Neuroprotection

Most of the current strategies for treatment of ischaemic stroke are based on re-establishing perfusion through the blocked blood vessels, using pharmacologic and mechanical thrombolysis. Conversely, neuroprotection targets biochemical pathways that lead to cell injury and death in ischaemia in order to rescue salvageable nervous tissue.

Despite encouraging data in experimental animal models, no clinical trials have demonstrated any significant benefit of neuroprotective agents in human stroke patients.

There are too few data on other groups of agents, including colony-stimulating factors (including erythropoietin, granulocyte colony-stimulating factor and analogues), theophylline, aminophylline, caffeine and analogues, edaravone, minocycline, and arundic acid (ONO2506).

Hypothermia has been studied for its potential neuroprotective effects, including physical cooling or use of paracetamol to reduce body temperature, but evidence supporting it is also limited.

For current research and evidence-based recommendations see our Clinical Guidelines.