Limiting Neurological Damage After Stroke

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Abstract
Acute ischaemic stroke is a leading cause of death and a major cause of long term disability worldwide. Effective treatments for limiting the neurological damage after stroke have proven elusive. An improved understanding of the complicated cascade of cellular events following the onset of cerebral ischaemia has led to exploration of a number of avenues for early intervention. Reperfusion of the ischaemic territory using thrombolytic drugs has shown promise in clinical trials as a method for achieving tissue salvage. Antithrombotic and antiplatelet agents have not demonstrated efficacy as acute therapies, although the early use of aspirin (acetylsalicylic acid) appears to produce a reduction in early stroke recurrence. A wide variety of drugs which interfere at various points in the ischaemic cascade, so-called ‘neuroprotective agents’, have also been studied, but with mixed success. Of these, antagonists of voltage-gated calcium channels, antagonists at the N-methyl-D-aspartate (NMDA) receptor and scavengers of free radicals have been most extensively studied. Despite proving effective in animal models of cerebral ischaemia, these drugs have largely failed to fulfil their promise in clinical trials. While individual compounds have proven ineffective, combinations of drugs with different mechanisms of action may yet provide the best treatment for acute ischaemic stroke.