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Different patterns of N-acetylaspartate loss in subcortical ischemic vascular dementia and AD

From the Magnetic Resonance Unit (Drs. Schuff, Du, Amend, and Weiner), DVA Medical Center San Francisco, and Departments of Radiology (Drs. Norman and Weiner), Neurology (Drs. Miller, Yaffe, and Weiner), Medicine (Dr. Weiner), and Psychiatry (Drs. Kramer and Reed), University of California, San Francisco; MRI Unit (Dr. Capizzano), Fernández Hospital, Buenos Aires, Argentina; Department of Psychiatry (Dr. O’Neill), University of California, Los Angeles; Department of Neurology (Dr. Jagust), University of California, Davis; and Department of Neurology (Dr. Chui), University of Southern California, Los Angeles.

Address correspondence and reprint requests to Dr. Norbert Schuff, DVA Medical Center, 4150 Clement St., 114M, San Francisco, CA 94121; e-mail: nschuff{at}itsa.ucsf.edu

Objectives: 1) To determine the regional pattern of reduced N-acetylaspartate (NAA) in subcortical ischemic vascular dementia (SIVD); 2) to explore the relationship between NAA reduction and subcortical vascular disease; and 3) to test if MR spectroscopic imaging (MRSI) in combination with structural MRI improves differentiation between SIVD and Alzheimer disease (AD).

Methods: Thirteen patients with SIVD (71 ± 8 years old) and 43 patients with AD of comparable age and dementia severity were studied using MRSI and MRI. Patients were compared to 52 cognitively normal subjects with and without lacunes.

Results: Compared to controls, patients with SIVD had lower NAA by 18% (p < 0.001) in frontal cortex and by 27% (p < 0.003) in parietal cortex, but no significant NAA reduction in white matter and medial temporal lobe. Compared to patients with AD, patients with SIVD had lower NAA by 13% (p < 0.02) in frontal cortex and by 20% (p < 0.002) in left parietal cortex. Cortical NAA decreased in SIVD with increasing white matter lesions (r = 0.54, p < 0.02) and number of lacunes (r = 0.59, p < 0.02). Thalamic lacunes were associated with greater NAA reduction in frontal cortex than were lacunes outside the thalamus (p < 0.02) across groups, after adjusting for cognitive impairments. Adding parietal NAA to MRI-derived hippocampal atrophy improved separation between SIVD and AD (p = 0.02) from 79 to 89%.

Conclusions: These results emphasize the importance of cortical dysfunction as a factor in SIVD and indicate a characteristic pattern of metabolite change that might serve as a basis for improved diagnosis.

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