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. 2024 Apr 9;15:1383494. doi: 10.3389/fneur.2024.1383494

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Copyright © 2024 Schmidt-Pogoda, Kaesmacher, Bonberg, Werring, Strecker, Koecke, Beuker, Gralla, Meier, Wiendl, Minnerup, Fischer and Minnerup.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Delayed infarct volume growth is the target of neuroprotection in animal stroke, but most stroke patients with successful recanalization do not offer this target. (A,B) Infarct growth after tMCAO in rodents without neuroprotective treatment. (A) Black and green lines connect the mean infarct volumes of untreated animals determined at timepoints 1 and 2 in each individual study. (B) Each cross represents the change in mean infarct volumes in an individual study. The median change in mean infarct volumes was 74%. (C,D) Infarct growth after tMCAO in rodents with neuroprotective treatment. (C) Black and green lines connect the mean infarct volumes of treated animals determined at timepoints 1 and 2 in each individual study. (D) Each cross represents the change in mean infarct volumes in an individual study. The median change in mean infarct volumes was 23%. (E,F) Infarct growth in stroke patients with TICI 2b-3 thrombectomy. (E) Black lines connect the infarct volumes at timepoints 1 and 2 in each patient. The red line represents an overall regression line given by the fixed effects of the mixed model. (B) Each cross represents the infarct volume growth in a patient. The median change in infarct volumes was only 2%.