Background-Leukoaraiosis, a term that defines an abnormal appearance of the subcortical white matter of the brain on neuroimaging (bilateral patchy or diffuse areas of low attenuation on CT or hyperintense T2 MR areas), has gained evidence in retrospective studies to demonstrate its association with stroke and in prospective studies to demonstrate its prognostic value related to the occurrence of stroke, both ischemic and hemorrhagic, or the occurrence of vascular death. Summary of Review-The subtype of ischemic stroke most strongly predicted by leukoaraiosis is lacunar infarct, which is likely caused by the same underlying small-vessel pathology. Leukoaraiosis has been shown to predispose to intracerebral hemorrhage at both the basal-ganglionic and lobar sites, primarily when leukoaraiosis is extensive and patients are treated with anticoagulants because of prior ischemic events. Conclusions-Leukoaraiosis shares with stroke common pathophysiological mechanisms and, because it is likely an expression of the same disease, must be regarded as an intermediate surrogate of stroke rather than a true stroke risk factor. Key Words: leukoaraiosis Ⅲ risk factors Ⅲ stroke I n 1987, Hachinski and coworkers 1 used the term leukoaraiosis (LA) (from the Greek: leukoϭwhite; araiosisϭrarefaction) to describe an abnormal CT appearance of the subcortical brain white matter, seen as bilateral patchy or diffuse areas of reduced x-ray attenuation with ill-defined margins, limited to the periventricular regions or extended to the centrum semiovale ( Figure 1). On T2 or fluid-attenuated inversion recovery (FLAIR) MRI sequences, LA appears as hyperintense periventricular caps or rims or halos or subcortical multiple punctuate or patchy, partially confluent or confluent areas. The degree of these changes is variable. Examples of MRI-disclosed LA of increasing severity are shown in Figure 2. On the basis of multiple findings, including some recent observations using MRI perfusion, 2 these changes are likely ischemic in nature and are caused by hypoperfusion in the distal deep arterial or arteriolar territories. 3 Lipohyalinosis (arteriolosclerosis), produced by chronic hypertension with or without diabetes, also related to lacunar infarction (LI) and intracerebral hemorrhage (ICH), is thought to be the hallmark pathological process altering small vessels. Pontine hyperintense lesions, usually combined with hemispheric LA, have been reported as a LA subtype, possibly produced through the same mechanisms. 4 LA may also be caused by cerebral amyloid angiopathy (CAA) or cerebral autosomal dominant arteriopathy stroke and ischemic leukoencephalopathy (CADASIL). 3 Evidence is being accumulated to document that the presence of LA is associated with a history of stroke and also predicts the future occurrence of either ischemic or hemorrhagic stroke. The aim of this article is to review the evidence on the risk of stroke among patients presenting with LA and to discuss whether LA should be considered more properly a stroke risk factor or an inter...