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Stroke illness remains the single greatest cause of serious physical disability in western countries and is a major consumer of scarce medical resources. In the United Kingdom, it is estimated that the management of stroke patients accounts for 4%–5% of the National Health Service budget.1 Clearly, any intervention that reduces cerebral infarct size will have a major impact on the personal and health budget costs of stroke illness. At present, low dose aspirin and early referral to a dedicated “stroke unit” seem to be the two positive things that physicians can do for patients with acute ischaemic stroke that significantly reduce mortality and dependency levels, for which there is a firm evidence base. Treatment with thrombolytic drugs may be beneficial in those with acute stroke who are fortunate enough to obtain treatment within 3 hours of onset of symptoms.2 However, with such a narrow therapeutic time window, early thrombolysis is applicable in only a small minority of patients. Similarly, human trials of several neuroprotective agents which work in animals have so far proved disappointing.
In the midst of this therapeutic gloom, scientists and clinicians have been forced to re-evaluate the potential therapeutic targets in the cerebral ischaemic cascade. Perhaps the reason for the failure of neuroprotective interventions is that trials have concentrated on inhibiting the early components of the cascade which are triggered within minutes of onset of ischaemia. Attempts to block these processes after several hours, particularly glutamate activation of N-methyl-D-aspartate receptors and intracellular calcium influx may be a futile exercise. Or, it may be that potentially beneficial drugs simply do not reach their site of action because of the ischaemia affecting the penumbral zone during the putative therapeutuc time window. Is there then scope for effective therapeutic intervention beyond the first few hours of onset of …