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American Journal of Neuroradiology 21:621-630 (4 2000)
© 2000 American Society of Neuroradiology

ARTICLE

Subcortical Ischemic Vascular Dementia: Assessment with Quantitative MR Imaging and ¹H MR Spectroscopy

Aristides A. Capizzano^a, Norbert Schuff^a, Diane L. Amend^a, Jody L. Tanabe^a, David Norman^a, Andrew A. Maudsley^a, William Jagust^a, Helena C. Chui^a, George Fein^a, Mark R. Segal^a and Michael W. Weiner^,a

^a From the Department of Veterans Affairs Medical Center (A.A.C., N.S., D.L.A., J.L.T., A.A.M., M.W.W.), Magnetic Resonance Spectroscopy Unit, San Francisco, CA; the Departments of Radiology (A.A.C., N.S., D.L.A., J.L.T., D.N., M.W.W.), Medicine (M.W.W.), Psychiatry (G.F., M.W.W.), and Neurology (M.W.W.) and the Division of Biostatistics (M.R.S.), University of California, San Francisco, San Francisco, CA; The Center for Functional Imaging (W.J.), Ernest Orlando Lawrence Berkeley National Laboratory, Berkeley, CA; and the Department of Neurology (H.C.C.), University of Southern California, Rancho Los Amigos Medical Center, Downey, CA.

BACKGROUND AND PURPOSE: Subcortical ischemic vascular dementia is associated with cortical hypometabolism and hypoperfusion, and this reduced cortical metabolism or blood flow can be detected with functional imaging such as positron emission tomography. The aim of this study was to characterize, by means of MR imaging and ¹H MR spectroscopy, the structural and metabolic brain changes that occur among patients with subcortical ischemic vascular dementia compared with those of elderly control volunteers and patients with Alzheimer's disease.

METHODS: Patients with dementia and lacunes (n = 11), cognitive impairment and lacunes (n = 14), and dementia without lacunes (n = 18) and healthy age-matched control volunteers (n = 20) underwent MR imaging and ¹H MR spectroscopy. ¹H MR spectroscopy data were coanalyzed with coregistered segmented MR images to account for atrophy and tissue composition.

RESULTS: Compared with healthy control volunteers, patients with dementia and lacunes had 11.74% lower N-acetylaspartate/creatine ratios (NAA/Cr) (P = .007) and 10.25% lower N-acetylaspartate measurements (NAA) in the cerebral cortex (P = .03). In white matter, patients with dementia and lacunes showed a 10.56% NAA/Cr reduction (P = .01) and a 12.64% NAA reduction (P = .04) compared with control subjects. NAA in the frontal cortex was negatively correlated with the volume of white matter signal hyperintensity among patients with cognitive impairment and lacunes (P = .002). Patients with dementia, but not patients with dementia and lacunes, showed a 10.33% NAA/Cr decrease (P = .02) in the hippocampus compared with healthy control volunteers.

CONCLUSION: Patients with dementia and lacunes have reduced NAA and NAA/Cr in both cortical and white matter regions. Cortical changes may result from cortical ischemia/infarction, retrograde or trans-synaptic injury (or both) secondary to subcortical neuronal loss, or concurrent Alzheimer's pathologic abnormalities. Cortical derangement may contribute to dementia among patients with subcortical infarction.

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