and guidelines in this dynamic field, providing clear summaries and practical evaluations of all relevant data. Contains updates throughout, including the latest clinical trials (thrombectomy, DAWN, DEFUSE), genetics research, prevention research, new therapies, and the new guidelines from the ASA. Includes new slides for lectures, covering basic science, case studies, and interventional treatment overviews. Features a Key Points summary at the beginning of each chapter so you can quickly find important information. Provides abundant full-color CT images and pathology slides that help you make efficient and accurate diagnoses. Enhanced eBook version included with purchase. Your enhanced eBook allows you to access all of the text, figures, and references from the book on a variety of devices.

Additional Edition: Print version: Stroke. Philadelphia, PA : Elsevier, [2022] ISBN 9780323694247

Language: English

UID:

Format: 1 online resource (1481 p.)

Edition: Sixth edition.

ISBN: 0-323-29544-4

Content: Offered in print, online, and downloadable formats, this updated edition of Stroke: Pathophysiology, Diagnosis, and Management delivers convenient access to the latest research findings and management approaches for cerebrovascular disease. Picking up from where J. P. Mohr and colleagues left off, a new team of editors - Drs. Grotta, Albers, Broderick, Kasner, Lo, Mendelow, Sacco, and Wong - head the sixth edition of this classic text, which is authored by the world's foremost stroke experts. Comprehensive, expert clinical guidance enables you to recognize the clinical manifestations of stroke.

