Treatment of Cerebral Infarction: Experimental and Clinical Study

ISBN-13: 9783709188637 / Angielski / Miękka / 2012 / 385 str.

Jiro Suzuki

Opis

It is a great honor and pleasure for cerebral infarction have been carried me to have Springer-Verlag publish out. Dr. Yoshimoto hoped that the this volume entitled Treatment of results of research done in our depart Cerebral Infarction. I am much in ment over the last sixteen years con debted to my colleagues for my success cerning cerebral infarction could be in publishing this book. published. Moved by his enthusiasm, I have engaged in clinical work in my colleagues took their share in writ the field of neurosurgery for these few ing each article. I suggested to them decades and I have performed more that this volume should cover primarily than 5,000 major operations of intra the results of our own research, but that cranial surgery. Throughout this time, at the same time it should also include it has been my privilege to conduct a 2- the results of related work done by neurosurgical experts throughout the hour-morning research seminar in our department every Wednesday and to world. Therefore, I hope that this book supervise a great deal of research. At will interest many investigators who these seminars my fellow research have devoted themselves to research in workers and I have exchanged many the field of neuroscience. ideas about the study of neurosurgery My colleagues acknowledge that and we have designed many animal our research has been stimulated and experiments.

Spis treści

I Experimental Study.- 1. Experimental Models.- 1 1 Introduction.- 1.2 Cerebral Infarction Models.- 1.2.1 Experimental Models Using the Monkey.- 1.2.2 Experimental Models Using the Dog.- 1.2.3 Experimental Models Using the Cat.- 1.2.4 Experimental Models Using the Rat.- 1.2.5 Experimental Models Using the Gerbil.- 1.3 The Cerebral Infarction Model Developed in Sendai.- 1.3.1 Production of Various Cerebral Infarction Models in the Dog by Means of Occlusion of Intracranial Trunk Arteries.- 1.3.1.1 Thalamic Infarction Model.- 1.3.1.2 Cerebral Mantle Infarction Model.- 1.3.1.3 Complete Cerebral Hemisphere Infarction Model.- 1.3.1.4 Incomplete Cerebral Hemisphere Infarction Model.- 1.3.1.5 Complete Ischemic Brain Regulated with the Perfusion Method.- 1.3.2 A 3-Vessel Occlusion Model for Bilateral Hemispheric Infarction Using the Rat.- 1.3.2.1 Production of the Ischemia-Model.- 1.3.2.2 EEG Studies.- 1.3.2.3 Studies of the Cerebral Blood Flow Using Autoradiography.- 2. Histological Study.- 2.1 Introduction.- 2.2 Sequential Changes in Cerebral Ischemia.- 2.2.1 Sequential Changes in Focal Ischemia.- 2.2.1.1 Acute Stage Changes in an Ischemic Focus.- 2.2.1.2 Changes in the Ischemic Focus Following Acute Stage Recirculation.- 2.2.1.3 Changes in Ischemic Foci During the Subacute and Chronic Stages.- 2.2.2 Sequential Changes in Global Ischemia.- 2.2.2.1 Observations Using the Light Microscope.- 2.2.2.2 Observations Using the Electron Microscope.