22. European Stroke Conference 441 Small vessel stroke and white matter disease High prevalence of cerebral amyloid angiopathy (CAA) at post-mortem examination in elderly stroke service patients. M.J. Crowe1, I. Noone2, M. Farrell3, D. O’Shea4 St.Vincent’s University Hospital, Elm Park,, Dublin 4, IRELAND1, St.Vincent’s University Hos-pital, Elm Park,, Dublin 4, IRELAND2, St.Vincent’s University Hospital, Elm Park,, Dublin 4, IRE-LAND3, St.Vincent’s University Hospital, Elm Park,, Dublin 4, IRELAND4 BACKGROUND Sporadic CAA is associated with a spectrum of clinical disorders including cere-bral haemorrhage; rapidly progressive cognitive and neurological decline, transient focal neurolog-ical episodes and dementia. Definitive diagnosis of CAA depends on neuropathologic demonstra-tion of vascular amyloid METHODS We reviewed the post–mortem neuropathologic findings in 8 patients (mean age 81 years, range 67-95) of a total of 48 inpatients who died in 2011 on the stroke service. Representative brain tissue blocks, stained with haematoxylin & eosin and immunostained with anti-βA4 and tau were microscopically examined for vascular deposition of βA4 as well as plaque and tangle density. RESULTS In 5 patients the acute neurological event was due to intra-cranial haemorrhage (intracerebral, subarachnoid, subdural, alone or in combination). In one other patient intracerebral haemorrhage complicated thrombolysis for an acute cerebral infarct. Of the 6 patients, 4 had CAA in parenchymal, meningeal and perivascular distributions. Of the remaining 2 patients with acute cerebral infarcts, one had capillary CA. Although 5/8(62%) had CAA, none had a high probability of Alzheimer Disease (AD) based on the ABC scores for AD neuropatholog-ic change (1) . CONCLUSION The high prevalence of CAA (62%) in this study is consistent with other population based autopsy studies(20-60%)in the elderly(2). However the role of CAA in the pathogenesis of acute neurological events in our patients requires further evaluation. 520 © 2013 S. Karger AG, Basel Scientific Programme 442 Small vessel stroke and white matter disease Spatial relationships between incident lacunes and white matter hyperintensities in cerebral small vessel disease: a systematic analysis M. Duering1, E. Csanadi2, B. Gesierich3, E. Jouvent4, D. Hervé5, S. Seiler6, B. Belaroussi7, S. Ropele8, R. Schmidt9, H. Chabriat10, M. Dichgans11 Institute for Stroke and Dementia Research, University of Munich, Munich, GERMANY1, Department of Neurology, University of Munich, Munich, GERMANY2, Institute for Stroke and Dementia Research, University of Munich, Munich, GERMANY3, Department of Neurology, CHU Lariboisière, APHP, Paris, FRANCE4, Department of Neurology, CHU Lariboisière, APHP, Paris, FRANCE5, Department of Neurology, Medical University of Graz, Graz, AUSTRIA6, Bioclinica SAS, Lyon, FRANCE7, Department of Neurology, Medical University of Graz, Graz, AUSTRIA8, Department of Neurology, Medical University of Graz, Graz, AUSTRIA9,Department of Neurology, CHU Lariboisière, APHP, Paris, FRANCE10, Institute for Stroke and Dementia Research, University of Munich, Munich, GERMANY11 Background: The mechanisms of cerebral small vessel disease (SVD) are incompletely understood. The pathological processes underlying white matter hyperintensities (WMH) and lacunes are of growing interest since small vessel disease has been identified as the major cause of vascular cogni-tive impairment. Methods: We analyzed the distribution and spatial relationships of incident lacunes and WMH in a large cohort of subjects with pure small vessel disease. We followed 276 patients with CADASIL over a total of 633 patient years. Using difference images and Jacobian maps from registered T1 im-ages we identified 104 incident lacunes. The spatial relationships with WMH were evaluated using a visual rating scale on FLAIR images. The vascular topology was taken into account by comparison with an atlas of the cerebral microvasculature. Furthermore, we added cross-sectional data from a cohort with age-related, sporadic small vessel disease (n=588). Results: The main findings can be summarized as follows: The majority of incident lacunes devel-oped at the edge of a WMH. This pattern was also found for prevalent lacunes (n=14) in age-related small vessel disease. Most incident lacunes developed proximal to a white matter hyperintensitiy with regard to the anatomy of perforating vessels. Lesion prevalence maps across different disease stages showed a spread of lesions from the periventricular to subcortical regions in both inherited and age-related SVD. Conclusion: The link between WMH and lacunes regarding their spatial relationship argues for a common, chronically advancing process underlying both WMH and lacunes. This process seems to start in the periventricular vascular end zone and spread converse to the blood flow direction along perforating arteries.
Karger_ESC London_2013
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