Choroid plexus calcification detection using quantitative susceptibility mapping MRI
Hett, K.; Dubois, A.; Bonitz, I.; Considine, C. M.; Eaton, J.; Mcknight, C. D.; Claassen, D. O.; Donahue, M. J. J.; Trujillo, P.
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Purpose. The choroid plexus (ChP) is the primary source of cerebrospinal fluid and an emerging marker of cerebral health, with enlargement and hypoperfusion reported in aging and neurodegeneration. However, frequent ChP calcifications can confound volumetric and perfusion measures. Although computed tomography (CT) is the gold standard for detecting calcification, it is rarely available in research MRI. Quantitative susceptibility mapping (QSM) offers an alternative sensitive to diamagnetic mineralization but lacks validated susceptibility thresholds. Method. Participants underwent CT and MRI within four weeks, including 3D T1-weighted and a multi-echo gradient echo QSM MRI. ChP calcifications were identified on CT using standard diagnostic criteria. Using the Bayes decision boundary framework, we identified optimal susceptibility thresholds for detecting diamagnetic signals consistent with calcification and compared these thresholds with multiple density levels measured on gold standard CT images. Results. Across all participants (n=20; age=62.2+-12.0 yrs), the optimal susceptibility threshold separating background ChP signal from calcifications was -0.10 ppm at 60 HU (low-density) and -0.15 ppm at 100 HU (high-density). Susceptibility values within calcified tissue exhibited a linear relationship with CT-derived tissue density. A significant positive association was observed between ChP volume and calcification volume among participants with detectable calcification (beta=2.26, p=0.047). Conclusion. This work should provide a practical framework for quantifying ChP calcifications routinely from MRI. The observed relationship between ChP volume and calcification volume highlights the importance of accounting for calcified tissue, particularly when calcification burden is substantial, when investigating ChP abnormalities in aging and neurodegenerative disease.
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