FENG / Feng / Mao Early Brain Injury or Cerebral Vasospasm

Vol 1: Pathophysiology
2011
ISBN: 978-3-7091-0353-1
Verlag: Springer Wien
Format: PDF
Kopierschutz: Wasserzeichen (»Systemvoraussetzungen)

E-Book, Englisch, Band 110/1, 256 Seiten, eBook

Reihe: Acta Neurochirurgica Supplement

More than 40 articles provide an extensive coverage of clinical and basic science advances over the last three years of research on subarachnoid hemorrhage-induced brain injuries. Early brain injury, the new frontier of subarachnoid hemorrhage research, which may be a key contributor to the high mortality and morbidity, promotes collaborative efforts from neurosurgery, neurology, neuro-ICU into other interrelated fields and basic neurosciences. For the first time, subarachnoid hemorrhage research is almost equally divided by early brain injury and cerebral vasospasm, mechanistic investigations and therapeutic approaches, demonstrating a translational feature of the future direction.

Zielgruppe

Research

Autoren/Hrsg.

Feng, Hua

Mao, Ying

FENG, HUA

Zhang, John H.

Inhaltsverzeichnis

1;Preface;6
2;Acknowledgement;8
3;Contents;10
4;Part I: Advances in Subarachnoid Hemorrhage and Cerebral Vasospasm;14
4.1;Section I: Honored Guest & Honored Speaker Speeches;15
4.1.1;A Clinical Review of Cerebral Vasospasm and Delayed Ischaemia Following Aneurysm Rupture;16
4.1.2;New Regulatory, Signaling Pathways, and Sources of Nitric Oxide;18
4.2;Section II: Advances in Subarachnoid Hemorrhage Research;24
4.2.1;Advances in Experimental Subarachnoid Hemorrhage;25
4.2.2;Advances in Treatment of Cerebral Vasospasm: an Update;32
4.2.3;Roles of Signal Transduction Mechanisms in Cerebral Vasospasm Following Subarachnoid Hemorrhage: Overview;36
5;Part II: Mechanistic Studies;40
5.1;Section III: Early Brain Injury After Subarachnoid Hemorrhage;41
5.1.1;Hypoperfusion in the Acute Phase of Subarachnoid Hemorrhage;42
5.1.2;Association of APOE Polymorphism with the Change of Brain Function in the Early Stage of Aneurysmal Subarachnoid Hemorrhage;46
5.1.3;Apoptotic Mechanisms for Neuronal Cells in Early Brain Injury After Subarachnoid Hemorrhage;50
5.1.4;Early Micro Vascular Changes After Subarachnoid Hemorrhage;56
5.1.5;Immunological Response in Early Brain Injury After SAH;63
5.1.6;Mechanisms of Early Brain Injury After SAH: Matrixmetalloproteinase 9;68
5.1.7;Tyrosine Phosphatase Inhibition Attenuates Early Brain Injury After Subarachnoid Hemorrhage in Rats;71
5.1.8;Protection of Minocycline on Early Brain Injury After Subarachnoid Hemorrhage in Rats;75
5.1.9;Role of Osteopontin in Early Brain Injury After Subarachnoid Hemorrhage in Rats;79
5.1.10;Matrix Metalloproteinase 9 Inhibition Reduces Early Brain Injury in Cortex After Subarachnoid Hemorrhage;84
5.2;Section IV: Nitric Oxide & Cortical Spreading Depolarization After Subarachnoid Hemorrhage;88
5.2.1;Nitric Oxide Synthase Inhibitors and Cerebral Vasospasm;89
5.2.2;The Role of Nitric Oxide Donors in Treating Cerebral Vasospasm After Subarachnoid Hemorrhage;94
5.2.3;Nitric Oxide in Early Brain Injury After Subarachnoid Hemorrhage;99
5.2.4;Nitric Oxide Related Pathophysiological Changes Following Subarachnoid Haemorrhage;104
5.2.5;Endothelin-1(1–31) Induces Spreading Depolarization in Rats;109
5.2.6;The Gamut of Blood Flow Responses Coupled to Spreading Depolarization in Rat and Human Brain: from Hyperemia to Prolonged Ischemia;116
5.2.7;Cerebral Microdialysis in Acutely Brain-Injured Patients with Spreading Depolarizations;122
5.3;Section V: Pathophysiology of Cerebral Vasospasm;128
5.3.1;Mitogen-Activated Protein Kinases in Cerebral Vasospasm After Subarachnoid Hemorrhage: A Review;129
5.3.2;Association of Apolipoprotein E Polymorphisms with Cerebral Vasospasm After Spontaneous Subarachnoid Hemorrhage;136
5.3.3;Impact of Subarachnoid Hemorrhage on Local and Global Calcium Signaling in Cerebral Artery Myocytes;140
5.3.4;Enhanced Angiogenesis and Astrocyte Activation by Ecdysterone Treatment in a Focal Cerebral Ischemia Rat Model;146
5.3.5;Bilirubin Oxidation Products Seen Post Subarachnoid Hemorrhage Have Greater Effects on Aged Rat Brain Compared to Young;151
5.3.6;Preliminary Results of an ICP-Controlled Subarachnoid Hemorrhage Rabbit Model for the Study of Delayed Cerebral Vasospasm;157
5.3.7;PKGIa Inhibits the Proliferation of Cerebral Arterial Smooth Muscle Cell Induced by Oxyhemoglobin After Subarachnoid Hemorrhage;160
5.3.8;Characteristics of In Vivo Animal Models of Delayed Cerebral Vasospasm;165
5.3.9;Endothelin Related Pathophysiology in Cerebral Vasospasm: What Happens to the Cerebral Vessels?;168
5.3.10;Expression and Role of COMT in a Rat Subarachnoid Hemorrhage Model;172
5.4;Section VI: Clinical Manifestations of Subarachnoid Hemorrhage;179
5.4.1;Monitoring of the Inflammatory Response After Aneurysmal Subarachnoid Haemorrhage in the Clinical Setting: Review of Literature and Report of Preliminary Clinical Experience;180
5.4.2;Perimesencephalic Subarachnoid Hemorrhage: Risk Factors, Clinical Presentations, and Outcome;186
5.4.3;The Relationship Between IL-6 in CSF and Occurrence of Vasospasm After Subarachnoid Hemorrhage;191
5.4.4;Non-Aneurysm Subarachnoid Hemorrhage in Young Adults;197
5.4.5;Cardiac Damage After Subarachnoid Hemorrhage;202
5.4.6;Analysis on Death-Associated Factors of Patients with Subarachnoid Hemorrhage During Hospitalization;206
5.4.7;Clinical Study of Changes of Cerebral Microcirculation in Cerebral Vasospasm After SAH;211
5.4.8;Effect of Weekend Admission on in-Hospital Mortality After Subarachnoid Hemorrhage in Chongqing China;215
5.4.9;The Correlation Between COMT Gene Polymorphism and Early Cerebral Vasospasm After Subarachnoid Hemorrhage;219
5.4.10;Fever Increased In-Hospital Mortality After Subarachnoid Hemorrhage;225
5.4.11;Subarachnoid Hemorrhage in Old Patients in Chongqing China;230
6;Author Index;234
7;Subject Index;236
8;Table of Contents for Vol. 1;242
9;Table of Contents for Vol. 2;246