Treatment of Cerebral Infarction

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.

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 $$\left( {{{\text{O}}_{\text{2}}}\bar \cdot } \right)$$.- 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.