Note: "Get full acces and more at ExpertConsult.com"--Cover. , Front Cover -- Stroke -- Copyright Page -- Table Of Contents -- Foreword to the Sixth Edition -- Preface -- List of Contributors -- AHA Evidence-based Classifications -- I Pathophysiology -- 1 Vascular Biology and Atherosclerosis of Cerebral Vessels -- Key Points -- Introduction -- Physiological Regulation of Cerebral Vascular Tone -- Cyclic AMP-mediated Mechanisms -- Nitric Oxide (NO) and Cyclic Guanosine Monophosphate -- K+ Channels -- KCa-activated K+ Channels -- KATP Channels -- KV Channels -- KIR Channels -- K2P Channels -- Rho/rho-kinase -- Reactive Oxygen Species (ROS) -- Transient Receptor Potential (TRP) Channels -- Alterations in Cerebral Vascular Function During Hypertension and Atherosclerosis -- Atherosclerosis -- Cerebral Vascular Oxidative Stress in Models of Atherosclerosis -- Cerebral Vascular Endothelial Dysfunction in Models of Atherosclerosis -- Cerebral Vascular Inflammation in Models of Atherosclerosis -- Hypertension -- Oxidative Stress In Hypertension Involving Elevated Ang II -- Endothelial Dysfunction in Hypertension Involving Elevated Ang II -- Cerebrovascular Inflammation in Hypertension Involving Elevated Ang II -- K+ Channel Function in Chronic Hypertension -- BKCa Channels. -- KATP Channels. -- KV Channels. -- KIR Channels. -- Rho-kinase in Hypertension -- Conclusion -- References -- 2 Mechanisms of Thrombosis and Thrombolysis -- Key Points -- Thrombus Formation -- Fibrinolysis -- Plasminogen -- Plasminogen Activation -- Thrombus Dissolution -- Plasminogen Activators -- Endogenous Plasminogen Activators -- Tissue-type Plasminogen Activator -- Urokinase-type Plasminogen Activator (u-PA) -- Exogenous Plasminogen Activators -- Streptokinase -- Staphylokinase -- Plasminogen Activators Derived from Desmodus rotundus -- Novel Plasminogen Activators -- Regulation of Endogenous Fibrinolysis. , α2-Antiplasmin and α2-Macroglobulin -- Inhibitors of Plasminogen Activators and Fibrinolysis -- Clinical Consequences of Therapeutic Plasminogen Activation -- Limitations to the Clinical Use of Fibrinolytic Agents for Ischemic Stroke -- Plasminogen Activators in Cerebral Tissue -- Plasminogen Activators and Neuronal Functions -- Plasminogen Activators and Cerebral Microvessel Integrity -- Plasminogen Activators in Experimental Cerebral Ischemia -- Plasminogen Activators and Recanalization in Ischemic Stroke -- Plasminogen Activators and Cerebral Hemorrhage in Ischemic Stroke -- Conclusion -- References -- 3 Cerebral Blood Flow and Metabolism: -- Key Points -- Normal Cerebral Energy Metabolism and Hemodynamics -- Introduction -- Cerebral Blood Flow and Other Measurements of Cerebral Perfusion -- Normal Values of Cerebral Blood Flow and Cerebral Metabolism -- Control of Cerebral Blood Flow -- Relationship of Cerebral Blood Flow and Metabolism -- Response of Cerebral Blood Flow to Changes in Arterial Partial Pressure of Oxygen and Oxygen Content -- Response of Cerebral Blood Flow to Changes in Blood Glucose -- Response of Cerebral Blood Flow to Changes in Arterial pCO2 -- Response of Cerebral Blood Flow to Changes in Blood Viscosity -- Autoregulation of Cerebral Blood Flow to Changes in Cerebral Perfusion Pressure -- Compensatory Responses to Reduced Cerebral Blood Flow -- Response of Cerebral Blood Flow to Multiple Simultaneous Stimuli -- Hemodynamic Effects of Arterial Occlusive Disease -- Three-stage Classification System of Cerebral Hemodynamics -- Hemodynamic Effects of Arterial Stenosis -- Correlation of Cerebral Hemodynamics with Stroke Risk -- Ischemic Stroke -- Changes in Cerebral Blood Flow and Metabolism with Acute Ischemic Stroke -- Flow-Metabolism Thresholds of Tissue Function and Viability in Acute Ischemic Stroke. , Vasoreactivity and Autoregulation in Ischemic Stroke -- Remote Flow and Metabolic Effects of Ischemic Stroke -- Intracerebral Hemorrhage -- Cerebral Blood Flow and Metabolism -- Autoregulation -- Arteriovenous Malformations -- Aneurysmal Subarachnoid Hemorrhage -- Cerebral Blood Flow and Metabolism -- Autoregulation -- Conclusions -- Acknowledgments -- Key References -- References -- 4 Histopathology of Brain Tissue Response to Stroke and Injury -- Key Points -- Four Broad Categories of Cerebral Ischemia -- Large Vessel Strokes -- Heart Disease and Cerebral Emboli -- Carotid Artery Atherosclerosis -- Infarction Versus Selective Neuronal Necrosis -- Small Vessel Strokes -- Hypertensive Arteriolosclerosis -- White Matter Incomplete Infarction -- Amyloid Angiopathy -- CADASIL -- Tissue Response to Therapy of Cerebral Ischemia -- References -- 5 Molecular and Cellular Mechanisms of Ischemia-Induced Neuronal Death -- Key Points -- Global Ischemia -- Focal Ischemia -- Experimental Models of Global and Focal Ischemia -- Models of Global Ischemia -- Models of Focal Ischemia -- Hypoxia/Ischemia -- Modalities of Ischemic Cell Death -- Necrosis -- Apoptosis -- The Caspase Death Cascade -- Alternative Pathways of Caspase Activation -- The Bcl-2 Family of Proteins -- Inhibitors of Apoptosis -- Caspase-Independent Programmed Cell Death -- Autophagy -- Cell Death Pathways -- Triggers of Ischemic Cell Death -- Glutamate Excitotoxicity -- NMDARs -- Ca2+-Permeable AMPARs -- Non-excitotoxic Mechanisms -- TRP Channels -- ASIC Channels -- Calcium -- Zinc -- Mechanisms of Ischemic Cell Death -- Metabolic Stress -- Mitochondrial Permeabilization -- Nitric Oxide -- Free Radicals and Lipid Peroxidation -- Epigenetic Mechanisms and Transcriptional Regulation -- The Transcription Activator CREB -- Nuclear Factor-κB: A Balance between Neuronal Survival and Death. , The Pro-Death Transcription Activator FOXO -- The Signal Transducer and Activator of Transcription 3 (STAT3) -- The Restrictive Element-1 Silencing Transcription Factor (REST)/Neuron Restrictive Silencing Factor (NRSF) -- Inflammation -- Acknowledgments -- Key References -- References -- 6 Intracellular Signaling: -- Key Points -- Preconditioning -- Windows of Preconditioning -- Induction of Preconditioning -- Cross-Tolerance -- Cellular Defense -- Reactive Oxygen Species -- Mitochondria -- Neurotrophin Support -- Survival Kinases -- Erythropoietin -- Inhibition of Cell Death -- Cellular Maintenance -- Regeneration and Repair -- Clinical Implications -- Acknowledgments -- References -- 7 The Neurovascular Unit and Responses to Ischemia -- Key Points -- Introduction -- Architecture of the CNS and the Neurovascular Unit -- Structural Relationships: Anatomy of the Cerebral Vasculature -- Functional Relationships -- Neuron-Microvessel Communication -- Neuron-Astrocyte Communication. -- Astrocyte-Endothelial Cell (Vascular) Communication. -- Astrocyte-Smooth Muscle Communication. -- Microvessel-Neuron Communication -- Astrocyte-Neuron Communication. -- Endothelial Cell-Astrocyte Communication. -- Evidence for the Neurovascular Unit -- Interactions Suggesting Unit Communication -- Structural Changes During Focal Ischemia. -- Microvessel (Endothelial-Astrocyte) Communication. -- Innate Inflammation. -- Propagating Depolarizations and Neurovascular Unit Dysfunction. -- Summary and Implications -- References -- 8 Mechanisms of Cerebral Hemorrhage -- Key Points -- Experimental Models of Intracerebral Hemorrhage -- Mechanism of Brain Injury after Intracerebral Hemorrhage -- Inflammatory Responses after Intracerebral Hemorrhage -- Oxidative Stress after Intracerebral Hemorrhage -- Blood Components and Intracerebral-Hemorrhage-induced Injury. , Red Blood Cell Lysis and Hemoglobin Toxicity -- Brain Iron Overload -- Thrombin Formation -- Mechanisms of Cell Death After Intracerebral Hemorrhage -- Apoptosis -- Excitotoxicity and Cell Death after Intracerebral Hemorrhage -- Additional Caveats about the Apoptosis and Other Forms of Death after Intracerebral Hemorrhage -- Blood-Brain Barrier Disruption -- Modifiers of Intracerebral-hemorrhage- induced Injury -- Hypertension -- Gender -- Age -- Therapeutic Approaches Targeting Intracerebral Hemorrhage Pathogenesis in Animal Research -- Surgical Treatment for Intracerebral Hemorrhage -- Pharmacologic and other Experimental Treatment for Intracerebral Hemorrhage -- Conclusion -- Key References -- References -- 9 White Matter Pathophysiology -- Key Points -- White Matter Anatomy and Physiology -- Model Systems for Studying White Matter Ischemia -- Cell Culture -- In vitro Tissue Models -- In vivo Models -- Effects of Ischemia on White Matter -- Derangement of Transmembrane Ion Gradients -- The Ca2+ Hypothesis and Anoxic-Ischemic White Matter Injury -- Mechanisms of White Matter Injury -- Ca2+ Entry and Intracellular Ca2+ Release in Axons during Ischemia -- Reversal of Na+-Ca2+ Exchange -- Activation of Voltage-Gated Ca2+ Channels -- Activation of Intracellular Ca2+ Release -- Excitotoxic Pathways Injure Glia in White Matter -- Autoprotection in White Matter -- Strategies for Protecting White Matter from Anoxic-Ischemic Injury are Diverse -- Acknowledgments -- References -- 10 Inflammation and Immune Response -- Key Points -- Cerebral Ischemia, Cytokines, and Inflammation -- Mechanisms by Which Inflammation Contributes to Ischemic Brain Injury -- Immune Cells Participating in Ischemic Injury and Tissue Repair -- Microglia, Monocytes/Macrophages, and Dendritic Cells -- Neutrophils -- Mast Cells -- Lymphocytes. , Danger Sensors: Scavenger Receptors and Toll-Like Receptors. , English

