London, United Kingdom 2013 7 Stroke prognosis 9:30 - 9:40 Influence of lesion location on early recovery in acute ischemic stroke: a voxel-lesion map-ping Cerebrovasc Dis 2013; 35 (suppl 3)1-854 19 study of 550 patients P. Bentley1, G. Kumar2, P. Rinne3, S. Buddha4, J. Kalligan5, P. Sharma6, A. Mehta7, C. Beck-mann8 Imperial College London, London, UNITED KINGDOM1,Imperial College London, Lon-don, UNITED KINGDOM2, Imperial College London, London, UNITED KINGDOM3, Im-perial College London, London, UNITED KINGDOM4, Imperial College London, London, UNITED KINGDOM5, Imperial College London, London, UNITED KINGDOM6, Imperial College London, London, UNITED KINGDOM7, University of Twente, Twente, THE NETH-ERLANDS8 Background – The wide heterogeneity of stroke recovery depends partly upon whether certain critical regions of the brain are lesioned. Here we ask the broader questions of: which of all common stroke locations influence early recovery, and how much variance can be accounted for by these? Methods – Functional scores (NIH Stroke Scale, modified Rankin Scale) over the first week were derived from the clinical records of 550 consecutive acute ischemic stroke patients, all of whom presented to a single centre, and underwent MRI. Baseline severity and percentage re-covery rates were related to DWI-positive lesion location using a multivariate voxel-lesion sta-tistical mapping approach that interrogated both single voxels in isolation and conjunctions of spatially-separate voxels. Results - High NIHSS baseline deficit was associated with lesions to left capsule, striatum and thalamic white matter relays, whereas high recovery rates (of overall NIHSS and its motor and aphasia components) occurred with lesions to left frontal cortico-cortical tracts and left insu-lar- opercular cortices. Low NIHSS (and motor component) recovery rates were associated with lesions to bilateral parietal, medial frontal, right insula, capsule, and brainstem. The inclusion of these regions in a multivariate conjunction model of stroke recovery rate increased variance explained (r-squared) from 6% to 52% (or from 46% to 71% in a binary logistic model of com-plete versus incomplete recovery). Conclusions – A large proportion of stroke recovery heterogeneity can be explained by lesion location. Associations between lesion topography and outcome can be improved by data-inten-sive techniques that assess location in more than one place at a time. 6 Stroke prognosis 9:20 - 9:30 IST-3 trial: impact of rt-PA on survival to 18 months post ischaemic stroke W.N. Whiteley1, G. Cohen2, J. Wardlaw3, R. Lindley4, P.A.G. Sandercock5 on behalf of the IST-3 collaborative group University of Edinburgh, Edinburgh, UNITED KINGDOM1,University of Edinburgh, Ed-inburgh, UNITED KINGDOM2, University of Edinburgh, Edinburgh, UNITED KINGDOM3, Sydney Medical School – Westmead Hospital and The George Institute for Global Health, University of Sydney, Australia, Sydney, AUSTRALIA4, University of Edinburgh, Edinburgh, UNITED KINGDOM5 BACKGROUND The effect of rtPA on long-term survival after ischaemic stroke is uncertain. A Cochrane me-ta- analysis of summary data from rtPA trials before IST-3 demonstrated a non-significant in-crease in the odds of death (OR 1.14, 95%CI: 0.95 to 1.38) by final follow up. However, the du-ration of follow up in most studies was short, and the reduction of disability by rtPA treatment could lead to longer term survival gains. METHODS IST-3 was a randomised, open label, trial of rtPA in patients with acute ischaemic stroke. At 6 months follow up, IST-3 found a small non-significant difference between rtPA and control in the odds of the primary outcome ‘death or dependence’, but a statistically significant benefit from rtPA with an ordinal analysis of the whole Oxford Handicap Scale. All patients were fol-lowed to least until 18 months in most countries. We analysed data with Kaplan Meier (KM) and proportional hazard methods. RESULTS 3035 patients were randomised in the trial: 1515 to rtPA and 1520 to control. By 18 months, there was no detectable difference in the KM survival probability between groups: rtPA 0.64 (95%CI:0.62-0.66, 532 deaths) versus control 0.63 (95%CI:0.61-0.66, 542 deaths) log rank p=0.54. Between randomisation and 18 month follow up there was a non-significant reduction in the hazard of death with rtPA treatment after adjustment for age, NIHSS, delay from stroke to randomisation, and infarct visible on brain imaging (hazard ratio:0.96, 95%CI: 0.85-1.09). CONCLUSIONS There was no detectable difference in survival between patients treated with rtPA and control over the 18 months of follow up. The benefits of rtPA on the distribution of the 6 month Oxford Handicap Scale did not translate into a significant longer term survival benefit.
Karger_ESC London_2013
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