Stroke is a heterogenous disease, but about 85% of strokes are as a result
of cerebral ischaemia due to arterial occlusion. It seems logical to assume
that, as in myocardial infarction, treatment designed to dissolve clots sh
ould be helpful.
We now have a substantial amount of data on the use of aspirin, heparin and
thrombolytic drugs in the treatment of acute ischaemic stroke. Aspirin 300
mg daily has a modest effect in reducing mortality and handicap when used
within 48 hours of stroke onset. The beneficial effects of low dose, medium
dose subcutaneous unfractionated heparin, and various low molecular weight
heparins in reducing early recurrent ischaemic stroke seem to be outweighe
d by haemorrhagic side effects. Streptokinase used within six hours of stro
ke onset results in excess mortality with some reduction in handicap in sur
vivors, while in carefully selected patients recombinant tissue plasminogen
activator (r-TPA) may be less hazardous. At the moment it is unclear which
stroke patients will benefit from the use of r-TPA, and the use of criteri
a, as outlined by the NINDS group, means that only a very small proportion
of stoke victims are suitable for thrombolytic therapy.
Further research is necessary, while the concept of a 'Brain Attack' with a
ppropriate urgency being used in the assessment of possible stoke needs dev
elopment.