Additional Edition: ISBN 1-336-23984-0

Additional Edition: ISBN 0-323-32805-9

Language: English

UID:

Format: 1 online resource (xvii, 235 pages) : , digital, PDF file(s).

Edition: Second edition.

ISBN: 9780511794568 (ebook)

Series Statement: Pocket clinician

Content: You have just encountered a possible stroke patient. You ask yourself: what should I do first? How do I know it is a stroke? Is it too late to reverse the damage? How do I do the right things in the right order? This book will help you answer these critical questions. It provides practical advice on the care of stroke patients in a range of acute settings. The content is arranged in chronological order, covering the things to consider in assessing and treating the patient in the emergency department, the stroke unit and then on transfer to a rehabilitation facility. All types of stroke are covered. This new edition provides updated information from recently completed clinical trials and added information on endovascular therapy, hemicraniectomy for severe stroke, DVT prophylaxis and stroke prevention. A comprehensive set of appendices contain useful reference information including dosing algorithms, conversion factors and stroke scales.

Note: Title from publisher's bibliographic system (viewed on 05 Oct 2015).

Additional Edition: Print version: ISBN 9780521184847

Language: English

URL: https://doi.org/10.1017/CBO9780511794568

URL: Volltext

UID:

Format: Tab.; Lit.

ISSN: 0016-867X

Note: Band: 43; Heft: 7; Seiten: 40-46

In: Geriatrics, Cleveland, Ohio : Advanstar Communications, 1946, 43(1988), 7, Seite 40-46, 0016-867X

In: volume:43

In: year:1988

In: number:7

In: pages:40-46

Language: English

UID:

Format: 1 online resource : , illustrations (chiefly color)

Edition: Seventh edition

ISBN: 0-323-69425-X

Content: Authored by the world's foremost stroke experts, this classic text brings you fully up to date with current research findings and management approaches for cerebrovascular disease. Stroke: Pathophysiology, Diagnosis, and Management, 7th Edition, covers every aspect of this fast-moving field, and is an ideal resource for stroke specialists, general neurologists, and other medical professionals with an interest in stroke. You'll find expert clinical guidance, comprehensive pathophysiology coverage, data from recent trials, advances in diagnostic tests, full-color CT images, pathology slides, and much more, for a complete picture of today's stroke medicine. Helps you recognize the clinical manifestations of stroke, use the latest laboratory and imaging studies to arrive at a diagnosis, and generate an effective medical and surgical treatment plan. Keeps you abreast of the overwhelming volume of studies and guidelines in this dynamic field, providing clear summaries and practical evaluations of all relevant data. Contains updates throughout, including the latest clinical trials (thrombectomy, DAWN, DEFUSE), genetics research, prevention research, new therapies, and the new guidelines from the ASA. Includes new slides for lectures, covering basic science, case studies, and interventional treatment overviews. Features a Key Points summary at the beginning of each chapter so you can quickly find important information. Provides abundant full-color CT images and pathology slides that help you make efficient and accurate diagnoses. Enhanced eBook version included with purchase. Your enhanced eBook allows you to access all of the text, figures, and references from the book on a variety of devices.

