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Neurology 2002;58:1635-1641
© 2002 American Academy of Neurology

Effects of subcortical ischemic vascular dementia and AD on entorhinal cortex and hippocampus

A. T. Du, MD, N. Schuff, PhD, M. P. Laakso, MD PhD, X. P. Zhu, MD PhD, W. J. Jagust, MD, K. Yaffe, MD, J. H. Kramer, PsyD, B. L. Miller, MD, B. R. Reed, MD, D. Norman, MD, H. C. Chui, MD and M. W. Weiner, MD

From the Magnetic Resonance Unit (Drs. Du, Schuff, Zhu, and Weiner), Department of Veterans Affairs Medical Center, San Francisco, CA; Departments of Radiology (Drs. Schuff, Norman, and Weiner), Psychiatry (Drs. Yaffe, Kramer, and Weiner), Neurology (Drs. Yaffe, Miller, and Weiner), Epidemiology (Dr. Yaffe), and Medicine (Dr. Weiner), University of California, San Francisco; Departments of Neurology and Clinical Radiology (Dr. Laakso), Kuopio University Hospital, Kuopio, Finland; Department of Neurology (Drs. Reed and Jagust), University of California, Davis; and Department of Neurology (Dr. Chui), University of Southern California, Los Angeles.

Address correspondence and reprint requests to Dr. Michael W. Weiner, MR Unit, VA Medical Center (114M), University of California, San Francisco, 4150 Clement Street, San Francisco, CA 94121; e-mail: mweiner{at}itsa.ucsf.edu

Objective: To determine the effects of subcortical ischemic vascular dementia (SIVD) and AD on entorhinal cortex (ERC) and hippocampus.

Methods: Thirty-eight cognitively normal subjects, 18 patients with SIVD, and 22 patients with AD were included. Volumes of ERC and hippocampus were manually measured based on MRI. Global cerebral changes of cortical gray matter, subcortical gray matter, white matter, sulcal CSF, ventricular CSF (vCSF), and white matter signal hyperintensities (WMSH) were assessed.

Results: Patients with SIVD had 21.7% (p < 0.01) smaller ERC and 18.2% (p < 0.01) smaller hippocampi than cognitively normal subjects and 24.4% (p < 0.01) larger ERC and 11.1% (p < 0.05) larger hippocampi than patients with AD. In addition, patients with SIVD had less cortical gray matter and white matter and more vCSF and WMSH (all p < 0.01) than cognitively normal subjects and more vCSF and WMSH (p < 0.01) than patients with AD. The volumes of ERC and hippocampus were positively correlated to similar extents (p < 0.01) in SIVD and AD. Cortical gray matter loss was positively correlated (p < 0.01) with hippocampal atrophy, but not with ERC atrophy, in SIVD and AD. Hippocampal volume alone could classify 82% of patients with SIVD from cognitively normal subjects and 63% of patients with SIVD from subjects with AD. Adding global cerebral changes to hippocampus substantially improved the classification to 96% between patients with SIVD and cognitively normal subjects and 83% between subjects with SIVD and those with AD, whereas adding ERC change to hippocampus did not significantly improve the discrimination.

Conclusions: The entorhinal cortex and hippocampus are less affected by subcortical ischemic vascular dementia than by AD.




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