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From the Department of Neurology (Drs. Bakker and Koudstaal), University Hospital Rotterdam, Department of Epidemiology & Biostatistics (Drs. Bakker, de Leeuw, de Groot, Hofman, and Breteler), Erasmus University Medical School, Rotterdam, the Netherlands.
Address correspondence and reprint requests to Dr. Stef L.M. Bakker, Department of Neurology, University Hospital Rotterdam, Dr. Molewaterplein 40, 3015 GD Rotterdam, the Netherlands.
OBJECTIVE: The pathogenesis of white matter lesions is still uncertain, but an ischemic-hypoxic cause has been suggested. Cerebral vasomotor reactivity reflects the compensatory dilatory mechanism of the intracerebral arterioles to a vasodilatory stimulus and provides a more sensitive hemodynamic index than the level of resting flow.
METHODS: The authors determined the association between vasomotor reactivity and white matter lesions in 73 consecutive individuals from the Rotterdam Scan Study who also participated in the Rotterdam Study, a large population-based prospective follow-up study of individuals
55 years old. Vasomotor reactivity was measured by means of CO2-enhanced transcranial Doppler, and in all individuals axial T1*-, T2*-, and proton density (PD)-weighted MRI scans (1.5 T) were obtained. White matter lesions were scored according to location, size, and number by two independent readers.
RESULTS: Vasomotor reactivity was inversely associated with the deep subcortical and total periventricular white matter lesions (OR 0.5, 95% CI 0.3 to 1.1; and OR 0.7, 95% CI 0.4 to 1.1, respectively). A strong association was found between impaired vasomotor reactivity and periventricular white matter lesions adjacent to the lateral ventricular wall (OR 0.6, 95% CI 0.4 to 1.0; p = 0.001). No association was found with periventricular white matter lesions near the frontal and occipital horns.
CONCLUSIONS: Our data confirm the association between vasomotor reactivity and white matter lesions and support the hypothesis that some white matter lesions may be associated with hemodynamic ischemic injury to the brain.
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