{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,19]],"date-time":"2026-09-19T05:58:30Z","timestamp":1789797510980,"version":"4.0.1"},"reference-count":19,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2025,6,5]],"date-time":"2025-06-05T00:00:00Z","timestamp":1749081600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100012550","name":"Nemzeti Kutat\u00e1si, Fejleszt\u00e9si \u00e9s Innovaci\u00f3s Alap","doi-asserted-by":"publisher","award":["TKP\u20102021\u2010EGA\u201032"],"award-info":[{"award-number":["TKP\u20102021\u2010EGA\u201032"]}],"id":[{"id":"10.13039\/501100012550","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100012550","name":"Nemzeti Kutat\u00e1si, Fejleszt\u00e9si \u00e9s Innovaci\u00f3s Alap","doi-asserted-by":"publisher","award":["2017\u20101\u20101.1.2.1\u2010NKP\u20102017\u20100002"],"award-info":[{"award-number":["2017\u20101\u20101.1.2.1\u2010NKP\u20102017\u20100002"]}],"id":[{"id":"10.13039\/501100012550","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Neuropathology"],"published-print":{"date-parts":[[2025,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Cerebral amyloid angiopathy (CAA) has been implicated as a risk for developing lobar intracerebral hemorrhage (ICH) after intravenous thrombolysis (IVT) applied for acute ischemic stroke (AIS). However, there is a paucity of cases reported with histopathological CAA diagnosis in this setting, with a single report to imply the role of CAA\u2010related inflammation (CAA\u2010RI). We report clinical, radiological, and neuropathological observations of a 65\u2010year\u2010old woman who presented with acute left\u2010hemispheric symptoms with an initially unrevealing cranial computed tomography (CT) and received IVT for presumed AIS. The course was rapidly complicated by a huge lobar ICH and a fatal outcome. The autopsy revealed severe CAA, unexpectedly with transmural CAA\u2010RI, a.k.a. amyloid\u2010\u03b2\u2010related angiitis (ABRA), and histopathological evidence for vascular amyloid\u2010\u03b2 phagocytosis. Re\u2010evaluation of initial imaging did not reveal signs of asymmetric confluent white matter edema characteristic of CAA\u2010RI, but raised the suspicion of a tiny left central convexity subarachnoid hemorrhage, a substrate of amyloid spells. The genotype of the apolipoprotein E (ApoE) gene (<jats:italic>ApoE<\/jats:italic>) was \u03b53\/\u03b53. Being the second published thrombolysis\u2010associated fatality with ABRA and among the few with definite CAA, the present case confirms CAA\/CAA\u2010RI to be a potential hidden risk for IVT\u2010associated ICHs, urging for awareness of CAA\u2010associated pathologies and clinical\u2010radiological hints in an AIS setting. The findings implicate the relevance of vascular A\u03b2 phagocytosis in the pathogenesis, confirm that CAA\u2010RI may present without prominent edema, highlight that CAA\/CAA\u2010RI\u2010related focal neurological deficits (including amyloid spells) can be potential AIS mimics within the IVT time window, and urge for rigorous analysis of pre\u2010IVT CT scans for even subtle sulcal hyperdensities suggesting cSAH\/amyloid spell in elderly patients, prompting consideration of magnetic resonance imaging.<\/jats:p>","DOI":"10.1111\/neup.70013","type":"journal-article","created":{"date-parts":[[2025,6,6]],"date-time":"2025-06-06T00:39:35Z","timestamp":1749170375000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Fatal Outcome of Intravenous Thrombolysis With an Unexpected Finding of Amyloid\u2010\u03b2\u2010Related Angiitis\u2014A Case Report Highlighting a Relevant Scenario With Acute Focal Neurological Deficits and Minimal Radiological Presentation"],"prefix":"10.1111","volume":"45","author":[{"given":"Kristof","family":"Babarczy","sequence":"first","affiliation":[{"name":"Department of Neurology, Albert Szent\u2010Gy\u00f6rgyi Medical School, Albert Szent\u2010Gy\u00f6rgyi Clinical Center University of Szeged  Szeged Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bence L.","family":"Radics","sequence":"additional","affiliation":[{"name":"Institute of Pathology, Albert Szent\u2010Gy\u00f6rgyi Medical School, Albert Szent\u2010Gy\u00f6rgyi Clinical Center University of Szeged  Szeged Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Orsolya","family":"Horvath","sequence":"additional","affiliation":[{"name":"Department of Neurology, Albert Szent\u2010Gy\u00f6rgyi Medical School, Albert Szent\u2010Gy\u00f6rgyi Clinical Center University of Szeged  Szeged Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5389-3266","authenticated-orcid":false,"given":"Peter","family":"Klivenyi","sequence":"additional","affiliation":[{"name":"Department of Neurology, Albert Szent\u2010Gy\u00f6rgyi Medical School, Albert Szent\u2010Gy\u00f6rgyi Clinical Center University of Szeged  Szeged Hungary"},{"name":"HUN\u2010REN\u2010SZTE Neuroscience Research Group  Szeged Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1084-6195","authenticated-orcid":false,"given":"Levente","family":"Szalardy","sequence":"additional","affiliation":[{"name":"Department of Neurology, Albert Szent\u2010Gy\u00f6rgyi Medical School, Albert Szent\u2010Gy\u00f6rgyi Clinical Center University of Szeged  Szeged Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2025,6,5]]},"reference":[{"key":"e_1_2_12_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1474-4422(22)00208-3"},{"key":"e_1_2_12_3_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00702-020-02174-2"},{"key":"e_1_2_12_4_1","doi-asserted-by":"publisher","DOI":"10.1002\/alz.12366"},{"key":"e_1_2_12_5_1","doi-asserted-by":"publisher","DOI":"10.1161\/STROKEAHA.112.657759"},{"key":"e_1_2_12_6_1","doi-asserted-by":"publisher","DOI":"10.1111\/nan.12946"},{"key":"e_1_2_12_7_1","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.0000000000209647"},{"key":"e_1_2_12_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1474-4422(18)30006-1"},{"key":"e_1_2_12_9_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1789.2011.01219.x"},{"key":"e_1_2_12_10_1","doi-asserted-by":"publisher","DOI":"10.1186\/s12883-022-03029-x"},{"key":"e_1_2_12_11_1","doi-asserted-by":"publisher","DOI":"10.1002\/ana.27164"},{"key":"e_1_2_12_12_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1474-4422(04)00825-7"},{"issue":"1","key":"e_1_2_12_13_1","article-title":"Cerebral Amyloid Angiopathy: A Hidden Risk for IV Thrombolysis?","volume":"2","author":"Felling R. 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