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PET Imaging of Neuroinflammation Using [11C]DPA-713 in a Mouse Model of Ischemic Stroke
Published on: June 14, 2018
Temporal Imaging Dynamics in ischemic Stroke: Intensity- vs. volume-based metrics.
Horst Urbach1, Alexander Rau2, Ömer Bagcilar2
1From the Dept. of Neuroradiology, Medical Center - University of Freiburg, Faculty of Medicine (H.U., A.R., Ö.B., E.K.), University of Freiburg; Center for Stroke Research Berlin (I.G., J.F.), Charite - Universitätsmedizin Berlin; and Dept. of Medical Physics, Medical Center, University of Freiburg, Faculty of Medicine (M.R., E.K.), University of Freiburg. horst.urbach@uniklinik-freiburg.de.
Tissue signal intensities in acute ischemic stroke change more with time than volumetric measures. This suggests infarct evolution is progressive tissue injury, not just expansion, with intensity metrics better reflecting this change.
Area of Science:
- Neurology
- Radiology
- Biomedical Imaging
Background:
- The progression of ischemic tissue damage after a thromboembolic occlusion is influenced by hypoperfusion and reperfusion timing.
- Temporal dynamics of hypoperfusion and tissue damage in acute ischemic stroke remain incompletely understood.
Purpose of the Study:
- To compare the association between onset-to-imaging time and volumetric versus intensity-based imaging markers in acute ischemic stroke.
- To investigate how different imaging modalities (CT and MRI) and metrics reflect tissue damage over time.
Main Methods:
- Retrospective analysis of 288 CT and 275 MR acute stroke examinations.
- Estimation of hypoperfusion and infarct core volumes using VEOcore software with standard thresholds.
- Quantification of tissue damage using ASPECTS and normalized signal intensities (NCCT, ADC, DWI, CBF, Tmax).
- Multivariable linear regression was used to assess associations with onset-to-imaging time, adjusting for covariates.
Main Results:
- Volumetric measures showed limited time-dependence: ASPECTS decreased by -0.33 points/h and ADC-core volume increased by +1.8 mL/h.
- Perfusion-related volumetric measures (CBF < 30%, Tmax > 6s) did not significantly change with time.
- Intensity measures demonstrated significant time-dependence: NCCT intensity decreased by -1.1%/h, ADC intensity by -0.69%/h, while DWI-b0 and DWI-b1000 increased by +2.3%/h and +4.9%/h, respectively.
Conclusions:
- Tissue signal intensities in acute ischemic stroke exhibit a stronger time-dependence compared to volumetric measures.
- Infarct evolution appears to reflect progressive tissue injury rather than solely volumetric expansion.
- Intensity-based metrics from NCCT and DWI may be more suitable for assessing "infarct growth rate" than perfusion-based metrics.
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