Subcortical ischemic vascular dementia: Assessment with quantitative MR imaging and H-1 MR spectroscopy

BACKGROUND AND PURPOSE: Subcortical ischemic vascular dementia is associate d with cortical hypometabolism and hypoperfusion, and this reduced cortical metabolism or blood flow can be detected with functional imaging such as p ositron emission tomography, The aim of this study was to characterize, by means of MR imaging and H-1 MR spectroscopy, the structural and metabolic b rain changes that occur among patients with subcortical ischemic vascular d ementia 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 H-1 MR spectr oscopy. H-1 MR spectroscopy data were coanalyzed with coregistered segmente d MR images to account for atrophy and tissue composition. RESULTS: Compared with healthy control volunteers, patients with dementia a nd lacunes had 11.74% lower N-acetylaspartate/creatine ratios (NAA/Cr) (P = .007) and 10.25% lower N-acetylaspartate measurements (NAA) in the cerebra l cortex (P = .03), In white matter, patients with dementia and lacunes sho wed 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 pati ents with cognitive impairment and lacunes (P = .002), Patients with dement ia, but not patients with dementia and lacunes, showed a 10.33% NAA/Cr decr ease (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 patholo gic abnormalities. Cortical derangement may contribute to dementia among pa tients with subcortical infarction.