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From the Department of Neurology (Y.W.C.), Li-Shin Hospital and National Taiwan University Hospital, Taipei; Department of Neurology (M.E.G.), University of Iowa Hospitals and Clinics, Iowa City; and Department of Neurology, Neurology Clinical Trials Unit (J.R., A.V., S.M.R., T.R.G., S.M.G., E.E.S.), and Center for Human Genetics Research (J.R.), Massachusetts General Hospital and Harvard Medical School, Boston.
Address correspondence and reprint requests to Dr. Eric E. Smith, Massachusetts General Hospital, VBK 725, 55 Fruit Street, Boston, MA 02114; e-mail: eesmith{at}partners.org
Objective: To determine the rate of progression of white matter lesions and hemorrhages in a cohort with cerebral amyloid angiopathy (CAA).
Methods: The authors analyzed data from 26 patients with possible (3) or probable (23) CAA, diagnosed by the Boston Criteria. Brain maps of white matter hyperintensities, normalized to head size (nWMH), were created by blinded computer-assisted segmentation of MRI images obtained at baseline and after a median follow-up interval of 1.1 year.
Results: There was a substantial nWMH volume increase over the interscan interval (median 0.5 mL/year, interquartile range 0.1 to 2.8, p < 0.001). The median yearly increase, expressed as a percentage of the baseline WMH volume, was 18%. The characteristic most strongly associated with nWMH volume increase was the baseline nWMH volume (r = 0.57, p = 0.002). The volume of nWMH progression was also associated with history of cognitive impairment (median 5.0 mL/year in cognitively impaired subjects vs 0.3 mL/year in cognitively unimpaired, p = 0.02) but not age or hypertension. This association remained present in an analysis stratified by baseline WMH volume. New hemorrhages, including asymptomatic microbleeds, were seen in 46% of subjects. The number of new MRI hemorrhages correlated strongly with baseline nWMH (r = 0.53, p = 0.005) but not with nWMH progression (r = 0.22, p = 0.28).
Conclusions: There is a progressive increase in white matter lesions in subjects with cerebral amyloid angiopathy. The association of white matter lesions with incident lobar hemorrhages suggests that white matter damage may reflect a progressive microangiopathy due to cerebral amyloid angiopathy.
Supported by a grant from the National Institute of Neurologic Disorders and Stroke (K23 NS-046327, principal investigator Dr. Eric Smith).
Disclosure: The authors report no conflicts of interest.
Received December 20, 2005. Accepted in final form March 20, 2006.
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