- 2.2.2.3 Observation Using the Freeze Fracture Method.- 3. Cerebral Blood Flow.- 3.1 Introduction.- 3.2 Correlation Between Regional EEG and rCBF.- 3.3 Regional Cerebral Hemodynamics Following Recirculation.- 3.3.1 Hemodynamics at the Center of an Ischemic Focus.- 3.3.2 Hemodynamics of the Border and Periphery of an Ischemic Focus.- 3.4 Sequential Changes in Vascular Reactivities.- 3.4.1 Autoregulation.- 3.4.1.1 Sequential Change in Autoregulation Occurring at the Center of an Ischemic Focus.- 3.4.1.2 Sequential Changes in Autoregulation at the Border and in the Periphery of an Ischemic Focus.- 3.4.2 CO2 Response.- 3.5 Hemorrhagic Infarction.- 3.5.1 Conditions Conductive to Hemorrhagic Infarction.- 3.5.2 Hemodynamics Following Recirculation.- 4. Ischemic Brain Edema.- 4.1 Introduction.- 4.1.1 The Definition of Ischemic Brain Edema.- 4.1.2 Pathophysiology of Ischemic Brain Edema.- 4.1.2.1 Causal Factors.- 4.1.2.2 The Onset and Natural Course of Ischemic Brain Edema.- 4.1.2.3 Ischemic Brain Edema Following Recirculation.- 4.1.2.4 The Disappearance of Edema.- 4.1.3 The Treatment of Ischemic Brain Edema.- 4.1.3.1 General Therapeutic Steps.- 4.1.3.2 Drug Therapy.- 5. Cerebral Metabolism and Free Radical Pathology.- 5.1 Introduction.- 5.2 Phospholipids as Biomembrane Constituents.- 5.3 Ca2+ Homeostasis.- 5.4 Lipid Metabolism in Cerebral Ischemia.- 5.5 The Free Radical Reaction in Cerebral Ischemia.- 5.5.1 Fundamental Knowledge Concerning Free Radicals.- 5.5.2 Lipid Peroxidation.- 5.5.3 Detection of Free Radicals.- 5.5.3.1 Chemiluminescence.- 5.5.3.2 Electron Spin Resonance (ESR).- 5.5.4 Initiators of Autoxidative Lipid Peroxidation.- 5.5.4.1 Superoxide Anion $$\left( {{{\text}_{\text}}\bar \cdot } \right)$$.- 5.5.4.2 Hydroxy Radical (OH ·).- 5.5.4.3 Oxygen-Metal Complexes.- 5.5.4.4 Singlet Oxygen (1O2).- 5.5.5 Energy Metabolism and Free Radical Generation.- 5.5.6 The Problem of “Intra-Ischemic Peroxidation” and “Post-Ischemic Peroxidation”.- 5.6 Pharmacological Mechanisms of Mannitol, Vitamin E, Glucocorticoids and Phenytoin.- 5.6.1 Mannitol.- 5.6.2 Vitamin E (?-tocopherol).- 5.6.3 Glucocorticoids.- 5.6.4 Combined Therapy with Mannitol, Vitamin E and Glucocorticoid.- 5.6.5 Phenytoin (Aleviatin).- 6. The Development of New Brain Protective Agents.- 6.1 Introduction.- 6.2 Brain Protective Agents—Short Review.- 6.2.1 Barbiturates.- 6.2.2 Naloxone.- 6.2.3 Prostaglandins and Indomethacin.- 6.3 Development of a New Brain Protective Substance—Our Study.- 6.3.1 Mannitol.- 6.3.1.1 The Effect of Mannitol on Cerebral Ischemia—Histological Study.- 6.3.1.2 Recirculation in the Acute Period of Cerebral Infarction: Brain Swelling and Its Suppression Using Mannitol.- 6.3.1.3 The Effect of Mannitol on Cerebral Ischemia—CBF Study.- 6.3.2 Perfluorochemicals (PFC).- 6.3.2.1 Introduction.- 6.3.2.2 PFC and Brain Tissue Partial Oxygen Pressure (PtO2).- 6.3.3 Combined Administration of Mannitol and PFC.- 6.3.3.1 Recovery of Brain Electrical Activity in the Severely Ischemic Brain.- 6.3.3.2 Suppression of Hemorrhagic Infarction.