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22. European Stroke Conference 8 Small vessel stroke and white matter disease 15:40 - 15:50 Evidence for an ischemic origin of deep brain ‘microbleeds’ P. G. Ince1, B. Janaway2, S. B. Wharton3, J. E. Simpson4, J. R. Highley5, F. E. Matthews6, G. Forster7, C. Brayne8 Sheffield Institute for Translational Neuroscience, University of Sheffield, Sheffield, UNITED KINGDOM1,Sheffield Institute for Translational Neuroscience, University of Shef-field, Sheffield, UNITED KINGDOM2, Sheffield Institute for Translational Neuroscience, University of Sheffield, Sheffield, UNITED KINGDOM3, Sheffield Institute for Translational Neuroscience, University of Sheffield, Sheffield, UNITED KINGDOM4, Sheffield Institute for Translational Neuroscience, University of Sheffield, Sheffield, UNITED KINGDOM5, MRC Biostatistics Unit, Cambraidge, UNITED KINGDOM6, Sheffield Institute for Translational Neuroscience, University of Sheffield, Sheffield, UNITED KINGDOM7, Institute of Public Health, Cambridge, UNITED KINGDOM8 Background: MRI microbleeds have uncertain clinical implications. Microscopy of ageing brain shows abundant haemosiderin (HM) in macrophages with no evidence of previous hem-orrhage. These two approaches to the demonstration of non-metabolic iron need rationalising. We hypothesise that brain HM can be derived from haem-containing proteins and stored ferri-tin- iron released by ischemia in addition to bleeding. Methods: Foci of HM in H&E sections of putamen were counted in 200 brain donations to a population-representative cohort of old people (www.cfas.org.uk). Ischemic change and the extent of local degenerative vascular pa-thology in the putamen was recorded. Frontal lobe tissue from 5 cases with high HM, and 5 with low HM were imaged for microbleeds, in an imaging chamber designed to present coronal slices of formalin fixed brain submerged in oil to optimise tissue contrast and lesion detection, using a 3T MRI susceptibility-weighted protocol. The relationship of putamen HM with local and global pathological changes, clinical risk factors, dementia status, HFE gene mutations, and the frequency of microbleed signal voids in frontal white matter was analysed. Results: High putamen HM density by microscopy is associated with more local small vessel ischemia (microinfarcts, p<0.05; arteriolosclerosis, p<0.05; perivascular attenuation, p<0.001) and the presence of lacunes in any brain region (p<0.05), but not large vessel disease. Putamen HM increases with age (p<0.01) but not with more severe Alzheimer pathology, HFE gene muta-tions, clinical stroke, diabetes, heart attack or dementia. Cases with more putamen HM had more MRI microbleeds outside the putamen (p<0.003). Conclusion: Basal ganglia and white matter MRI-microbleeds may better reflect brain iron homeostasis and small vessel ischaemic change in later life rather than minor episodes of cerebrovascular extravasation. These finding are therefore of clinical relevance in the management of stroke. 7 Small vessel stroke and white matter disease 15:30 - 15:40 Prevalence and mechanisms of cortical superficial siderosis in cerebral amyloid angiopa-thy A. Charidimou1, H.R. Jäger2, Z. Fox3, A. Peeters4, Y. Vandermeeren5, P. Laloux6, J.C. Baron7, D.J. Werring8 Stroke Research Group, UCL Institute of Neurology and The National Hospital for Neu-rology and Neurosurgery, Queen Square, London, UNITED KINGDOM1,Lysholm Depart-ment of Neuroradiology, UCL Institute of Neurology and National Hospital for Neurology and Neurosurgery, London, UNITED KINGDOM2, Education Unit, UCL Institute of Neurology, Queen Square, London, UNITED KINGDOM3, Department of Neurology, Cliniques Univer-sitaires UCL Saint Luc, Avenue Hippocrate, Brussels, BELGIUM4, Department of Neurology, CHU Mont-Godinne, Université Catholique de Louvain, Avenue Dr G. Therasse, Yvoir, Brus-sels, BELGIUM5, Department of Neurology, CHU Mont-Godinne, Université Catholique de Louvain, Avenue Dr G. Therasse, Yvoir, Brussels, BELGIUM6, Department of Clinical Neu-rosciences, University of Cambridge, Addenbrooke’s Hospital, Cambridge, UNITED KING-DOM7, Stroke Research Group, UCL Institute of Neurology and The National Hospital for Neurology and Neurosurgery, Queen Square, London, UNITED KINGDOM8 Background: Cortical superficial siderosis (cSS) is a promising neuroimaging marker of ce-rebral amyloid angiopathy (CAA), but the prevalence, strength of association and underlying mechanisms remain uncertain. We therefore investigated the prevalence of cSS in patients with strictly lobar ICH (probable CAA) compared to patients with spontaneous intracerebral haem-orrhage (ICH) not attributed to CAA. To gain insights into mechanisms underlying cSS, we in-vestigated associations between cSS and other clinical and imaging findings. Methods: Retrospective multicentre cohort study of 120 patients with probable CAA and 89 control subjects with non-CAA ICH (67 with “mixed” deep/lobar and 22 with “strictly deep” haemorrhage). We rated cSS, ICH, white matter changes (WMC) and cerebral microbleeds (CMBs) using validated scales. Results: cSS was detected in 48/120 (40%; 95%CI: 31.2%-49.3%) patients with probable CAA, compared to 10/67 (14.9%; 95%CI: 7.4-25.7%) with “mixed” and 1/22 (4.6%) patients with “strictly deep” haemorrhage (p<0.001 for trend). Disseminated cSS was present in 29/120 (24%: 95%CI: 16.8-32-8%) probable CAA patients but in none of the other ICH patients (p<0.001). In probable CAA, age (OR: 1.09; 95%CI: 1.03-1.15; p=0.002), chronic lobar ICH (OR: 3.94, 95%CI: 1.54-10.08; p=0.004) and transient focal neurological episodes (OR: 11.08; 95%CI: 3.49-35.19; p<0.001) were independently associated with cSS. However, cSS occurred in 17 of 48 CAA patients (35.4%, 95%CI: 22.2-50.5%) without evidence of chronic ICH. Conclusion: Our findings further support cSS (especially if disseminated) as a characteristic neuroimaging marker of CAA. In some cases cSS may be due to blood leakage into the sub-arachnoid space from previous lobar ICH, but other mechanisms, independent of lobar ICH, must also contribute. Transient focal neurological episodes are the strongest clinical marker for cSS in CAA. 42 © 2013 S. Karger AG, Basel Scientific Programme


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