Treating acute ischaemic strokeBMJ 1995; 311 doi: https://doi.org/10.1136/bmj.311.6998.139 (Published 15 July 1995) Cite this as: BMJ 1995;311:139
- Philip M W Bath, Wolfson senior lecturer in stroke medicine
- Department of Medicine, King's College School of Medicine and Dentistry, London SE5 9PJ
Still no effective drug treatment available
Now that drug treatment for acute myocardial infarction has been largely sorted out, the world of vascular medicine has moved on to acute stroke. Given that stroke is the third commonest cause of death in the West and the most important cause of adult disability,1 it is surprising that no treatment exists that has been conclusively shown to reduce the risk of death or disability. Despite a massive worldwide effort to rectify this, early results are disappointing.
In the West most (85%) strokes result from cerebral infarction after arterial occlusion. Ischaemia induces activation of the glutamate-calcium cascade and cytodestructive enzymes, the release of free radicals, and ultimately cell death.2 Surrounding the core of dead neural tissue lies a penumbra of neurones that may survive or die, which has become the focus of pharmacological activity.
The main classes of agents include thrombolytics (to accelerate reperfusion), anticoagulants and antithrombotics (to prevent further occlusion), vasodilators (to increase cerebral blood flow), antileucocytic drugs (to prevent inflammation), glutamate antagonists, calcium antagonists, and free radical scavengers. Anticoagulants, antithrombotics, and antileucocytic drugs may also reduce the early risk of deep vein thrombosis and pulmonary embolism, which are important complications of stroke.
Two sets of events have occurred recently that considerably advance our knowledge …
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