London, United Kingdom 2013 E-Poster Session Red Cerebrovasc Dis 2013; 35 (suppl 3)1-854 229 E-Poster Terminal 2 1 Brain imaging Long-term development of cerebral microbleeds in the APP23-transgenic mouse model of ce-rebral amyloid angiopathy B. Reuter1, A. Venus2, S. Grudzenski3, P. Heiler4, L. Schad5, M. Staufenbiel6, M.G. Hennerici7, M. Fatar8 Department of Neurology, Universitätsmedizin Mannheim, University of Heidelberg, Mann-heim, GERMANY1, Department of Neurology, Universitätsmedizin Mannheim, University of Heidelberg, Mannheim, GERMANY2, Department of Neurology, Universitätsmedizin Mannheim, University of Heidelberg, Mannheim, GERMANY3, Computer Assisted Clinical Medicine, Uni-versitätsmedizin Mannheim, University of Heidelberg, Mannheim, GERMANY4, Computer As-sisted Clinical Medicine, Universitätsmedizin Mannheim, University of Heidelberg, Mannheim, GERMANY5, Neuroscience Discovery, Novartis Institutes for BioMedical Research, Basel, SWIT-ZERLAND6, Department of Neurology, Universitätsmedizin Mannheim, University of Heidelberg, Mannheim, GERMANY7, Department of Neurology, Universitätsmedizin Mannheim, University of Heidelberg, Mannheim, GERMANY8 Background In Western societies, neurodegenerative diseases including cerebral amyloid angiopathy (CAA) manifest increasingly with age. In CAA, deposition of amyloid beta (AB) in brain vessels is the main early pathological substrate of CAA, potentially anticipating the risk of sequential sponta-neous intracerebral hemorrhage (ICH). Silent cerebral microbleeds (cMBs) illustrated on magnetic resonance imaging (MRI) is the most appropriate non-invasive tool to investigate the burden of AB deposition and identifies typical imaging patterns, sometimes already in healthy subjects. Experi-mental findings are scarce and selection of best suitable conditions to estimate the risk for cMBs and ICH are unknown. Methods APP23-transgenic (tg) mice overexpress amyloid precursor protein with the Swedish mutation. Vas-cular AB deposition starts with the age of 8 months, while cMBs occur later. We performed a 9.4 Tesla high field MRI study using T2, T2* (coronal plane, 18 slides each) and time of flight-MRA (TOF-MRA, raw data 128 slides) in 8 to 24 month old APP23-tg mice. Results APP23-tg mice (n=6 per group) were analyzed at ages of 8, 12, 16, 20, and 24 months, respectively. MRI revealed the occurrence of cMBs at the age of 16 months at the earliest (2.33 ± 1.75 cMBs). We discovered an exponential increase over time, with 14.5 ± 4.03 cMBs at 20 months, and 39.5 ± 22 cMBs at 24 months. Irregularities of the large intracranial arterial vessels were detectable for the first time at 16 months. Conclusion Numbers of cMBs increase exponentially over time, beginning at the age of 16 months. At 24 months the interindividual distribution of cMBs is increasingly variable. MRI studies in APP23-tg mice should be performed in animals > 20 to 24 months of age for future experimental therapeutic studies of the prognosis of CAA and the risk of cMBs and ICH. 2 Brain imaging Multi-modal MRI may detect embolic mechanisms in lacunar stroke M.E. Wolf1, M.G. Hennerici2, K. Szabo3, R. Kern4 Department of Neurology; UniversitaetsMedizin Mannheim; University of Heidelberg, Mann-heim, GERMANY1, Department of Neurology; UniversitaetsMedizin Mannheim; University of Heidelberg, Mannheim, GERMANY2, Department of Neurology; UniversitaetsMedizin Mannheim; University of Heidelberg, Mannheim, GERMANY3, Department of Neurology; UniversitaetsMediz-in Mannheim; University of Heidelberg, Mannheim, GERMANY4 Background: Acute subcortical lacunar infarction is mostly caused by small vessel disease due to local occlusion of a small penetrating cerebral artery. However, in rare cases, lacunar lesions may also be caused by other aetiologies, e.g. large artery disease or cardiac embolism. Multi-modal MRI including MR angiography, diffusion (DWI)- and perfusion weighted imaging (PWI) can provide valuable information about the underlying aetiology of stroke e.g. macrovascular obstruction and “PWI-/DWI-mismatch”. We hypothesized that multi-modal MRI is also useful to detect an alterna-tive (i.e. embolic) mechanism of lacunar infarction rather than small vessel disease. Methods: From a prospectively collected stroke-/MR-database of more than 7000 stroke patients, 105 patients with acute ischemic stroke and PWI-/DWI-mismatch were screened for isolated subcor-tical acute ischemic lesions (<15 mm Ø). Clinical data and technical investigations from all patients were collected and recorded according to a standardized acute stroke care protocol. Results: The vast majority of patients with PWI-/DWI-mismatch had territorial infarcts. Only six pa-tients (5.7%) with isolated lacunar infarction on DWI were identified, of whom 4 patients presented with a typical lacunar stroke syndrome (Figure). In 2 patients a cardiac source of embolism could be identified, the cause was undetermined in the remaining 4 patients. Conclusion: Multi-modal MRI including PWI and MR angiography may identify rare cases of acute lacunar infarction and typical clinical presentation but additional, larger perfusion deficits not being compatible with the classical mechanism of small vessel disease. This additional information might have an impact on the stroke work-up as well as on secondary prevention.
Karger_ESC London_2013
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