ABSTRACT
It is well known that stroke is one of the leading causes of death and disability in Western societies (1). However, progress in the treatment of stroke has been slow. For many years, neurologists could only localize lesions and describe the resulting syndromes, i.e., establish clinicopathological correlations. Little was known about the etiology of stroke, and the prevailing presumption was that in situ thrombosis of the intracranial vasculature was the most common culprit (2). The observation that thrombotic material could embolize from the carotid artery to the intracranial vessels (3) and the description of lacunar syndromes and their underlying pathophysiology (4) were pivotal in helping neurologists advance to the next stage, which was to assess the etiology of stroke. Thus, strategies for secondary prevention could emerge, but there was still no acute treatment available.
