상세정보

Intro -- Contents -- Part I: Stroke Epidemiology-Diagnosis -- Chapter 1: Stroke Therapy Development Successes: Research Guidelines and Embolic Stroke Models for Monotherapy and Adjuvant Therapy Development -- 1.1 Introduction -- 1.2 Chronological Successes -- 1.2.1 Thrombolysis -- 1.2.2 Select rt-PA Clinical Trials -- 1.2.3 Thrombolysis Cost-Effectiveness (USA Compared to China) -- 1.2.4 Endovascular Procedures -- 1.2.4.1 Summary of MR CLEAN -- 1.2.4.2 Summary of ESCAPE -- 1.2.4.3 Summary of REVASCAT -- 1.2.4.4 Summary of SWIFT PRIME -- 1.2.4.5 Summary of EXTEND-IA -- 1.2.4.6 Summary of THRACE -- 1.2.4.7 Cumulative Summary -- 1.2.4.8 Patient Selection and Treatment -- 1.2.5 Cost-Effectiveness -- 1.3 Future Stroke Therapy Development -- 1.3.1 Translational Research to Complement Existing Clinical Practice -- 1.3.2 Option 1: Rabbit Embolic Stroke Model [81, 82, 92–95] -- 1.3.2.1 No Anesthetic or Analgesic Interference [81] -- 1.3.2.2 Use of a Heterogeneous Population Endpoint -- 1.3.2.3 Clinically Relevant Endpoint -- 1.3.2.4 Positive Controlled Studies -- 1.3.2.5 Combination Drug Testing for Efficacy and Safety -- 1.3.2.6 Cost-Effective Analysis -- 1.3.3 Option 2: Rodent Embolic Stroke Model [122, 123] -- 1.4 Conclusions -- References -- Chapter 2: Recent Success with Endovascular Stroke Therapy -- 2.1 Introduction -- 2.2 Evolution of Endovascular Techniques -- 2.3 Endovascular Trials: Path to Success -- 2.3.1 First-Generation Neutral Trials -- 2.3.2 Second-Generation Landmark Trials -- 2.4 Factors Involved in Success of Endovascular Trials -- 2.4.1 Patient Selection Based on Neuroimaging -- 2.4.2 State-of-the-Art Mechanical Thrombectomy Devices -- 2.4.3 Quality Metrics for Revascularization -- 2.4.4 Speed of Revascularization -- 2.5 Future Trends -- 2.6 Conclusion -- References -- Chapter 3: Stroke Epidemiology -- 3.1 Introduction -- 3.1.1 Ischemic Stroke -- 3.1.2 Hemorrhagic Stroke -- 3.2 Stroke Morbidity and Mortality -- 3.3 Risk Factors -- 3.4 Conclusion -- References -- Chapter 4: Pathophysiology of Ischemic Stroke -- 4.1 Introduction -- 4.2 Altered Ion Balance -- 4.2.1 Ionic Changes Following Ischemic Stroke over Time -- 4.2.1.1 Na+-K+ Pump Dysfunction and Increased Intracellular Na+ -- 4.2.1.2 Calcium Overload -- 4.2.1.3 Acid-Sensing Ion Channels -- 4.2.2 Peri-infarct Depolarization -- 4.3 Altered Cell Energy and Metabolism Activity -- 4.3.1 Decreased ATP and pH Levels -- 4.3.2 Excitotoxicity Response to Ischemic Stroke -- 4.3.3 Global Inhibition of Protein Synthesis and Changes in Protein Kinase and Phosphatases -- 4.4 Increased Free Radical Generation During and After Ischemia -- 4.5 Cell Changes and Death During and After Ischemic Stroke -- 4.5.1 Apoptotic Cell Death -- 4.5.2 Necrotic Cell Death -- 4.5.3 Autophagy in Cell Death -- 4.6 Blood-Brain Barrier Pathophysiology Following Ischemic Stroke -- 4.7 Inflammation in Ischemic Stroke -- 4.8 Summary -- References -- Chapter 5: Pathophysiology of Hemorrhagic Stroke -- 5.1 Introduction -- 5.