It is now generally accepted by neurologists that most transient ischaemic attacks, particularly in the carotid artery territory, have a thromboembolic basis. These emboli are, for the most part, fibrin-platelet aggregates. Others which contain atheromatous debris are more likely to produce longer lasting neurological deficits. If one assumes this hypothesis then it is reasonable to employ drugs which interfere with platelet aggregation in order to prevent cerebrovascular symptoms and signs. Acetylsalicylic acid (aspirin) prevents aggregation by inhibiting the ‘release reaction’ initiated by thromboxane A2. This inhibition lasts for the life of the affected platelets. Recent trials in the United States and Canada have demonstrated a positive clinical benefit from the employment of aspirin in patients suffering from transient cerebral ischaemic attacks and amaurosis fugax. There was a reduction or cessation of the attacks in both males and females and a 50% reduction of stroke morbidity and mortality in males.