Mechanisms of Secondary Brain Damage (häftad)
Format
Häftad (Paperback / softback)
Språk
Engelska
Antal sidor
165
Utgivningsdatum
2012-01-24
Upplaga
Softcover reprint of the original 1st ed. 1993
Förlag
Springer Verlag GmbH
Medarbetare
Baethmann, Alexander (ed.), Kempski, Oliver (ed.), Schürer, Ludwig (ed.)
Illustrationer
VIII, 165 p.
Dimensioner
279 x 210 x 10 mm
Vikt
418 g
Antal komponenter
1
Komponenter
1 Paperback / softback
ISBN
9783709192689
Mechanisms of Secondary Brain Damage (häftad)

Mechanisms of Secondary Brain Damage

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Häftad Engelska, 2012-01-24
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Great progress has been made in the understanding and prevention of secondary brain damage from acute cerebral disorders, such as trauma and ischemia. Advances may be concerned in particular with better organization and logistics of preclinical emergency care, including rapid arrival of well-trained medical staff on the scene of an accident and of transportation to a competent hospital. Nevertheless, it is a safe assumption that development of secondary brain damage from both intra- and extracranial causes still represents a major factor for the final outcome in severe head injury. Thus, exchanges of experiences and information between various disciplines involved with this important clinical problem - trauma still assumes the number one position as a cause of morbidity and mortality up to an age of 45 years - may provide a basis for in-depth analysis of remaining problems as well as of methods of their solution. This exactly is the purpose of the present publication on concepts and findings pertinent for the general subject of secondary brain damage from various experimental as well as clinical viewpoints. An internationally high-ranking group of experts has been contributing to this collection of reviews on cerebral trauma and ischemia and its adverse sequelae, including cerebral exploration by most modern technologies, such as NMR spectroscopy or PET scanning, among others.
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Innehållsförteckning

Brain Damage Studied by NMR and Other Methods.- NMR Spectroscopy: Current Status and Future Possibilities.- Cerebral Metabolic Studies in vivo by Combined 1H/31P and 1H/13C NMR Spectroscopic Methods.- NMR-Spectroscopic Investigation of Cerebral Reanimation After Prolonged Ischemia.- Magnetite as a Potent Contrast-Enhancing Agent in Magnetic Resonance Imaging to Visualize Blood-Brain Barrier Disruption.- Absent Recruitment of Capillaries in Brain Tissue Recovering from Stroke.- Quantification of Primary and Secondary Lesions in Severe Head Injury.- Traumatic Damage to the Nodal Axolemma: An Early, Secondary Injury.- Morphometrical Evaluation of Triflusal in Brain Infarction.- Mediators and Antagonism in Secondary Brain Damage.- In vivo and in vitro Regulation of Acid-Base Control of Brain Cells During Ischemic and Selective Acidic Exposure.- Mediators of Vascular and Parenchymal Mechanisms in Secondary Brain Damage.- Glutamate Receptor Antagonists in Experimental Focal Cerebral Ischaemia.- Cerebral Protection by Adenosine.- Effects of Acute Isotonic Saline Administration on Serum Osmolality, Serum Electrolytes, Brain Water Content and Intracranial Pressure.- Ischemia as an Excitotoxic Lesion: Protection Against Hippocampal Nerve Cell Loss by Denervation.- Recovery of Brain Function Following Ischemia.- Systematic Development of Cerebral Resuscitation After Cardiac Arrest. Three Promising Treatments: Cardiopulmonary Bypass, Hypertensive Hemodilution, and Mild Hypothermia.- Functional Consequences of Cerebral Lesions.- Taxonomy of Subjective Phenomena: a Neuropsychological Basis of Functional Assessment of Ischemic or Traumatic Brain Lesions.- Blood Flow and Clinical Course in Patients with Ischemic Stroke without Cerebrospecific Therapy.- Emergency Care and Treatment in Acute Cerebral Insults.- Assessment of Emergency Care in Trauma Patients.- C. Current Level of Prehospital Care in Severe Head Injury - Potential for Improvement.- Prehospital Management of Head Injuries: International Perspectives.- Management of Intracranial Hypertension in Head Injury: Matching Treatment with Cause.- Traumatic Brain Tissue Acidosis: Experimental and Clinical Studies.