Published online by Cambridge University Press: 07 December 2009
Stroke is the third biggest cause of death in Western countries. As the commonest form of long-term adult disability it is a major consumer of health spending. Eighty percent of strokes are due to ischemic infarcts and 20% due to hemorrhages. Despite the magnitude of the problem successful active treatment of ischemic stroke was almost nonexistent until the mid-1990s. Medical management was predominantly prophylactic, particularly concentrated upon the control of hypertension. The role of diagnostic tests was limited to confirmation of stroke diagnosis, differentiation of infarct from hemorrhage and identification of those entities, which may present with stroke like symptoms and signs (”pseudostroke”). Chronic subdural hematoma, slow growing tumors, demyelination and arteriovenous malformations (AVM) are all potentially treatable lesions which may present as pseudostroke. As many as 20% of stroke like presentations can be due to entities other than stroke (Libman et al., 1995).
Thrombolysis in ischemic stroke
The catalyst for enormously renewed interest in ischemic stroke was the publication in 1995 of the first trial suggesting patient outcome benefit following active thrombolytic treatment in patients treated within 3 h of the onset of symptoms (National Institute of Neurological Disorders and Stroke rtPA Stroke Study Group, 1995). In 1999 a prospective randomised trial of intra-arterial pro-urokinase in patients with occluded middle cerebral arteries (MCA) showed patient outcome benefit when treatment was initiated between 3 and 6 h after the onset of the stroke symptoms (Furlan et al., 1999).