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on June 8, 2006

Stroke. 2006
Published online before print June 8, 2006, doi: 10.1161/01.STR.0000227328.86353.a7
A more recent version of this article appeared on July 1, 2006
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*Amyloidosis
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Submitted on January 13, 2006
Revised on April 27, 2006
Accepted on May 2, 2006

White Matter Alterations in Cerebral Amyloid Angiopathy Measured by Diffusion Tensor Imaging

David H. Salat PhD*; Eric E. Smith MD, MPH, FRCPC; David S. Tuch PhD; Thomas Benner PhD; Vasanth Pappu BS; Kristin M. Schwab BA; M. Edip Gurol MD; H. Diana Rosas MD; Jonathan Rosand MD; and Steven M. Greenberg MD, PhD

From the Massachusetts General Hospital/Massachusetts Institute of Technology/Harvard Medical School Athinoula A. Martinos Center for Biomedical Imaging (D.H.S., D.S.T., T.B., V.P., H.D.R.), Charlestown, Mass; the MGH Department of Neurology/Clinical Trials Unit (E.E.S., K.S., M.E.G., J.R., S.M.G.), Boston, Mass; the MGH Department of Neurology/Memory Disorders Unit (H.D.R., S.M.G.), Boston, Mass; and the MGH Center for Human Genetic Research (J.R.), Boston, Mass.

* To whom correspondence should be addressed. E-mail: salat{at}nmr.mgh.harvard.edu.

Background and Purpose--Cerebral amyloid angiopathy (CAA) represents {beta}-amyloid deposition in the small- and medium-sized vessels of the brain and meninges. CAA contributes to altered vessel function and is associated with white matter damage, cognitive impairment, and most salient, hemorrhagic stroke. We used diffusion tensor imaging to evaluate the anatomic distribution of white matter degeneration in participants diagnosed with advanced CAA.

Methods--Diffusion tensor imaging was obtained from 11 participants diagnosed with CAA-related intracerebral hemorrhage and 13 matched healthy control participants. Fractional anisotropy (FA) and diffusivity maps were compared using voxel based t test and region-of-interest analyses.

Results--FA was reduced in CAA in temporal white matter and in the splenium of the corpus callosum (P<0.001 with {approx}17% reduction in temporal white matter and 15% reduction in the splenium). FA was marginally increased in CAA in the posterior limb of the internal capsule and subthalamic gray matter regions ({approx}7% increase in subthalamic gray). FA changes were bilateral, remained significant in cluster analysis controlling for multiple comparisons, and did not depend on the hemisphere of the cerebral hemorrhage. Diffusivity was not substantially altered.

Conclusions--These findings suggest that a pattern of regional brain tissue degeneration is a characteristic feature of advanced CAA.


Key words: aging • amyloid • cerebral hemorrhage • dementia • diffusion




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