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.

Table of Contents:
ForewordAcknowledgmentsAbbreviationsChapter 1 History I. Introduction II. Clinical Description III. Pathology IV. Radiology A. Angiography B. Computed Tomography C. Blood Flow Measurements D. Transcranial Doppler V. Medical Aspects A. Hemodynamic Therapy B. Avoidance of Adverse Factors C. Vasodilator and Neuroprotectant Medication VI. Etiology VII. Surgical Aspects A. Clot Removal B. Timing of Surgery C. Angioplasty VIII. Physiology IX. State of the Art X. Farewell Message ReferencesChapter 2 Epidemiology I. Introduction II. Incidence of Subarachnoid Hemorrhage III. Incidence of Vasospasm IV. Timing of Angiography and Incidence of Vasospasm V. Prognostic Factors for Vasospasm A. Blood on CT Scan B. Hypertension C. Anatomical and Systemic Factors D. Clinical Grade E. Antifibrinolytics F. Age and Sex G. Smoking H. Physiological Parameters I. Hydrocephalus VI. Factors Unrelated to Vasospasm VII. Effect of Vasospasm on Outcome VIII. Influence of Surgery on Vasospasm IX. Relative Significance of Vasospasm X. Vasospasm and Cerebral Infarction XI. The Incidence of Vasospasm over Time XII. Vasospasm and Nonaneurysmal Subarachnoid Hemorrhage A. Nonaneurysmal Subarachnoid Hemorrhage B. Arteriovenous Malformations C. Other Causes XIII. Endovascular Coiling and Vasospasm ReferencesChapter 3 Hematology I. Introduction II. Blood A. Cellular Elements B. Plasma C. Erythrocytes D. Endothelial Cells E. Platelets F. Neutrophils G. Mast Cells and Basophils H. Eosinophils I. Monocytes and Macrophages J. Lymphocytes III. Coagulation A. Coagulation Pathways B. Coagulation Inhibitors C. Anticoagulants D. Fibrinolytics E. Antifibrinolysis F. Thrombin ReferencesChapter 4 Pathology and Pathogenesis I. Introduction II. The Subarachnoid Space, Pia-arachnoid, Arachnoid Villi, and Cerebrospinal Fluid A. Subarachnoid Space and Pia-Arachnoid B. Arachnoid Villi C. Cerebrospinal Fluid III. Cytopathology of Cerebrospinal Fluid and Subarachnoid Hemorrhage A. Cellular Responses B. Red Blood Cell Clearance IV. Arterial Changes in Vasospasm A. Systemic Arterial Response to Injury B. Morphometry of Vasospasm C. Pathology of Arteries in Vasospasm D. Changes in Arterial Innervation E. Arterial Wall Barrier Disruptions F. The Functional Significance of Morphologic Changes G. Blood-Brain Barrier V. Changes in Composition of Cerebrospinal Fluid, Blood, and Adjacent Tissues A. Cerebrospinal Fluid B. Changes in Blood Serum and Plasma C. Changes in Vessel Wall, Leptomeningeal Cells, Brain, and Clot VI. Cerebral Infarction from Vasospasm A. Physiology of Aneurysmal Rupture and Vasospasm B. Impairment of Autoregulation C. Cerebral Edema D. Cerebral Volume Changes E. Cerebrospinal Fluid and Intracranial Pressure F. Cerebral Blood Flow G. Cerebral Metabolism H. Histopathology I. Clinical Studies of Infarction ReferencesChapter 5 Radiology I. Introduction II. Angiography A. Definition and Classification of Angiographic Vasospasm B. Method of Diagnosis C. Clinical Series D. Very Delayed Vasospasm E. Nonaneurysmal Vasospasm F. Acute Angiographic Vasospasm G. Vertebrobasilar Vasospasm H. Operation and Vasospasm I. The Venous System and Vasospasm J. Automated Assessment K. Mean Transit Time and the Intraparenchymal Circulation L. Extradural Vasospasm III. CT Scan A. Early Demonstration of Subarachnoid Hemorrhage B. Duration of Subarachnoid Hemorrhage on CT Scan C. Relationship of Subarachnoid Hemorrhage on CT Scan to Angiographic Vasospasm and Infarction D. Relationship of Blood on CT Scan to Hydrocephalus E. Computed Tomographic Prognostic Factors for Poor Outcome F. Computed Tomographic Demonstration of Ischemic and Hemorrhagic Infarction G. Quantification of Degree of Subarachnoid Hemorrhage on CT Scan H. Time Course of Low-Density Areas on CT Scan I. Demonstration of Rebleeding on CT Scan J. Effect of Nimodipine on Infarction K. The Basal Cisterns in Subarachnoid Hemorrhage L. Computed Tomographic Findings in Patients Dying Early from Subarachnoid Hemorrhage M. Seizures N. Coiling of Aneurysms O. Contrast Enhancement P. Computed Tomographic Angiographic Direct Demonstration of Vasospasm IV. Transcranial Doppler