The Cardiovascular Outcome of Patients With Motor Impairment and Extensive Leukoaraiosis

Background and Purpose-White matter lesions (WMLs) have been shown to be associated with the risk of stroke in previous studies but little is known about the prediction of other vascular events. We evaluated the risk of stroke and other vascular events according to WML volume in a large population-based sample. We also studied WML volume by type (deep or periventricular) in relation to these events. Methods-The 3-City Study is a population-based prospective cohort of people aged Ն65 years followed up for, on average, 4.9 years. Among them, 1643 participants free of prevalent vascular events had quantitative measurements of WML volume at baseline using a fully automatic method. The risks of incident major vascular events according to WML volume were evaluated using Cox proportional hazards models. Results-The risk of incident stroke significantly increased with increasing baseline WML volume and was multiplied by 5 for those in the highest quartile of WML volume. Nonstroke vascular events' incidence was not associated with WML volumes, whatever their type. Conclusions-WMLs are an independent predictor of stroke in the elderly. This association is specific because WMLs are not associated with the risk of other vascular events.

Section: Discussionmentioning

confidence: 99%

Cerebral White Matter Lesions Are Associated With the Risk of Stroke But Not With Other Vascular Events

Buyck

Dufouil²,

Mazoyer³

et al. 2009

“…4 Prospective observations further corroborated the relationship between LA and stroke and the distinct role of LI. The presence of LA on CT scan predicted subsequent stroke in patients with first-ever lacunar stroke, 15 in those with lacunar or cortical infarction, 16 in elderly patients with gait problems and LA on CT scan, 17 and in patients with lacunar stroke or trivial neurological symptoms. 18 Recurrent stroke was predominantly of the lacunar type.…”

Section: La As a Predictor Of Ischemic Stroke Or Vascular Deathmentioning

confidence: 98%

Leukoaraiosis

Inzitari

2003

119

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...

“…Notwithstanding thè fact that some studies failed to demonstrate an association between WM abnormalities and cerebrovascular risk factors,7 LA is usually seen more frequently in patients with history of strokes and in individuals with cognitive deterioration of presumed vascular origin.22-27 Also, persons with severe LA are at increased risk to develop stroke and myocardial infarction. 28 The most common risk factor for LA is aging7'27; arterial hypertension, diabetes mellitus, and cardiac diseases are additional risk factors frequently associated with LA.29-31 Aging, chronic hypertension, and diabetes share a common substrato in thè type of alterations that these conditions induce on thè small penetrating arteries and arterioles of thè WM. Such changes include replacement of thè smooth muscle cells by fibro-hyaline material with thickening of thè wall and narrowing of thè vascular lumen (arteriolosclerosis).32'34 Arteriolosclerosis, almost always detected within areas of LA,35-37 may be one of thè reasons thè blood supply to thè WM is altered, and this vascular alteration may lead to either localized ischemie areas of necrosis and cavitation (ie, lacunes) or diffuse rarefaction (ie, LA).…”

Section: Cllnica! and Pathological Features Of Leukoaraiosismentioning

confidence: 99%

Pathogenesis of Leukoaraiosis

Pantoni

García²

1997

1,139

933

Background Changes in the cerebral hemispheric white matter, detectable with increasing frequency by modern neuroimaging methods, are associated with aging and conceivably may contribute to the development of specific cognitive deficits. The pathogenesis of these cerebral white matter abnormalities (sometimes described as leukoaraiosis) is unknown. This review evaluates the available evidence in support of the hypothesis that the etiology of leukoaraiosis is related to a specific type of cerebral ischemia and highlights mechanisms by which ischemic injury to the brain may induce selected structural alterations limited to the cerebral white matter. Summary of Review The review is based on the critical analysis of over 100 publications (most appearing in the last decade) dealing with the anatomy and physiology of the arterial circulation to the cerebral white matter and with the pathogenesis of leukoaraiosis. Conclusions A significant number of clues support the hypothesis that some types of leukoaraiosis may be the result of ischemic injury to the brain. Structural changes affecting the small intraparenchymal cerebral arteries and arterioles that are associated with aging and with stroke risk factors, altered cerebral blood flow autoregulation, and the conditions created by the unique arterial blood supply of the hemispheric white matter each seem to contribute to the development of leukoaraiosis. To the best of our ability to interpret current information, the type of ischemic injury that is most likely responsible for these white matter changes involves transient repeated events characterized by moderate drops in regional cerebral blood flow that induce an incomplete form of infarction. This hypothesis could be tested in appropriate experimental models.