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From the Center for Imaging of Neurodegenerative Diseases (A.T.D., G.D.J., S.H., M.W.W., N.S.), Department of Veterans Affairs Medical Center, San Francisco, and Departments of Radiology (G.H.J., S.H., M.W.W., N.S.), Psychiatry (J.H.K., M.W.W.), Neurology (H.J.R., M.L.G.-T., K.P.R., B.L.M., M.W.W.), and Medicine (M.W.W.), University of California San Francisco.
Address correspondence and reprint requests to Dr. N. Schuff/A. Du, MR Unit (114M), VA Medical Center, 4150 Clement St., San Francisco, CA 94121; e-mail: Norbert.Schuff{at}ucsf.edu/Antao.Du{at}ucsf.edu or antao{at}wayne.edu
Objectives: To test if arterial spin labeling (ASL) MRI could detect a pattern of hypoperfusion in frontotemporal dementia (FTD) vs cognitively normal (CN) control subjects; to determine the regional difference of perfusion between FTD and Alzheimer disease (AD); and to determine whether hypoperfusion in FTD correlates with cognitive impairment.
Methods: We included 21 patients with FTD, 24 patients with AD, and 25 CN subjects in this cross-sectional MRI study. All subjects had MRI scans including T1-weighted structural images and ASL-MR images.
Results: ASL-MRI detected a pattern of hypoperfusion in right frontal regions in patients with FTD vs CN subjects, similar to PET and SPECT. FTD had higher perfusion than AD in the parietal regions and posterior cingulate. Frontal hypoperfusion in FTD correlated with deficits in judgment and problem solving. Adding frontal perfusion to gray matter (GM) atrophy significantly improved the classification of FTD from normal aging to 74%, and adding parietal perfusion to GM atrophy significantly improved the classification of FTD from AD to 75%. Combining frontal and parietal lobe perfusion further improved the classification of FTD from AD to 87%.
Conclusion: Frontotemporal dementia and Alzheimer disease display different spatial distributions of hypoperfusion on arterial spin labeling MRI. With further development and evaluation, arterial spin labeling MRI could contribute to the differential diagnosis between frontotemporal dementia and Alzheimer disease.
Supported in part by a research applications grant of the Department of Veterans Affairs REAP, NIH grant AG10897, a Program Project Grant from the National Institute of Aging (PO1AG19724), ADRC (P50-AG023501), and a Network grant from the Hillblom Foundation.
Disclosure: The authors report no conflicts of interest.
Received December 6, 2005. Accepted in final form May 25, 2006.
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