Ultrasonography A. History B. Technical Aspects C. Normal Values and Indices D. Time Course of Velocity Changes E. Velocity Changes and Angiographic Vasospasm F. Velocity Changes and Distal Angiographic Vasospasm G. Velocities, Delayed Ischemic Deficits, and Infarction in Clinical Studies H. Clinical Factors Affecting Velocities I. Effect of Age on Velocities J. Velocities and Blood Pressure K. Velocities and Physiological Parameters L. Velocity Changes during Aneurysmal Rupture M. Velocity Changes during Brain Death N. Velocity Changes Correlated with Angiographic Diameter O. Velocity Changes Correlated with Single Photon Emission Computed Tomography Studies P. The Effect of Hyperosmotic Agents on Velocities Q. The Transient Hyperemic Response R. Intracranial Pressure and Velocities S. Cerebral Blood Flow and Velocities T. Velocities in Traumatic Subarachnoid Hemorrhage U. Velocities and Angioplasty V. The Clinical Value of Transcranial Doppler Ultrasonography V. Magnetic Resonance Imaging A. Basic Mechanisms B. Clinical Series C. Imaging Techniques D. Diffusion-Weighted Imaging E. Magnetic Resonance Spectroscopy F. Magnetic Resonance Angiography G. Advantages and Disadvantages VI. Positron Emission Tomography A. Changes with Vasospasm B. Flow and Metabolism with Infarction C. Oxygen Delivery VII. Single Photon Emission Computed Tomography A. History B. Technique C. Findings in Vasospasm D. Activation Studies (Induced Parenchymal Vasodilation) E. Postoperative Changes F. Angioplasty G. Attempted Quantification H. Eclampsia I. Comparative Studies VIII. Cerebral Blood Flow Studies A. 133Xe Studies B. Xe CT Studies ReferencesChapter 6 Pharmacology I. Introduction II. General Considerations A. Experimental Variables B. Hypoxia III. Neurogenic Factors A. Adrenergic Nerves B. Cholinergic Nerves C. Intracerebral Pathways D. Effect of Subarachnoid Hemorrhage on Nerves E. Effect of Electrical Stimulation IV. Biogenic Amines A. Definitions B. Catecholamines C. Norepinephrine as a Potential Spasminogen D. Human Studies E. Serotonin (5-Hydroxytryptamine) F. Acetylcholine G. Histamine V. Neuropeptide Transmitters A. Tension Experiments B. Effects of SAH C. Intracisternal Injections D. Human Studies E. Bradykinin VI. Eicosanoids A. Biochemistry B. Prostaglandins C. Thromboxanes D. Leukotrienes VII. Endothelin A. History B. Basic Science C. Putative Spasmogens D. Vasoconstriction E. Pharmacological Interactions VIII. Blood and Cerebrospinal Fluid A. Circulating Factors B. Blood Derivatives C. Studies of CSF after Subarachnoid Hemorrhage D. Thrombin E. Fibrin and Fibrinogen Degradation Products F. Bilirubin G. Iron H. Adenosine Triphosphate IX. Hemoglobin A. Overview with Subarachnoid Hemorrhage B. Biochemistry C. Heme, Hemin, and Hematin D. In Vitro Studies E. Hemoglobin and Isolated Cells F. In Vitro Long-Term Studies G. Spectrophotometric Experiments H. Attempted Reversal of Hemoglobin-Induced Vasoconstriction I. Hemoglobin Interactions J. Ultrapure Hemoglobin K. Heme Oxygenase L. Hemoglobin and Arterial Wall M. Endothelin and Hemoglobin N. Endothelium-Derived Hyperpolarizing Factor X. Nitric Oxide A. Nitric Oxide as a Vasodilator B. Injury Induced by Nitric Oxide C. Nitric Oxide Synthase D. Nitric Oxide Synthase Inhibitors XI. Nitrovasodilators A. Mechanisms of Action B. Animal Models of Subarachnoid Hemorrhage C. Intrathecal Nitrovasodilators D. Effect on Vascular Smooth Muscle Cells XII. Free Radicals A. Oxygen and Free Radicals B. Superoxide Radical C. Hydroxyl Radical D. Nitric Oxide Radical E. Free Radicals and Stroke F. Production of Vasospasm by Free Radicals G. Effect of Free Radicals on Vascular Smooth Muscle H. Lipid Peroxidation I. Amino Steroids J. Oxidation of Hemoglobin K. Free Radical Scavengers XIII. Recent Novel Pharmacological Approaches ReferencesChapter 7 Structure, Physiology, and Biochemistry of Vascular Smooth Muscle I. Introduction II. Tension, Tone, and Work III. Structural Components A. Blood Vessel Walls B. Vascular Endothelium C. Vascular Smooth Muscle Cells IV. Actin and Myosin A. Sliding Filament Theory B. Structure and Interactions C. Rigor and Latch States V. Modulating Proteins A. Calmodulin B. Caldesmon C. Tropomyosin