title: Subcortical ischemic vascular dementia: assessment with quantitative MR imaging and 1H MR spectroscopy.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Veterans Affairs Medical Center, Magnetic Resonance Spectroscopy Unit, San Francisco, CA 94121, USA.
authors.forename: A A
authors.initials: AA
authors.lastname: Capizzano
authors.forename: N
authors.initials: N
authors.lastname: Schuff
authors.forename: D L
authors.initials: DL
authors.lastname: Amend
authors.forename: J L
authors.initials: JL
authors.lastname: Tanabe
authors.forename: D
authors.initials: D
authors.lastname: Norman
authors.forename: A A
authors.initials: AA
authors.lastname: Maudsley
authors.forename: W
authors.initials: W
authors.lastname: Jagust
authors.forename: H C
authors.initials: HC
authors.lastname: Chui
authors.forename: G
authors.initials: G
authors.lastname: Fein
authors.forename: M R
authors.initials: MR
authors.lastname: Segal
authors.forename: M W
authors.initials: MW
authors.lastname: Weiner
mesh_terms: D000368:Aged; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000378:metabolism; D002545:Brain Ischemia / Q000150:complications / Q000175:diagnosis* / Q000378:metabolism*; D003401:Creatine / Q000378:metabolism; D015140:Dementia, Vascular / Q000150:complications / Q000175:diagnosis* / Q000378:metabolism*; D005260:Female; D006801:Humans; D008279:Magnetic Resonance Imaging; D009682:Magnetic Resonance Spectroscopy; D008297:Male
chemical_list: D001224:Aspartic Acid; C000179:N-acetylaspartate; D003401:Creatine