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.