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Neurology · 1999

Brain arteriolosclerosis and hemodynamic disturbance may induce leukoaraiosis.

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Yamauchi H, Fukuyama H, Nagahama Y, Shiozaki T, Nishizawa S, Konishi J, Shio H, Kimura J

Аннотация

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.

CONCLUSION: 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.

Предметные рубрики MeSH

ИП Урсолов Владлен Сергеевич

ИНН 500118482352 · ОГРНИП 314500117700049

Реквизиты и контакты