Mechanisms of Secondary Brain Damage in Cerebral Ischemia and Trauma (Acta Neurochirurgica Supplement, 66)

The publication of the Vth International Symposium 1995 on "Mechanisms of Secondary Brain Damage" in Mauls/ltaly is a collection of focused reviews reaching from novel molecular- and cell biological findings to aspects of clinical management in head injury and cerebral ischemia. A specific purpose of these series of meetings introduced in 1984 is for an exchange on problems of mutual interest by international high ranking experts from the basic sciences and related clinical disciplines, such as intensive care medicine, neurology, or neurosurgery. The present volume covers three major areas: (a) Molecular and cell biological mechanisms including inflammation (b) Novel findings on mechanisms and treatment in cerebral ischemia (c) Secondary processes in head injury, regeneration and treatment Molecular-and cell biology is currently attracting attention towards activation of genomic processes associated with the demise of cells referred to as "programmed cell death" and "apoptosis" which, actually, might be distinguished from each other. Thus, the phenomenon of delayed neuronal death in selectively vulnerable brain areas following brief interruption of blood flow is scrutinized as to the contribution of the activation of suicide genes. The physiological role of such a response, among others, is removal of surplus neurons during ontogenesis of the brain. Yet, evidence is accumulating that similar mechanisms playa role in cerebral ischemia, probably also trauma, where nerve-and other cells demonstrate features of apoptosis. Observations on protection of neurons by administration of protein synthesis inhibitors in cerebral ischemia provide more direct support. Front Matter....Pages I-VIII Molecular Correlates of Delayed Neuronal Death Following Transient Forebrain Ischemia in the Rat....Pages 1-7 Molecular Mechanisms of Acidosis-Mediated Damage....Pages 8-14 Is Calcium Accumulation Post-Injury an Indicator of Cell Damage?....Pages 15-20 Apoptosis in Focal Cerebral Ischemia....Pages 21-26 Significance of the Inflammatory Response in Brain Ischemia....Pages 27-31 Leukocytes, Macrophages and Secondary Brain Damage Following Cerebral Ischemia....Pages 32-39 Inflammation of the Brain after Ischemia....Pages 40-43 Three-Dimensional Metabolic and Hemodynamic Imaging of the Normal and Ischemic Rat Brain....Pages 44-49 Origins of Glutamate Release in Ischaemia....Pages 50-55 Swelling, Intracellular Acidosis, and Damage of Glial Cells....Pages 56-62 Environmental Influence on Outcome After Experimental Brain Infarction....Pages 63-67 Fetal Neocortical Grafts Placed in Brain Infarcts Do Not Improve Paw-Reaching Deficits in Adult Spontaneously Hypertensive Rats....Pages 68-72 Extended Studies on the Effect of Glutamate Antagonists on Ischemic CA-1 Damage....Pages 73-75 Thrombolysis in Acute Ischemic Stroke....Pages 76-80 Traumatically Induced Axonal Damage: Evidence for Enduring Changes in Axolemmal Permeability with Associated Cytoskeletal Change....Pages 81-86 Expression of Microglial Markers in the Human CNS After Closed Head Injury....Pages 87-95 Altered β -APP Metabolism After Head Injury and its Relationship to the Aetiology of Alzheimer’s Disease....Pages 96-102 Principles of Neuronal Regeneration....Pages 103-106 Neuroprotective Efficacy of Microvascularly-Localized Versus Brain-Penetrating Antioxidants....Pages 107-113 “Small Volume Resuscitation” as Treatment of Cerebral Blood Flow Disturbances and Increased ICP in Trauma and Ischemia....Pages 114-117 Conduct of Head Injury Trials in the United States: The American Brain Injury Consortium (ABIC)....Pages 118-121 Back Matter....Pages 122-123 The publication is a progress report of the understanding of secondary brain damage from head injury and cerebral ischemia. The spectrum reaches from the molecular- and cell biological level up to the complex issues of clinical management. Specific topics on cerebral ischemia are concerned with apoptosis, inflammation, acidosis, cellular Ca2+-overflow, the role of the stimulatory input for maintenance of functional competence in stroke, effects of brain grafting in infarction, and the current state of glutamate antagonization or reestablishment of cerebral blood flow by thrombolysis, among others. Novel data on head injury relate with the cell biological response of the damaged axon, the activation of microglia, the role of b-amyloid precursor protein in the later development of Alzheimer's disease, and the current understanding of neuronal regeneration. Aspects of management and treatment have a spectrum from novel antioxidants to international consensus efforts