Carotid atherosclerosis and cerebral white matter lesions in a population based magnetic resonance imaging study

Citation
Fe. De Leeuw et al., Carotid atherosclerosis and cerebral white matter lesions in a population based magnetic resonance imaging study, J NEUROL, 247(4), 2000, pp. 291-296
Citations number
38
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROLOGY
ISSN journal
03405354 → ACNP
Volume
247
Issue
4
Year of publication
2000
Pages
291 - 296
Database
ISI
SICI code
0340-5354(200004)247:4<291:CAACWM>2.0.ZU;2-T
Abstract
Cerebral white matter lesions are frequently observed on magnetic resonance imaging of elderly, nondemented persons. There is evidence that white matt er lesions are involved in the pathophysiology of cognitive decline and dem entia. White matter lesions can be divided into those in the periventricula r and those in the subcortical region. Pathological and epidemiological stu dies suggest that atherosclerosis is involved in the pathogenesis of these lesions. Our study reports on the association between atherosclerosis in th e carotid arteries and white matter lesions in a population-based study amo ng 1077 elderly subjects. We randomly sampled 1077 subjects aged between 60 -90 years from two prospective population-based studies. All subjects under went ultrasonography of the carotid artery. In addition, 1.5 T magnetic res onance imaging was performed; white matter lesions in the subcortical and p eriventricular regions were rated separately. With increasing number of pla ques in the carotid artery the severity of periventricular white matter les ions increased (P-trend = 0.03), but not the severity of subcortical white matter lesions (P-trend = 0.19). In addition, an increase in intima media t hickness was borderline significantly associated with an increased severity of periventricular white matter lesions (P-trend = 0.09), but not of subco rtical white matter lesions (P-trend = 0.68). These findings suggest that p artly dissimilar pathogenetic mechanisms are involved in the etiology of pe riventricular and subcortical white matter lesions.