Additional Edition: Print version: Stroke. Philadelphia, PA : Elsevier, [2022] ISBN 9780323694247

Language: English

UID:

Format: 1 online resource : , illustrations (chiefly color)

Edition: Seventh edition

ISBN: 0-323-69425-X

Content: Authored by the world's foremost stroke experts, this classic text brings you fully up to date with current research findings and management approaches for cerebrovascular disease. Stroke: Pathophysiology, Diagnosis, and Management, 7th Edition, covers every aspect of this fast-moving field, and is an ideal resource for stroke specialists, general neurologists, and other medical professionals with an interest in stroke. You'll find expert clinical guidance, comprehensive pathophysiology coverage, data from recent trials, advances in diagnostic tests, full-color CT images, pathology slides, and much more, for a complete picture of today's stroke medicine. Helps you recognize the clinical manifestations of stroke, use the latest laboratory and imaging studies to arrive at a diagnosis, and generate an effective medical and surgical treatment plan. Keeps you abreast of the overwhelming volume of studies and guidelines in this dynamic field, providing clear summaries and practical evaluations of all relevant data. Contains updates throughout, including the latest clinical trials (thrombectomy, DAWN, DEFUSE), genetics research, prevention research, new therapies, and the new guidelines from the ASA. Includes new slides for lectures, covering basic science, case studies, and interventional treatment overviews. Features a Key Points summary at the beginning of each chapter so you can quickly find important information. Provides abundant full-color CT images and pathology slides that help you make efficient and accurate diagnoses. Enhanced eBook version included with purchase. Your enhanced eBook allows you to access all of the text, figures, and references from the book on a variety of devices.

Additional Edition: Print version: Stroke. Philadelphia, PA : Elsevier, [2022] ISBN 9780323694247

Language: English

UID:

Format: 1 online resource (1481 p.)

Edition: Sixth edition.

ISBN: 0-323-29544-4

Content: Offered in print, online, and downloadable formats, this updated edition of Stroke: Pathophysiology, Diagnosis, and Management delivers convenient access to the latest research findings and management approaches for cerebrovascular disease. Picking up from where J. P. Mohr and colleagues left off, a new team of editors - Drs. Grotta, Albers, Broderick, Kasner, Lo, Mendelow, Sacco, and Wong - head the sixth edition of this classic text, which is authored by the world's foremost stroke experts. Comprehensive, expert clinical guidance enables you to recognize the clinical manifestations of stroke.

