Cerebral ischaemia leads to a massive and time-dependent infiltration
of leukocytes into the nervous system. This process involves early upr
egulation of endothelial cell adhesion molecules in the area of develo
ping infarction. In experimental cerebral ischaemia blocking of leukoc
yte adhesion and migration by antibodies led to a dramatic reduction o
f ensuing cerebral infarcts. in humans, cerebral infarcts grow by exte
nsion into the penumbra up to several hours. it is therefore conceivab
le that antiinflammatory treatment strategies are applicable to human
stroke.