Semin Thromb Hemost 1996; 22(1): 53-60
DOI: 10.1055/s-2007-998991
Copyright © 1996 by Thieme Medical Publishers, Inc.

Acute Ischemic Stroke

Michael Huber, Wolf-Dieter Heiss
  • From the Max Planck Institute for Neurological Research, Cologne, Germany.
Further Information

Publication History

Publication Date:
06 February 2008 (online)

Abstract

While case fatality rates in ischemic stroke tend to decline, the total number of strokes is expected to increase further in the future because of more people reaching a greater age. Acute ischemic stroke, usually caused by chronic arterial hypertension, in most cases is induced either by a sudden loss of perfusion pressure or by thromboembolism. Reduction of oxygen supply to brain tissue then leads to a cascade of biochemical reactions. Cell death finally occurs after massive Ca2+ influx into the cell and breakdown of the membranes. A rim of viable tissue called the penumbra often exists around a central necrotic core within the ischemic region. This tissue compartment may be brought back to function if perfusion is restored within a short time. Since some cytotoxic reactions within ischemic tissue are irreversible, current efforts in stroke therapy focus on measures to decrease cellular vulnerability. Restoring perfusion remains the first important therapeutic goal. A variety of compounds have been tested for cytoprotection, but none can yet be recommended for routine clinical use. General management of stroke patients in every case should be implemented for emergency assessment, since the first few hours after onset are crucial for the outcome.