HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Figures Only Full Text Full Text (PDF) Correspondence: Submit a response Correspondence: View responses Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kimberly, W. T. Articles by Greenberg, S. M. Search for Related Content PubMed PubMed Citation Articles by Kimberly, W. T. Articles by Greenberg, S. M. Related Collections DWI Vascular dementia Intracerebral hemorrhage

Silent ischemic infarcts are associated with hemorrhage burden in cerebral amyloid angiopathy

From the Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston.

Address correspondence and reprint requests to Dr. Steven M. Greenberg, J.P. Kistler Stroke Research Center, Massachusetts General Hospital, 175 Cambridge St, Boston, MA 02114

Background: Neuropathologic studies suggest an association between cerebral amyloid angiopathy (CAA) and small ischemic infarctions as well as hemorrhages. We examined the prevalence and associated risk factors for infarcts detected by diffusion-weighted imaging (DWI).

Methods: We performed retrospective analysis of MR images from 78 subjects with a diagnosis of probable CAA and a similar aged group of 55 subjects with Alzheimer disease or mild cognitive impairment (AD/MCI) for comparison. DWI and apparent diffusion coefficient (ADC) maps were inspected for acute or subacute infarcts. We also examined the association between DWI lesions and demographic variables, conventional vascular risk factors, and radiographic markers of CAA severity such as number of hemorrhages on gradient-echo MRI and volume of T2-hyperintense white matter lesions.

Results: Twelve of 78 subjects with CAA (15%) had a total of 17 DWI-hyperintense lesions consistent with subacute cerebral infarctions vs 0 of 55 subjects with AD/MCI (p = 0.001). The DWI lesions were located primarily in cortex and subcortical white matter. CAA subjects with DWI lesions had a higher median number of total hemorrhages (22 vs 4, p = 0.025) and no difference in white matter hyperintensity volume or conventional vascular risk factors compared to subjects with CAA without lesions.

Conclusions: MRI evidence of small subacute infarcts is present in a substantial proportion of living patients with advanced cerebral amyloid angiopathy (CAA). The presence of these lesions is associated with a higher burden of hemorrhages, but not with conventional vascular risk factors. This suggests that advanced CAA predisposes to ischemic infarction as well as intracerebral hemorrhage.

AD = Alzheimer disease; ADC = apparent diffusion coefficient; CAA = cerebral amyloid angiopathy; DWI = diffusion-weighted imaging; FLAIR = fluid-attenuated inversion recovery; GRE = gradient-echo; HTN = hypertension; ICH = intracerebral hemorrhage; MCI = mild cognitive impairment; MGH = Massachusetts General Hospital; nWMH = normalized white matter hyperintensity volumes; WMH = white matter T2-hyperintense lesions.

sgreenberg{at}partners.org

Supported by NIH grants RO1 AG026484 and K24 NS056207.

Disclosure: The authors report no disclosures.

Medical Devices: Signa scanner (GE Medical Systems, Milwaukee, WI).

Received September 2, 2008. Accepted in final form January 21, 2009.

This article has been cited by other articles:

				R. S. Menon and C. S. Kidwell Neuroimaging Demonstration of Evolving Small Vessel Ischemic Injury in Cerebral Amyloid Angiopathy Stroke, December 1, 2009; 40(12): e675 - e677. [Abstract] [Full Text] [PDF]

				C. S. Kidwell and S. M. Greenberg Red meets white: Do microbleeds link hemorrhagic and ischemic cerebrovascular disease? Neurology, November 17, 2009; 73(20): 1614 - 1615. [Full Text] [PDF]

Correspondence: