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Updated: Mar 26, 2026

Brain Infarct Segmentation and Registration on MRI or CT for Lesion-symptom Mapping
Published on: September 25, 2019
Facing the Time Window in Acute Ischemic Stroke: The Infarct Core
C J Maurer1, K Egger2, A-K Dempfle2
1Department of Neuroradiology, University Medical Center Freiburg, Breisacher Straße 64, 79106, Freiburg, Germany. christoph.johannes.maurer@uniklinik-freiburg.de.
Background:
Increasing numbers needed to treat within the first hours after ischemic stroke onset indicate a strong time dependency of the viability of brain tissue. However, this time dependency is not reflected in recent randomized controlled trials of endovascular stroke treatment. This study evaluates whether and to which extent a time dependency exists in patients with embolic carotid T or M1 occlusions within the first 6 h of stroke onset.
Methods:
Patient data were retrieved from the Freiburg stroke data bank. Time from onset to acquisition of the diffusion weighted images (DWIs) varied between 49 and 357 min. Ischemic lesions were semiautomatically segmented on apparent diffusion coefficient maps with a threshold of 600 × 10 (- 6) mm(2)/s. Occlusion location and thrombus length were determined with magnetic resonance angiography, T2*, and more recently susceptibility weighted image (SWI) sequences. A hyperintense vessel sign in FLAIR images as a possible surrogate for collaterals was also identified.
Results:
A total of 155 patients with occlusions of the carotid T (n = 26), proximal M1 segment (n = 44), and distal M1 segment (n = 85) of the middle cerebral artery between 2011 and 2015 were included. Infarct volumes varied from 0.3 to 180.2 mL. Infarct size did not correlate with stroke onset to DWI times. Infarct volumes also did not associate with different locations of vessel occlusion, thrombus length, presence of the hyperintense vessel sign and initial infarct growth.
Conclusion:
We found no significant time dependency of the viability of brain tissue with embolic carotid T or M1 occlusions between 1 and 6 h after stroke onset. The early infarction volume is thus probably determined in the hyperacute phase by the quality of leptomeningeal collaterals and comparatively stable in this time period.
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