الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Stroke is the second leading cause of death worldwide. Mortality rates are declining, however. Over 75% of patients survive a first stroke during the first year, and over half survive beyond 5 years.
Calcium plays an important role in the pathogenesis of ischemic cell damage. Intracellular calcium accumulation leads neuronal damage by triggering the cycle of cytotoxic events.
Calcium levels levels obtained lately within 72 to 96 hours was found to be of prognostic significance after ischemic stroke. Clarifying the exact pathophysiological mechanism that may underlie these clinical observations has been challenging, especially because it is unclear whether serum Ca2+ level exerts a primary effect on ischemic stroke, or if it reflects a secondary epiphenomenon of ischemic stroke severity.
Although the better outcomes seen among patients with higher serum calcium levels in these prior studies were postulated to be caused by smaller infarct volumes, several potential mechanisms may explain why serum calcium levels are related to the extent of bioenergetically compromised tissue in patients with acute ischemic stroke. These mechanisms can be divided into 2 broad and non-mutually exclusive categories. First, raised serum calcium levels directly or indirectly attenuate the volume of ischemic tissue; second, serum calcium levels may alternately DROP in response in the presence of tissue ischemia. Most important, decreased extracellular serum calcium levels are an important factor in the positive feedback mechanism that potentiates the inward serum calcium level currents following ischemic injury.