- 6.3.4 The Protective Effects of Various Free Radical Scavengers.- 6.3.5 Combined Administration of Mannitol, Vitamin E, Dexamethasone and PFC.- 6.3.5.1 Experimental Results: Untreated Control Group (22 Dogs).- 6.3.5.2 Drug-Treated Animals (61 Dogs).- 6.3.6 Phenytoin (Aleviatin).- 6.3.7 Calcium Antagonist (Flunarizine).- II Clinical Study.- 7. Epidemiology and Symptomatology.- 7.1 Introduction.- 7.2 The Natural Course of the Acute Stage of Cerebral Infarction: a Study of 1,000 Cases.- 7.2.1 Analysis of 1,000 Cases: Prognosis.- 7.2.1.1 Description of the 1,000 Cases.- 7.2.1.2 Lesion Site and Outcome.- 7.2.1.3 Age and Prognosis.- 7.2.1.4 Study of Fatalities.- 7.2.2 Occlusion of the Internal Carotid Artery.- 7.2.2.1 ICA Occlusion and Prognosis.- 7.2.2.2 Acute Stage Disturbances of Consciousness and Prognosis.- 7.2.2.3 Acute Stage Motor Deficits and Prognosis.- 7.2.2.4 CT Findings in ICA Occlusion.- 7.2.2.5 Fatalities Among the ICA Cases.- 7.2.3 Occlusion of the Middle Cerebral Artery.- 7.2.3.1 MCA Occlusion and Prognosis.- 7.2.3.2 Acute Stage Disturbances of Consciousness and Prognosis.- 7.2.3.3 Acute Stage Motor Deficits and Prognosis.- 7.2.4 Ischemic Cerebrovascular Disease Without Positive Angiographical Findings.- 7.2.4.1 Relationship to Prognosis.- 7.2.4.2 Acute Stage Neurological Deficits and Prognosis.- 7.2.4.3 CT Findings.- 8. Diagnostic Techniques.- 8.1 Introduction.- 8.2 Techniques for Obtaining Information Concerning the Cerebral Vessels.- 8.2.1 Cerebral Angiography Using the Direct Puncture and Seldinger’s Methods.- 8.2.2 Digital Subtraction Angiography (DSA).- 8.3 Techniques for Obtaining Morphological Information.- 8.3.1 X-ray Computerized Tomography (CT).- 8.3.1.1 Low Density Areas.- 8.3.1.2 Mass Signs Due to Cerebral Edema.- 8.3.1.3 Cerebral Atrophy.- 8.3.1.4 Contrast Enhancement Effects.- 8.3.1.5 High Density Areas.- 8.3.2 Nuclear Magnetic Resonance Computed Tomography (NMR-CT).- 8.4 Techniques for Obtaining Information Concerning Cerebral Blood Flow and Metabolism.- 8.4.1 Two-dimensional Measurement Techniques.- 8.4.2 Three-dimensional Measurement Techniques.- 8.4.2.1 Dynamic CT.- 8.4.2.2 The Stable Xenon-enhanced CT Technique.- 8.4.2.3 Single Photon Emission CT Scanning (SPECT).- 8.4.2.4 PET Scanning.- 8.4.3 The Pathophysiology of Cerebral Infarction as Seen from Measurements of Cerebral Blood Flow and Metabolism.- 9A. Medical Treatment of Cerebral Infarction.- 9A.1 Introduction.- 9A.2 Control of Blood Pressure.- 9A.2.1 Control of Blood Pressure in the Acute Stage.- 9A.2.2 Control of Blood Pressure in the Chronic Stage.- 9A.3 Treatment to Suppress Cerebral Edema.- 9A.3.1 Hypertonic Solutions.- 9A.3.2 Corticosteroids.- 9A.4 Antithrombotic Therapy.- 9A.4.1 Antiplatelet Agents.- 9A.4.2 Anticoagulants.- 9A.4.3 Thrombolytic Agents.- 9A.5 Facilitators of Cerebral Blood Flow.- 9A.5.1 Cerebral Vasodilators.- 9A.5.2 Low Molecular Weight Dextran (Dextran 40).- 9A.5.3 Exsanguination.- 9A.6 Activators of Cerebral Metabolism.- 9A.7 Cerebral Protective Agents.- 9A.7.1 Barbiturate Therapy.