Glucocorticoids have been shown to reduce the levels of circulating inflammatory mediators (Hill et al. 1997). The release of interleukin-10, a potent anti-inflammatory cytokine, may play an important role in the anti-inflammatory effects of corticosteroids (Tabardel et al. 1996), but despite their anti-inflammatory potential, they have not turned out to be major neuroprotectants.

Critical evaluation of the data has demonstrated that free radical scavangers act more effectively at the level of the vascular endothelium than in the neuronal tissue per se (Hall et al. 1994). The use of alpha-phenyl-tert -butyl nitrone before HCA attenuated the normal response to ischaemia and improved recovery by affording protection from free radical-mediated damage. (Langley et al. 2000)

Tirilazad mesylate, a non-glucocorticoid 21-aminosteroid lipid peroxidation inhibitor, has proved promising as a neuroprotectant in experimental models of focal cerebral ischaemia, but it failed to improve the functional outcome after cerebral stroke. (Haley 1998).

A challenging therapeutic prospect is to aim directly at cytokine suppressive agents. Soluble TNF receptor I (a physiological inhibitor of TNF-a) has been shown to be neuroprotective, and TNF-a Mab treatment has been found to effectively prevent the expansion of infarct size in the brain (Barone et al. 1997). Another possibility is to inhibit interactions between the endothelium and the leukocytes. The potential of the experimentally demonstrated anti-ischaemic effect of cytokine inhibition and anti-adhesion molecules for clinically effective therapy is obscure, but these strategies evidently hold a promise for the future (Feuerstein et al. 1998).