Titlebook: Cerebral Ischemia and Basic Mechanisms; Alexander Hartmann,Frank Yatsu,Wolfgang Kuschinsky Conference proceedings 1994 Springer-Verlag Ber

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Anoxic Injury of Central Myelinated Axons: Nonsynaptic Ionic Mechanismsd axons. We have been interested in the pathophysiology of CNS axonal injury and have developed a reliable model system for studying the basic mechanisms of injury to CNS-myelinated axons caused by anoxia (Stys et al. 1990a; Ransom et al. 1993). The nonsynaptic ionic mechanisms which are critical in

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Uncoupling of Flow and Metabolism in Early Ischemic Stroketive for different therapeutic approaches: one short period during which improvement of perfusion is successful in reversing functional deficits and preventing morphological damage, and a probably longer period during which the progressive infarction could be ameliorated by intervention with ongoing

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Head Injuries: A Target for Neuroprotection and the increasing frequency with which younger patients are injured. There is evidence from several sources that ischaemic brain damage is the most important component of secondary brain damage either due to cerebral compression, or from poor oxygenation and perfusion, due to post-traumatic lung o

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Aspects of Acid-Base Homeostasis in Ischemia damage resulting from inadequate oxygen supply to the brain or head trauma (see Rosner and Becker 1984 for review). Intracellular acidosis has been extensively investigated and nuclear magnetic resonance spectroscopy has provided new insights (Siesjo 1985; Allen et al. 1988), but it is also importa

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In Vivo Nuclear Magnetic Resonance Observation of Cerebral Metabolismlular environment to a greater and greater degree. Position emission tomography (PET) and single photon emission computed tomography (SPECT) have provided important information on cerebral blood flow, metabolism, and receptor distributions. Here we review the recent improvements in nuclear magnetic