{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,22]],"date-time":"2026-01-22T18:27:05Z","timestamp":1769106425932,"version":"3.49.0"},"reference-count":21,"publisher":"S. Karger AG","issue":"2","license":[{"start":{"date-parts":[[2013,1,1]],"date-time":"2013-01-01T00:00:00Z","timestamp":1356998400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2013,1,1]],"date-time":"2013-01-01T00:00:00Z","timestamp":1356998400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cerebrovasc Dis"],"published-print":{"date-parts":[[2013]]},"abstract":"<b><i>Introduction:<\/i><\/b> Hyperglycaemia (HG) occurs in 30-40% of the patients with acute ischaemic stroke and is associated with larger infarct size and poor functional outcome. It is unknown whether HG is also associated with larger perfusion deficits in the acute stage of ischaemic stroke. As perfusion computed tomography (CT) is a reliable technique to determine the infarct core and ischaemic penumbra, we aimed to determine if patients with acute ischaemic stroke and HG have larger perfusion deficits or infarct cores on admission perfusion CT than patients with normoglycaemia (NG). <b><i>Methods:<\/i><\/b> We identified 80 consecutive patients (mean age 69 \u00b1 11 years, 58% men) with acute supratentorial non-lacunar ischaemic stroke in whom CT showed a perfusion deficit within 24 h after stroke onset. The size of the total perfusion deficit area (mean transit time of >145% compared to the contralateral hemisphere) and the infarct core area (cerebral blood volume of <2.0 ml\/100 g) at the level of the basal ganglia (level 1) and at the level of the corona radiata (level 2) were compared between patients with HG (admission glucose \u22657.0 m<smlcap>M<\/smlcap>) and patients with NG with a MANOVA. Clinical outcome [modified Rankin Scale (mRS) score] after 6 months was correlated to glucose levels at admission. <b><i>Results:<\/i><\/b> Admission HG was present in 33 of the 80 patients (41%). A perfusion deficit was present in 79 (40% HG) patients at level 1 and 75 (43% HG) at level 2. The total area with a perfusion deficit (level 1 HG 22.1 \u00b1 11.3 and NG 23.3 \u00b1 12.3 cm<sup>2<\/sup>; level 2 HG 27.1 \u00b1 12.3 and NG 25.4 \u00b1 12.0 cm<sup>2<\/sup>) and the proportion of the infarct core (level 1 HG 31 \u00b1 30% and NG 25 \u00b1 22%; level 2 HG 33 \u00b1 27% and NG 26 \u00b1 23%) did not differ significantly between the groups. HG was associated with worse outcome (mRS \u22653) at 6 months (OR 2.6, 95% CI 0.72-9.1). <b><i>Conclusions:<\/i><\/b> As compared to patients with NG, patients with HG did not have larger perfusion deficits in the acute stage of ischaemic stroke. Nevertheless, functional outcome was worse in patients with HG, which means that poor clinical outcome in stroke patients with HG could not be explained by a larger perfusion deficit in the acute stage. Therefore, our study suggests that there might be a window of opportunity for glucose-lowering therapy in the future.<\/jats:p>","DOI":"10.1159\/000346588","type":"journal-article","created":{"date-parts":[[2013,2,21]],"date-time":"2013-02-21T09:28:43Z","timestamp":1361438923000},"page":"163-167","source":"Crossref","is-referenced-by-count":31,"title":["Admission Hyperglycaemia and Cerebral Perfusion Deficits in Acute Ischaemic Stroke"],"prefix":"10.1159","volume":"35","author":[{"given":"Merel J.A.","family":"Luitse","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tom","family":"van Seeters","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alexander D.","family":"Horsch","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hieke A.","family":"Kool","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Birgitta K.","family":"Velthuis","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L. Jaap","family":"Kappelle","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Geert Jan","family":"Biessels","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"127","published-online":{"date-parts":[[2013,2,21]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","DOI":"10.1161%2Fhs1001.096194"},{"key":"ref2","doi-asserted-by":"publisher","DOI":"10.1093%2Fbrain%2Fawm087"},{"key":"ref3","doi-asserted-by":"publisher","DOI":"10.1097%2F01.nrl.0000131800.77824.dd"},{"key":"ref4","doi-asserted-by":"publisher","DOI":"10.1016%2FS1474-4422%2812%2970005-4"},{"key":"ref5","doi-asserted-by":"publisher","DOI":"10.1159%2F000321332"},{"key":"ref6","doi-asserted-by":"publisher","DOI":"10.1161%2F01.STR.0000085087.41330.FF"},{"key":"ref7","doi-asserted-by":"publisher","DOI":"10.1038%2Fnrneurol.2009.231"},{"key":"ref8","doi-asserted-by":"publisher","DOI":"10.1002%2Fana.10241"},{"key":"ref9","doi-asserted-by":"publisher","DOI":"10.1161%2F01.STR.0000068406.30514.31"},{"key":"ref10","doi-asserted-by":"publisher","DOI":"10.1161%2F01.STR.0000023579.61630.AC"},{"key":"ref11","doi-asserted-by":"publisher","DOI":"10.1212%2F01.wnl.0000255959.30107.08"},{"key":"ref12","doi-asserted-by":"publisher","DOI":"10.1161%2F01.STR.0000131271.54098.22"},{"key":"ref13","doi-asserted-by":"publisher","DOI":"10.1007%2Fs00234-009-0575-y"},{"key":"ref14","doi-asserted-by":"publisher","DOI":"10.1161%2F01.STR.0000209238.61459.39"},{"key":"ref15","doi-asserted-by":"publisher","DOI":"10.1016%2Fj.jns.2008.02.020"},{"key":"ref16","doi-asserted-by":"publisher","DOI":"10.1161%2F01.STR.30.4.793"},{"key":"ref17","doi-asserted-by":"publisher","DOI":"10.1161%2F01.STR.19.5.604"},{"key":"ref18","doi-asserted-by":"publisher","DOI":"10.1159%2F000047756"},{"key":"ref19","doi-asserted-by":"publisher","DOI":"10.1161%2F01.STR.18.1.52"},{"key":"ref20","doi-asserted-by":"publisher","DOI":"10.1097%2F00004647-199705000-00009"},{"key":"ref21","doi-asserted-by":"publisher","DOI":"10.1212%2FWNL.41.6.899"}],"container-title":["Cerebrovascular Diseases"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/346588","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/346588","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,23]],"date-time":"2025-04-23T18:48:07Z","timestamp":1745434087000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000346588"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2013]]},"references-count":21,"journal-issue":{"issue":"2","published-online":{"date-parts":[[2013,3,1]]},"published-print":{"date-parts":[[2013,3,11]]}},"URL":"https:\/\/doi.org\/10.1159\/000346588","archive":["Portico"],"relation":{},"ISSN":["1015-9770","1421-9786"],"issn-type":[{"value":"1015-9770","type":"print"},{"value":"1421-9786","type":"electronic"}],"subject":[],"published":{"date-parts":[[2013]]}}}