Note: "Get full acces and more at ExpertConsult.com"--Cover. , Front Cover -- Stroke -- Copyright Page -- Table Of Contents -- Foreword to the Sixth Edition -- Preface -- List of Contributors -- AHA Evidence-based Classifications -- I Pathophysiology -- 1 Vascular Biology and Atherosclerosis of Cerebral Vessels -- Key Points -- Introduction -- Physiological Regulation of Cerebral Vascular Tone -- Cyclic AMP-mediated Mechanisms -- Nitric Oxide (NO) and Cyclic Guanosine Monophosphate -- K+ Channels -- KCa-activated K+ Channels -- KATP Channels -- KV Channels -- KIR Channels -- K2P Channels -- Rho/rho-kinase -- Reactive Oxygen Species (ROS) -- Transient Receptor Potential (TRP) Channels -- Alterations in Cerebral Vascular Function During Hypertension and Atherosclerosis -- Atherosclerosis -- Cerebral Vascular Oxidative Stress in Models of Atherosclerosis -- Cerebral Vascular Endothelial Dysfunction in Models of Atherosclerosis -- Cerebral Vascular Inflammation in Models of Atherosclerosis -- Hypertension -- Oxidative Stress In Hypertension Involving Elevated Ang II -- Endothelial Dysfunction in Hypertension Involving Elevated Ang II -- Cerebrovascular Inflammation in Hypertension Involving Elevated Ang II -- K+ Channel Function in Chronic Hypertension -- BKCa Channels. -- KATP Channels. -- KV Channels. -- KIR Channels. -- Rho-kinase in Hypertension -- Conclusion -- References -- 2 Mechanisms of Thrombosis and Thrombolysis -- Key Points -- Thrombus Formation -- Fibrinolysis -- Plasminogen -- Plasminogen Activation -- Thrombus Dissolution -- Plasminogen Activators -- Endogenous Plasminogen Activators -- Tissue-type Plasminogen Activator -- Urokinase-type Plasminogen Activator (u-PA) -- Exogenous Plasminogen Activators -- Streptokinase -- Staphylokinase -- Plasminogen Activators Derived from Desmodus rotundus -- Novel Plasminogen Activators -- Regulation of Endogenous Fibrinolysis. , α2-Antiplasmin and α2-Macroglobulin -- Inhibitors of Plasminogen Activators and Fibrinolysis -- Clinical Consequences of Therapeutic Plasminogen Activation -- Limitations to the Clinical Use of Fibrinolytic Agents for Ischemic Stroke -- Plasminogen Activators in Cerebral Tissue -- Plasminogen Activators and Neuronal Functions -- Plasminogen Activators and Cerebral Microvessel Integrity -- Plasminogen Activators in Experimental Cerebral Ischemia -- Plasminogen Activators and Recanalization in Ischemic Stroke -- Plasminogen Activators and Cerebral Hemorrhage in Ischemic Stroke -- Conclusion -- References -- 3 Cerebral Blood Flow and Metabolism: -- Key Points -- Normal Cerebral Energy Metabolism and Hemodynamics -- Introduction -- Cerebral Blood Flow and Other Measurements of Cerebral Perfusion -- Normal Values of Cerebral Blood Flow and Cerebral Metabolism -- Control of Cerebral Blood Flow -- Relationship of Cerebral Blood Flow and Metabolism -- Response of Cerebral Blood Flow to Changes in Arterial Partial Pressure of Oxygen and Oxygen Content -- Response of Cerebral Blood Flow to Changes in Blood Glucose -- Response of Cerebral Blood Flow to Changes in Arterial pCO2 -- Response of Cerebral Blood Flow to Changes in Blood Viscosity -- Autoregulation of Cerebral Blood Flow to Changes in Cerebral Perfusion Pressure -- Compensatory Responses to Reduced Cerebral Blood Flow -- Response of Cerebral Blood Flow to Multiple Simultaneous Stimuli -- Hemodynamic Effects of Arterial Occlusive Disease -- Three-stage Classification System of Cerebral Hemodynamics -- Hemodynamic Effects of Arterial Stenosis -- Correlation of Cerebral Hemodynamics with Stroke Risk -- Ischemic Stroke -- Changes in Cerebral Blood Flow and Metabolism with Acute Ischemic Stroke -- Flow-Metabolism Thresholds of Tissue Function and Viability in Acute Ischemic Stroke. , Vasoreactivity and Autoregulation in Ischemic Stroke -- Remote Flow and Metabolic Effects of Ischemic Stroke -- Intracerebral Hemorrhage -- Cerebral Blood Flow and Metabolism -- Autoregulation -- Arteriovenous Malformations -- Aneurysmal Subarachnoid Hemorrhage -- Cerebral Blood Flow and Metabolism -- Autoregulation -- Conclusions -- Acknowledgments -- Key References -- References -- 4 Histopathology of Brain Tissue Response to Stroke and Injury -- Key Points -- Four Broad Categories of Cerebral Ischemia -- Large Vessel Strokes -- Heart Disease and Cerebral Emboli -- Carotid Artery Atherosclerosis -- Infarction Versus Selective Neuronal Necrosis -- Small Vessel Strokes -- Hypertensive Arteriolosclerosis -- White Matter Incomplete Infarction -- Amyloid Angiopathy -- CADASIL -- Tissue Response to Therapy of Cerebral Ischemia -- References -- 5 Molecular and Cellular Mechanisms of Ischemia-Induced Neuronal Death -- Key Points -- Global Ischemia -- Focal Ischemia -- Experimental Models of Global and Focal Ischemia -- Models of Global Ischemia -- Models of Focal Ischemia -- Hypoxia/Ischemia -- Modalities of Ischemic Cell Death -- Necrosis -- Apoptosis -- The Caspase Death Cascade -- Alternative Pathways of Caspase Activation -- The Bcl-2 Family of Proteins -- Inhibitors of Apoptosis -- Caspase-Independent Programmed Cell Death -- Autophagy -- Cell Death Pathways -- Triggers of Ischemic Cell Death -- Glutamate Excitotoxicity -- NMDARs -- Ca2+-Permeable AMPARs -- Non-excitotoxic Mechanisms -- TRP Channels -- ASIC Channels -- Calcium -- Zinc -- Mechanisms of Ischemic Cell Death -- Metabolic Stress -- Mitochondrial Permeabilization -- Nitric Oxide -- Free Radicals and Lipid Peroxidation -- Epigenetic Mechanisms and Transcriptional Regulation -- The Transcription Activator CREB -- Nuclear Factor-κB: A Balance between Neuronal Survival and Death. , The Pro-Death Transcription Activator FOXO -- The Signal Transducer and Activator of Transcription 3 (STAT3) -- The Restrictive Element-1 Silencing Transcription Factor (REST)/Neuron Restrictive Silencing Factor (NRSF) -- Inflammation -- Acknowledgments -- Key References -- References -- 6 Intracellular Signaling: -- Key Points -- Preconditioning -- Windows of Preconditioning -- Induction of Preconditioning -- Cross-Tolerance -- Cellular Defense -- Reactive Oxygen Species -- Mitochondria -- Neurotrophin Support -- Survival Kinases -- Erythropoietin -- Inhibition of Cell Death -- Cellular Maintenance -- Regeneration and Repair -- Clinical Implications -- Acknowledgments -- References -- 7 The Neurovascular Unit and Responses to Ischemia -- Key Points -- Introduction -- Architecture of the CNS and the Neurovascular Unit -- Structural Relationships: Anatomy of the Cerebral Vasculature -- Functional Relationships -- Neuron-Microvessel Communication -- Neuron-Astrocyte Communication. -- Astrocyte-Endothelial Cell (Vascular) Communication. -- Astrocyte-Smooth Muscle Communication. -- Microvessel-Neuron Communication -- Astrocyte-Neuron Communication. -- Endothelial Cell-Astrocyte Communication. -- Evidence for the Neurovascular Unit -- Interactions Suggesting Unit Communication -- Structural Changes During Focal Ischemia. -- Microvessel (Endothelial-Astrocyte) Communication. -- Innate Inflammation. -- Propagating Depolarizations and Neurovascular Unit Dysfunction. -- Summary and Implications -- References -- 8 Mechanisms of Cerebral Hemorrhage -- Key Points -- Experimental Models of Intracerebral Hemorrhage -- Mechanism of Brain Injury after Intracerebral Hemorrhage -- Inflammatory Responses after Intracerebral Hemorrhage -- Oxidative Stress after Intracerebral Hemorrhage -- Blood Components and Intracerebral-Hemorrhage-induced Injury. , Red Blood Cell Lysis and Hemoglobin Toxicity -- Brain Iron Overload -- Thrombin Formation -- Mechanisms of Cell Death After Intracerebral Hemorrhage -- Apoptosis -- Excitotoxicity and Cell Death after Intracerebral Hemorrhage -- Additional Caveats about the Apoptosis and Other Forms of Death after Intracerebral Hemorrhage -- Blood-Brain Barrier Disruption -- Modifiers of Intracerebral-hemorrhage- induced Injury -- Hypertension -- Gender -- Age -- Therapeutic Approaches Targeting Intracerebral Hemorrhage Pathogenesis in Animal Research -- Surgical Treatment for Intracerebral Hemorrhage -- Pharmacologic and other Experimental Treatment for Intracerebral Hemorrhage -- Conclusion -- Key References -- References -- 9 White Matter Pathophysiology -- Key Points -- White Matter Anatomy and Physiology -- Model Systems for Studying White Matter Ischemia -- Cell Culture -- In vitro Tissue Models -- In vivo Models -- Effects of Ischemia on White Matter -- Derangement of Transmembrane Ion Gradients -- The Ca2+ Hypothesis and Anoxic-Ischemic White Matter Injury -- Mechanisms of White Matter Injury -- Ca2+ Entry and Intracellular Ca2+ Release in Axons during Ischemia -- Reversal of Na+-Ca2+ Exchange -- Activation of Voltage-Gated Ca2+ Channels -- Activation of Intracellular Ca2+ Release -- Excitotoxic Pathways Injure Glia in White Matter -- Autoprotection in White Matter -- Strategies for Protecting White Matter from Anoxic-Ischemic Injury are Diverse -- Acknowledgments -- References -- 10 Inflammation and Immune Response -- Key Points -- Cerebral Ischemia, Cytokines, and Inflammation -- Mechanisms by Which Inflammation Contributes to Ischemic Brain Injury -- Immune Cells Participating in Ischemic Injury and Tissue Repair -- Microglia, Monocytes/Macrophages, and Dendritic Cells -- Neutrophils -- Mast Cells -- Lymphocytes. , Danger Sensors: Scavenger Receptors and Toll-Like Receptors. , English

