ithout early detection and treatment significant permanent disability of Canadians stricken with stroke will result (Bahouth & LaMonte, 2000).
             The brain is unique in its vulnerability to ischemic damage and injury. While it only represents 2% of the human body, it receives up to 20% of cardiac output to meet its need for a steady supply of glucose and oxygen to meet its vast metabolic needs. The brain has limited capacities for compensation and minimal reserves if perfusion of is critically reduced or suspended (Fisher, 2001). Strokes occur when there is a disruption in cerebral perfusion. Cerebral tissue is oxygen-dependent, and ischemia occurs when oxygen delivery to the brain is interrupted, ultimately leading to immediate cell death. The longer the cerebral tissue goes without oxygen, the greater chance that permanent, irreversible ischemic tissue damage can occur. Unlike other organ systems that draw from the body's glucose reserves and function anaerobically, cerebral tissues are unable to compensate, and glucose and oxygen are rapidly depleted without reserves (Ingram & Sedlack, 2002). Normal cerebral blood flow is 55 mL/100 g of brain tissue per minute. Animal experiments suggest that ischemia occurs when cerebral blood flow falls to 23 mL/100 g/min. and infarction (cell death) occurs when cerebral blood flow falls to 17 mL/100 g/min (Kongable, 1997). Electroencephalographic activity is known to be suppressed at a cerebral blood flow of less than 20cc/100 gm/min and cellular viability is lost with anoxic depolarization of cell membranes at a threshold of less than 15 cc/100 gm/min. Ischemia also can interupt zinc homeostasis. As with calcium influx, excessive zinc in-flux might trigger cell death. (Meschia & Brott, 2002). With ischemia aerobic metabolism cannot be maintained and loss of function occurs (Felberg & Naidech, 2003). Factors influencing the period of ischemia are, degree of decreased blood flow, pattern of c...