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International Journal of Alzheimer’s Disease
Volume 2011 (2011), Article ID 483972, 6 pages
Research Article

MRI Shows More Severe Hippocampal Atrophy and Shape Deformation in Hippocampal Sclerosis Than in Alzheimer's Disease

1Rancho Los Amigos National Rehabilitation Center, University of Southern California, 7601 E Imperial Hwy., Medical Science Bldg., Room 26 Downey, CA 90242, USA
2Departments of Psychiatry and Behavioral Sciences and Radiology, Northwestern University Feinberg School of Medicine, 710 N. Lake Shore Drive, Abbott Hall 1312, Chicago, IL 60611, USA
3Department of Neurology, University of Southern California, 1510 San Pablo Street, Suite 618, Los Angeles, CA 90033, USA
4Center for Imaging of Neurodegenerative Disease, University of California, 4150 Clement Street, San Francisco, CA 94121, USA
5Department of Psychiatry and Behavioral Sciences, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA

Received 24 November 2010; Accepted 16 February 2011

Academic Editor: G. B. Frisoni

Copyright © 2011 C. Zarow et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


While hippocampal atrophy is a key feature of both hippocampal sclerosis (HS) and Alzheimer's disease (AD), the pathology underlying this finding differs in these two conditions. In AD, atrophy is due primarily to loss of neurons and neuronal volume as a result of neurofibrillary tangle formation. While the etiology of HS is unknown, neuron loss in the hippocampus is severe to complete. We compared hippocampal volume and deformations from premortem MRI in 43 neuropathologically diagnosed cases of HS, AD, and normal controls (NC) selected from a longitudinal study of subcortical ischemic vascular disease (IVD Program Project). HS cases (n=11) showed loss of neurons throughout the rostral-caudal extent of the hippocampus in one or both hemispheres. AD cases (n=24) met NIA-Reagan criteria for high likelihood of AD. Normal control cases (n=8) were cognitively intact and showed no significant AD or hippocampal pathology. The mean hippocampal volumes were significantly lower in HS versus AD groups (P<.001). Mean shape deformations in the CA1 and subiculum differed significantly between HS versus AD, HS versus NC, and AD versus NC (P<.0001). Additional study is needed to determine whether these differences will be meaningful for clinical diagnosis of individual cases.