Additional Edition: ISBN 1-336-23984-0

Additional Edition: ISBN 0-323-32805-9

Language: English

UID:

Format: 1 online resource (1481 p.)

Edition: Sixth edition.

ISBN: 0-323-29544-4

Content: Offered in print, online, and downloadable formats, this updated edition of Stroke: Pathophysiology, Diagnosis, and Management delivers convenient access to the latest research findings and management approaches for cerebrovascular disease. Picking up from where J. P. Mohr and colleagues left off, a new team of editors - Drs. Grotta, Albers, Broderick, Kasner, Lo, Mendelow, Sacco, and Wong - head the sixth edition of this classic text, which is authored by the world's foremost stroke experts. Comprehensive, expert clinical guidance enables you to recognize the clinical manifestations of stroke.

Note: "Get full acces and more at ExpertConsult.com"--Cover. , Front Cover -- Stroke -- Copyright Page -- Table Of Contents -- Foreword to the Sixth Edition -- Preface -- List of Contributors -- AHA Evidence-based Classifications -- I Pathophysiology -- 1 Vascular Biology and Atherosclerosis of Cerebral Vessels -- Key Points -- Introduction -- Physiological Regulation of Cerebral Vascular Tone -- Cyclic AMP-mediated Mechanisms -- Nitric Oxide (NO) and Cyclic Guanosine Monophosphate -- K+ Channels -- KCa-activated K+ Channels -- KATP Channels -- KV Channels -- KIR Channels -- K2P Channels -- Rho/rho-kinase -- Reactive Oxygen Species (ROS) -- Transient Receptor Potential (TRP) Channels -- Alterations in Cerebral Vascular Function During Hypertension and Atherosclerosis -- Atherosclerosis -- Cerebral Vascular Oxidative Stress in Models of Atherosclerosis -- Cerebral Vascular Endothelial Dysfunction in Models of Atherosclerosis -- Cerebral Vascular Inflammation in Models of Atherosclerosis -- Hypertension -- Oxidative Stress In Hypertension Involving Elevated Ang II -- Endothelial Dysfunction in Hypertension Involving Elevated Ang II -- Cerebrovascular Inflammation in Hypertension Involving Elevated Ang II -- K+ Channel Function in Chronic Hypertension -- BKCa Channels. -- KATP Channels. -- KV Channels. -- KIR Channels. -- Rho-kinase in Hypertension -- Conclusion -- References -- 2 Mechanisms of Thrombosis and Thrombolysis -- Key Points -- Thrombus Formation -- Fibrinolysis -- Plasminogen -- Plasminogen Activation -- Thrombus Dissolution -- Plasminogen Activators -- Endogenous Plasminogen Activators -- Tissue-type Plasminogen Activator -- Urokinase-type Plasminogen Activator (u-PA) -- Exogenous Plasminogen Activators -- Streptokinase -- Staphylokinase -- Plasminogen Activators Derived from Desmodus rotundus -- Novel Plasminogen Activators -- Regulation of Endogenous Fibrinolysis. , α2-Antiplasmin and α2-Macroglobulin -- Inhibitors of Plasminogen Activators and Fibrinolysis -- Clinical Consequences of Therapeutic Plasminogen Activation -- Limitations to the Clinical Use of Fibrinolytic Agents for Ischemic Stroke -- Plasminogen Activators in Cerebral Tissue -- Plasminogen Activators and Neuronal Functions -- Plasminogen Activators and Cerebral Microvessel Integrity -- Plasminogen Activators in Experimental Cerebral Ischemia -- Plasminogen Activators and Recanalization in Ischemic Stroke -- Plasminogen Activators and Cerebral Hemorrhage in Ischemic Stroke -- Conclusion -- References -- 3 Cerebral Blood Flow and Metabolism: -- Key Points -- Normal Cerebral Energy Metabolism and Hemodynamics -- Introduction -- Cerebral Blood Flow and Other Measurements of Cerebral Perfusion -- Normal Values of Cerebral Blood Flow and Cerebral Metabolism -- Control of Cerebral Blood Flow -- Relationship of Cerebral Blood Flow and Metabolism -- Response of Cerebral Blood Flow to Changes in Arterial Partial Pressure of Oxygen and Oxygen Content -- Response of Cerebral Blood Flow to Changes in Blood Glucose -- Response of Cerebral Blood Flow to Changes in Arterial pCO2 -- Response of Cerebral Blood Flow to Changes in Blood Viscosity -- Autoregulation of Cerebral Blood Flow to Changes in Cerebral Perfusion Pressure -- Compensatory Responses to Reduced Cerebral Blood Flow -- Response of Cerebral Blood Flow to Multiple Simultaneous Stimuli -- Hemodynamic Effects of Arterial Occlusive Disease -- Three-stage Classification System of Cerebral Hemodynamics -- Hemodynamic Effects of Arterial Stenosis -- Correlation of Cerebral Hemodynamics with Stroke Risk -- Ischemic Stroke -- Changes in Cerebral Blood Flow and Metabolism with Acute Ischemic Stroke -- Flow-Metabolism Thresholds of Tissue Function and Viability in Acute Ischemic Stroke. , Vasoreactivity and Autoregulation in Ischemic Stroke -- Remote Flow and Metabolic Effects of Ischemic Stroke -- Intracerebral Hemorrhage -- Cerebral Blood Flow and Metabolism -- Autoregulation -- Arteriovenous Malformations -- Aneurysmal Subarachnoid Hemorrhage -- Cerebral Blood Flow and Metabolism -- Autoregulation -- Conclusions -- Acknowledgments -- Key References -- References -- 4 Histopathology of Brain Tissue Response to Stroke and Injury -- Key Points -- Four Broad Categories of Cerebral Ischemia -- Large Vessel Strokes -- Heart Disease and Cerebral Emboli -- Carotid Artery