Carotid stenosis is an important cause of transient ischaemic attacks and stroke. The cause of carotid stenosis is most often atherosclerosis; contributing to the pathogenesis of the lesion are endothelial injury, inflammation, lipid deposition, plaque formation, fibrin, platelets and thrombin. Carotid stenosis accounts for 10–20% of cases of brain infarction, depending on the population studied. Despite successful treatment of selected patients who have had an acute ischaemic stroke with tissue plasminogen activator and the promise of other experimental therapies, prevention remains the best approach to reducing the impact of ischaemic stroke. High-risk or stroke-prone patients can be identified and targeted for specific interventions.At this juncture, treatment of carotid stenosis is a well established therapeutic target and a pillar of stroke prevention. There are two main strategies for the treatment of carotid stenosis. The first approach is to stabilise or halt the progression of the carotid plaque through risk factor modification and medication. Hypertension, diabetes mellitus, smoking, obesity and high cholesterol levels are closely associated with carotid stenosis and stroke; control of these factors may decrease the risk of plaque formation and progression. The second approach is to eliminate or reduce carotid stenosis through carotid endarterectomy or carotid angioplasty and stenting. Carotid endarterectomy, which is the mainstay of therapy for severe carotid stenosis, is beyond the scope of this review.Anticoagulants seem to play little role (if any) in the medical (i.e. non-surgical) treatment of carotid stenosis. Adoption of a healthy lifestyle combined with the reduction of risk factors has been shown to lead to a reduction in the extent of carotid stenosis. The medical treatment of carotid stenosis should be based on the triad of the reduction of risk factors, patient education, and use of antiplatelet agents.