الفهرس 
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Abstract
Thrombolytic therapy (TT) has been in use for cerebral infarction since 1958. In the era before CT, 7 case series were published describing thrombolytic therapy with ischaemic stroke. Treatment was almost always administered more than 6 hours after symptom onset. Because CT was unavailable, these early studies could not exclude patients with small intracerebral haematomas. All thrombolytic agents act by conversion of plasminogen to plasmin, an enzyme, which is capable of splitting fibrin to induce clot lysis and reperfusion, however, reperfusion is not the only mechanism by which TT may reduce morbidity and mortality, but other benflts of thrombolytic therapy include: maintenance of conduit for collateral supply, arrest of the process of clot extension, reduction of plasma fibrinogen concentration, increase in fibrinogen degradation products, modification of platelet activity, vasodilation, as well as cytoprotective (membrane) effect. Two methods of application of TT for ischaemic stroke are widely used nowadays; intravenous and intraarterial, using different thrombolytic agents; streptokinase. (SK), urokinase (UK) and tissue plasminogen activator (t-PA).