Atherosclerosis -- Infarction Versus Selective Neuronal Necrosis -- Small Vessel Strokes -- Hypertensive Arteriolosclerosis -- White Matter Incomplete Infarction -- Amyloid Angiopathy -- CADASIL -- Tissue Response to Therapy of Cerebral Ischemia -- References -- 5 Molecular and Cellular Mechanisms of Ischemia-Induced Neuronal Death -- Key Points -- Global Ischemia -- Focal Ischemia -- Experimental Models of Global and Focal Ischemia -- Models of Global Ischemia -- Models of Focal Ischemia -- Hypoxia/Ischemia -- Modalities of Ischemic Cell Death -- Necrosis -- Apoptosis -- The Caspase Death Cascade -- Alternative Pathways of Caspase Activation -- The Bcl-2 Family of Proteins -- Inhibitors of Apoptosis -- Caspase-Independent Programmed Cell Death -- Autophagy -- Cell Death Pathways -- Triggers of Ischemic Cell Death -- Glutamate Excitotoxicity -- NMDARs -- Ca2+-Permeable AMPARs -- Non-excitotoxic Mechanisms -- TRP Channels -- ASIC Channels -- Calcium -- Zinc -- Mechanisms of Ischemic Cell Death -- Metabolic Stress -- Mitochondrial Permeabilization -- Nitric Oxide -- Free Radicals and Lipid Peroxidation -- Epigenetic Mechanisms and Transcriptional Regulation -- The Transcription Activator CREB -- Nuclear Factor-κB: A Balance between Neuronal Survival and Death. , The Pro-Death Transcription Activator FOXO -- The Signal Transducer and Activator of Transcription 3 (STAT3) -- The Restrictive Element-1 Silencing Transcription Factor (REST)/Neuron Restrictive Silencing Factor (NRSF) -- Inflammation -- Acknowledgments -- Key References -- References -- 6 Intracellular Signaling: -- Key Points -- Preconditioning -- Windows of Preconditioning -- Induction of Preconditioning -- Cross-Tolerance -- Cellular Defense -- Reactive Oxygen Species -- Mitochondria -- Neurotrophin Support -- Survival Kinases -- Erythropoietin -- Inhibition of Cell Death -- Cellular Maintenance -- Regeneration and Repair -- Clinical Implications -- Acknowledgments -- References -- 7 The Neurovascular Unit and Responses to Ischemia -- Key Points -- Introduction -- Architecture of the CNS and the Neurovascular Unit -- Structural Relationships: Anatomy of the Cerebral Vasculature -- Functional Relationships -- Neuron-Microvessel Communication -- Neuron-Astrocyte Communication. -- Astrocyte-Endothelial Cell (Vascular) Communication. -- Astrocyte-Smooth Muscle Communication. -- Microvessel-Neuron Communication -- Astrocyte-Neuron Communication. -- Endothelial Cell-Astrocyte Communication. -- Evidence for the Neurovascular Unit -- Interactions Suggesting Unit Communication -- Structural Changes During Focal Ischemia. -- Microvessel (Endothelial-Astrocyte) Communication. -- Innate Inflammation. -- Propagating Depolarizations and Neurovascular Unit Dysfunction. -- Summary and Implications -- References -- 8 Mechanisms of Cerebral Hemorrhage -- Key Points -- Experimental Models of Intracerebral Hemorrhage -- Mechanism of Brain Injury after Intracerebral Hemorrhage -- Inflammatory Responses after Intracerebral Hemorrhage -- Oxidative Stress after Intracerebral Hemorrhage -- Blood Components and Intracerebral-Hemorrhage-induced Injury. , Red Blood Cell Lysis and Hemoglobin Toxicity -- Brain Iron Overload -- Thrombin Formation -- Mechanisms of Cell Death After Intracerebral Hemorrhage -- Apoptosis -- Excitotoxicity and Cell Death after Intracerebral Hemorrhage -- Additional Caveats about the Apoptosis and Other Forms of Death after Intracerebral Hemorrhage -- Blood-Brain Barrier Disruption -- Modifiers of Intracerebral-hemorrhage- induced Injury -- Hypertension -- Gender -- Age -- Therapeutic Approaches Targeting Intracerebral Hemorrhage Pathogenesis in Animal Research -- Surgical Treatment for Intracerebral Hemorrhage -- Pharmacologic and other Experimental Treatment for Intracerebral Hemorrhage -- Conclusion -- Key References -- References -- 9 White Matter Pathophysiology -- Key Points -- White Matter Anatomy and Physiology -- Model Systems for Studying White Matter Ischemia -- Cell Culture -- In vitro Tissue Models -- In vivo Models -- Effects of Ischemia on White Matter -- Derangement of Transmembrane Ion Gradients -- The Ca2+ Hypothesis and Anoxic-Ischemic White Matter Injury -- Mechanisms of White Matter Injury -- Ca2+ Entry and Intracellular Ca2+ Release in Axons during Ischemia -- Reversal of Na+-Ca2+ Exchange -- Activation of Voltage-Gated Ca2+ Channels -- Activation of Intracellular Ca2+ Release -- Excitotoxic Pathways Injure Glia in White Matter -- Autoprotection in White Matter -- Strategies for Protecting White Matter from Anoxic-Ischemic Injury are Diverse -- Acknowledgments -- References -- 10 Inflammation and Immune Response -- Key Points -- Cerebral Ischemia, Cytokines, and Inflammation -- Mechanisms by Which Inflammation Contributes to Ischemic Brain Injury -- Immune Cells Participating in Ischemic Injury and Tissue Repair -- Microglia, Monocytes/Macrophages, and Dendritic Cells -- Neutrophils -- Mast Cells -- Lymphocytes. , Danger Sensors: Scavenger Receptors and Toll-Like Receptors. , English

Additional Edition: ISBN 1-336-23984-0

Additional Edition: ISBN 0-323-32805-9

Language: English