Mechanisms of Ischemic Brain Damage

  • O. Kempski
  • F. Staub
  • G.-H. Schneider
  • M. Zimmer
  • A. Baethmann


One of the pathophysiological consequences of cerebral sinus vein thrombosis (SVT) is hypoperfusion of circumscript brain areas drained by the occluded veins. In some of these territories the supply of blood may fall below a critical threshold, resulting in an ischemic or hypoxemic lesion. Experimental SVT is indeed characterized by a significant rise of tissue electrical impedance [1] as an indication of ischemic cell swelling. Therefore, treatment of patients with SVT may require anti-ischemic measures. Unfortunately, after decades of research on cerebral ischemia, there has been little progress in the development of specific treatment protocols. New information is now available on the pathophysiological mechanisms activated during and after an ischemic insult. Thus, based on recent findings, novel therapeutic approaches may become available in the near future. A thorough understanding of pathophysiological events should help to design specific therapeutic schemes. The subject of ischemic brain damage, however, is too complex to cover it completely in a short review. Therefore, this chapter intends to summarize recent concepts of pathophysiological interactions implicated in ischemic brain damage.


Free Fatty Acid Brain Damage Ischemic Brain Damage Transient Cerebral Ischemia Neurochemical Pathology 
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Copyright information

© Springer Science+Business Media New York 1990

Authors and Affiliations

  • O. Kempski
    • 1
  • F. Staub
    • 1
  • G.-H. Schneider
    • 1
  • M. Zimmer
    • 1
  • A. Baethmann
    • 1
  1. 1.Institute for Surgical ResearchLudwig-Maximilians-University, Klinikum GroßhadernMunich 70Germany

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