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Cerebral Edema

  • Oliver Kempski
    Correspondence
    Address reprint requests to Oltver Kempski, MD, Institute for Neurosurgical Pathophysiology, Johannes Gutenberg-University Mainz, 55101 Mainz, Germany
    Affiliations
    From the Institute for Neurosurgical Pathophysiology, Johannes Gutenberg·University Mainz, Gennany
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      Two major types of brain edema may be discriminated, characterized by intra- or extracellular fluid accumulation. Intracellular (cytotoxic) edema is found after cerebral ischemia, trauma, intoxications, and metabolic disorders. Pathogenetic mechanisms include (1) failure of active Na+ export via Na/K-ATPase because of energy shortage, (2) Increased Na+-permeability, or (3) activation of Na+-driven membrane pumps. The latter mechanism reflects homeostatic functions of astroglia, which at reduced availability of energy resources uses the remaining Na+gradient to fuel uptake of transmitters such as glutamate, and for control of pHI. Extracellular (vasogenic) edema is caused by damage to the blood-brain barrier and consists of protein-rich fluid. It accompanies brain tumors, trauma, infections, and hypertensive crisis. Pathogenetic mechanisms include (1) opening of tight junctions responsible for barrier opening in acute conditions, or (2) sprouting of immature blood vessels in chronic conditions such as brain tumors.
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