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Ischaemic cerebral injury follows a well documented sequence of events, including three phases: depolarization, biochemical cascade and reperfusion injury. The importance of the failure of neurotransmitter transport as a common pathway in the pathogenesis of ischaemic cerebral injury has been attested. This substantial step has increased our understanding of the pathogenesis of ischaemic neuronal injury and at the same time has opened up new therapeutic prospects for improving brain protection. One such strategy is to use appropriate pharmacological agents (Baumgartner et al. 1997, Lipton and Rosenberg 1994). Previous studies also suggest that the reperfusion phase is of paramount importance with regard to the pathogenesis of ischaemic brain injury. Leukocyte infiltration can be detected following ischaemic insult to the brain, so that the blood vessels will be filled with leukocytes (primarily neutrophils) and oedema will develop. The adhesion of leukocytes to the wall of blood vessels and their infiltration into the ischaemic brain tissue can activate an inflammatory reaction driven by cytokines, which exacerbates the degree of tissue injury on account of interference with normal microvascular perfusion and the release of cytotoxic enzymes. (Feuerstein et al. 1998, Feuerstein et al. 1998). 

As you see ischaemic brain injury involves three sequential phases: depolarization, biochemical cascade and reperfusion injury.