Platelets and stroke

Platelets are anucleate cells with little or no capacity for de novo protei n synthesis. Their potential haemostatic reactivity is established at or be fore thrombopoiesis by their precursor cell, the bone marrow megakaryocyte. In some pathologic conditions, the megakaryocyte-platelet-haemostatic axis (MPHA) becomes perturbed, resulting in the formation of hyperfunctional pl atelets which may contribute to the development of vascular disease or an a cute thrombotic event such as ischaemic stroke or myocardial infarction. La boratory measurements of platelet function have established that platelet r eactivity is accentuated in acute ischaemic stroke, particularly following cortical rather than lacunar infarction. Whether accentuated platelet funct ion is a cause or a consequence of stroke is not yet clear, but it is likel y that patients with certain risk factor profiles have some degree of plate let activation preceding the stroke. Further work into the MPHA is required to establish whether enhanced post-stroke platelet reactivity can be refer red to the megakaryocyte. The antiplatelet agents tested to date are effect ive in secondary but not primary prevention of stroke. This probably reflec ts the diverse pathophysiology of stroke: accentuated platelet function is only likely to be a significant factor in cortical stroke.