D. Calponin VI. Relaxation A. General B. Phosphatases VII. Calcium A. Regulation of Calcium in Vascular Smooth Muscle B. Force and Sarcoplasmic Calcium C. Plasmalemma and Calcium Control D. Sacroplasmic Reticulum and Calcium Control E. Calcium and Hemolysate F. Calcium and Oxyhemoglobin VIII. Enzymes, Receptors, and Messenger Systems A. Myosin Light Chain Kinase B. Protein Kinase C C. Tyrosine Kinase D. Mitogen-Activated Protein Kinase E. G Proteins F. Rho A G. Phosphatidylinositol Cascade and Diacylglycerol H. Inositol Phosphates and Hemoglobin I. cGMP J. cAMP IX. Membrane Potential A. General B. Calcium Channels C. Potassium Channels X. Acidosis and Hypoxia A. Acidosis B. Hypoxia XI. Growth and Contraction XII. Metabolism A. General B. Arterial Metabolism after Experimental Subarachnoid Hemorrhage ReferencesChapter 8 Medical Aspects of Vasospasm I. Introduction II. Diagnosis A. Symptoms B. Signs C. Laboratory Findings III. Differential Diagnosis A. Respiratory Complications B. Electrolyte Disorders C. Infection and Fever D. Cardiac Complications E. Hypertension and Hypertensive Encephalopathy F. Seizures G. Rebleeding H. Gastrointestinal Complications I. Endocrine J. Metabolic K. Intracranial Hypertension and Hydrocephalus IV. Prophylaxis A. Calcium Antagonists B. Models Using Calcium Antagonists C. Avoidance of Antifibrinolytics D. Avoidance of Dehydration E. Optimal Hematocrit F. Sickle Cell Disease G. Avoidance of Hypotension and Hypertension H. Salicylates I. Cisternal Drainage J. Fibrinolytics V. Management of Delayed Ischemic Deficit A. Monitoring for Delayed Ischemic Deficit B. Immediate Actions on Detection of Delayed Ischemic Deficit C. Likelihood of Delayed Ischemic Deficit Developing D. Delayed Ischemic Deficit after Coiling E. Neuroprotective Strategies VI. Therapy A. Hypertension B. Hypervolemia C. Hemodilution D. HHH E. Cerebral Blood Flow F. Clinical Series G. Complications H. Fluids I. Models of Hypertension and Hypervolemia J. Assessing Cardiac Function K. Reducing Intracranial Pressure L. Respiratory Support M. Angioplasty N. Nitrovasodilator Therapy VII. Randomized Clinical Trials VIII. The Art of Treatment ReferencesChapter 9 Nonruptured Aneurysm Vasospasm I. Postoperative Cases A. Pituitary Tumors B. Other Tumors II. Vascular Lesions A. Arteriovenous Malformations B. Unruptured Aneurysms C. Aneurysms with Very Delayed Onset of Vasospasm D. Benign Perimesencephalic Hemorrhage III. Head Injury A. Clinical Series B. Experimental IV. Infections V. Eclampsia A. Magnesium Sulfate B. Pathology C. Angiography D. Transcranial Doppler Sonography E. Magnetic Resonance Studies VI. Migraine Headaches as a Vasoconstrictor Phenomenon VII. Coronary Artery Vasospasm ReferencesChapter 10 Surgical Aspects of Vasospasm I. Surgical Trauma Mimicking or Aggravating Vasospasm II. Clot Removal at Surgery A. Clinical Series B. Models of Clot Removal III. Timing of Surgery and Vasospasm A. Optimal Timing B. Treatment in the Presence of Established Vasospasm IV. Cisternal Drainage V. Fibrinolytic Therapy and Surgery ReferencesChapter 11 Animal Models I. Introduction II. Models In Vitro III. Acute Effects of SAH versus VSP IV. Species Differences V. Considerations in the Conduct of Animal Studies VI. Creation of SAH VII. Specific Animal Models A. Mouse B. Rat C. Cat D. Rabbit E. Dog F. Pig G. Nonhuman Primate H. Other VIII. Ethical Considerations ReferencesChapter 12 Molecular Biology and Genetics I. Introduction II. Genetic Predisposition to Vasospasm III. Molecular Biological Techniques A. Transgenic and Knockout Mice B. Screening for Changes in Gene Expression IV. Changes in Regulatory Mechanisms of Smooth Muscle Contraction A. Smooth Muscle Contraction B. Contractile Proteins C. Protein Kinase C D. Calpains E. Tyrosine Kinases F. Mitogen-Activated Protein Kinases G. Other Mechanisms V. Changes in Smooth Muscle Relaxation Mechanisms VI. Changes in Endothelium-Regulated Mechanisms VII. Changes in Genes That May Influence Vasospasm A. Heme Oxygenases B. Immediate Early Genes C. Inflammation D. Remodeling, Fibrosis, Proliferation, and Phenotype Change E. Apoptosis VIII. Microvascular Spasm IX. Changes in the Brain X. Gene Therapy ReferencesIndex