title: Brain arteriolosclerosis and hemodynamic disturbance may induce leukoaraiosis.
abstract: OBJECTIVE
  To investigate whether internal carotid artery (ICA) occlusive disease-induced hemodynamic disturbance is associated with extensive white matter high-intensity lesions (WMLs) on T2-weighted MR images in the hemisphere with lacunar infarct in the basal ganglia.
  
  
  BACKGROUND
  Hemodynamic disturbance in the brain with arteriolosclerosis may be one of the mechanisms by which ischemic injury induces extensive WMLs.
  
  
  METHODS
  The authors used MRI and PET to study 21 patients with unilateral ICA occlusion or stenosis and lacunar infarct in the bilateral basal ganglia. In hemispheres with ICA disease, the association of WMLs with the mean hemispheric values of oxygen extraction fraction (OEF)-an index of hemodynamic compromise-measured with the 15O-labeled gas steady-state technique was analyzed. Twenty-five patients with ICA occlusive disease without lacunar infarct were studied as control subjects.
  
  
  RESULTS
  In the hemispheres with ICA disease, patients with lacunar infarct had a significantly greater severity of WMLs than control subjects, although the mean hemispheric values of the OEF showed no significant difference. The severity of WMLs correlated significantly with the mean hemispheric values of the OEF in patients with lacunar infarct, but not in control subjects. Multivariate analysis revealed that lacunar infarcts and increased OEF were independent predictors of extensive WMLs, with lacunar infarcts the most heavily weighted factor.
  
  
  CONCLUSIONS
  Internal carotid artery occlusive disease-induced hemodynamic disturbance is associated with extensive WMLs in hemispheres with lacunar infarct. Hemodynamic disturbance may contribute to the development of extensive WMLs, although brain arteriolosclerosis may be a major contributing factor.
authors.affiliation: Department of Neurology, Faculty of Medicine, Kyoto University, Japan. yamauchi@shigamed.moriyama.shiga.jp
authors.forename: H
authors.initials: H
authors.lastname: Yamauchi
authors.forename: H
authors.initials: H
authors.lastname: Fukuyama
authors.forename: Y
authors.initials: Y
authors.lastname: Nagahama
authors.forename: T
authors.initials: T
authors.lastname: Shiozaki
authors.forename: S
authors.initials: S
authors.lastname: Nishizawa
authors.forename: J
authors.initials: J
authors.lastname: Konishi
authors.forename: H
authors.initials: H
authors.lastname: Shio
authors.forename: J
authors.initials: J
authors.lastname: Kimura
mesh_terms: D000368:Aged; D020144:Basal Ganglia Cerebrovascular Disease / Q000150:complications*; D001927:Brain Diseases / Q000175:diagnosis / Q000209:etiology*; D002340:Carotid Artery Diseases / Q000150:complications* / Q000503:physiopathology; D002343:Carotid Artery, Internal; D002544:Cerebral Infarction / Q000150:complications*; D002560:Cerebrovascular Circulation; D005260:Female; D006439:Hemodynamics; D006801:Humans; D002537:Intracranial Arteriosclerosis / Q000150:complications* / Q000503:physiopathology; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D014055:Tomography, Emission-Computed