- 9A.7.2 The Sendai Cocktail.- 9A.7.3 Other Drugs with Protective Effects on the Brain.- 9B. Surgical Treatment for Cerebral Infarction.- 9B.1 Introduction.- 9B.2 Surgical Treatment for Occlusive Diseases of the Extracranial Carotid Arteries.- 9B.2.1 Internal Carotid Endarterectomy (ICEA).- 9B.2.2 External Carotid Endarterectomy (ECEA).- 9B.2.3 Stumpectomy.- 9B.2.4 Tortuosity, Coiling and Kinking.- 9B.3 Surgical Therapy for Occlusive Lesions of the Extracranial Vertebral Artery.- 9B.4 Intracranial Vascular Reconstruction.- 9B.4.1 Vascular Reconstruction of the Anterior Circulation.- 9B.4.2 Vascular Reconstruction of the Posterior Circulation.- 9B.4.3 Vein Grafts.- 9C. Revascularization in Acute Stage.- 9C.1 Introduction.- 9C.2 Surgical Therapy in the Acute Stage of Major Stroke Cases.- 9C.3 Acute Stage Vascular Reconstruction Using the “Sendai Cocktail”—Our Series of Patients.- 9C.3.1 Treatment and Indication.- 9C.3.2 Materials.- 9C.3.3 Results.- 9C.3.3.1 Overall Results.- 9C.3.3.2 Results of Cases of Thrombosis and Embolism.- 9C.3.4 Conclusion.- 9C.4 Acute Vascular Reconstruction for Progressing Stroke.- 9C.5 The Present Series of Progressing Stroke Cases.- III Appendixes.- 10. Temporary Occlusion of Trunk Arteries of the Brain During Surgery.- 10.1 Introduction.- 10.2 Decrease in Cerebral Blood Flow Due to Temporary Clipping and Countermeasures—the Development of Methods to Prolong the Safe Time Limit for Vascular Occlusion.- 10.3 Damage to the Vascular Wall Due to the Temporary Clip.- 11. The Pathology of Cerebral Vasospasms and Its Treatment.- 11.1 Introduction.- 11.2 The Pathology of Cerebral Vasospasm.- 11.3 Mechanisms of Onset and Causal Factors of Vasospasm.- 11.4 Treatment of Cerebral Vasospasm.- 11.4.1 Drug Therapy.- 11.4.2 Surgical Treatment.- 11.4.3 Our Procedure for Prevention and Treatment.- 12. Surgical Therapy for Moyamoya Disease.- 12.1 Introduction.- 12.2 The Characteristic Pathophysiology of Moyamoya Disease.- 12.3 Surgical Therapy for Ischemic Moyamoya Disease.- 12.3.1 Durapexia.- 12.3.2 Cervical Perivascular Sympathectomy and Superior Cervical Ganglionectomy.- 12.3.3 Superficial Temporal Artery-Cortical Branch of the Middle Cerebral Artery Anastomosis (STA-MCA Anastomosis) and Encephalo-myo-synangiosis (EMS).- 12.3.4 Transplantation of Omentum.- 12.3.5 Encephalo-Duro-Arterio-Synangiosis (EDAS).- 12.3.6 Other Techniques for Improving Cerebral Blood Flow.- 12.4 Our Own Therapeutic Technique: Cervical Perivascular Sympathectomy (PVS) and Superior Cervical Ganglionectomy (SCG).- 12.4.1 The Surgical Method.- 12.4.2 Follow-up Clinical Symptoms.- 12.4.3 Angiographical Follow-up.- 12.4.4 Electroencephalographical Follow-up.- 12.4.5 The Effects of PVS and SCG, as Monitored During Surgery.- 12.5 Anesthesia, Pre- and Postoperative Management in Moyamoya Disease.- 12.5.1 Study of the “Re-build Up” Phenomenon Using EEG, Angiography and PET.- 12.5.2 Anesthesia, Pre- and Postoperative Management.- References.- 1.- 2.- 3.- 4.- 5.- 6.- 7.- 8.- 9A.- 9B.- 9C.- 10.- 11.- 12.