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Updated: Apr 28, 2026
Registered Bioimaging of Nanomaterials for Diagnostic and Therapeutic Monitoring
Published on: December 9, 2010
Characterizing the microstructural basis of "unidentified bright objects" in neurofibromatosis type 1: A combined in
Thibo Billiet1, Burkhard Mädler2, Felice D'Arco3
1Department of Imaging & Pathology, KU Leuven, Herestraat 49, Leuven 3000, Belgium ; Department of Radiology, University Hospitals Leuven, Herestraat 49, Leuven 3000, Belgium ; Medical Imaging Research Center (MIRC), Herestraat 49, Leuven 3000, Belgium ; Leuven Research Institute for Neuroscience & Disease (LIND), Herestraat 49, Leuven 3000, Belgium.
Introduction:
The histopathological basis of "unidentified bright objects" (UBOs) (hyperintense regions seen on T2-weighted magnetic resonance (MR) brain scans in neurofibromatosis-1 (NF1)) remains unclear. New in vivo MRI-based techniques (multi-exponential T2 relaxation (MET2) and diffusion MR imaging (dMRI)) provide measures relating to microstructural change. We combined these methods and present previously unreported data on in vivo UBO microstructure in NF1.
Methods:
3-Tesla dMRI data were acquired on 17 NF1 patients, covering 30 white matter UBOs. Diffusion tensor, kurtosis and neurite orientation and dispersion density imaging parameters were calculated within UBO sites and in contralateral normal appearing white matter (cNAWM). Analysis of MET2 parameters was performed on 24 UBO-cNAWM pairs.
Results:
No significant alterations in the myelin water fraction and intra- and extracellular (IE) water fraction were found. Mean T2 time of IE water was significantly higher in UBOs. UBOs furthermore showed increased axial, radial and mean diffusivity, and decreased fractional anisotropy, mean kurtosis and neurite density index compared to cNAWM. Neurite orientation dispersion and isotropic fluid fraction were unaltered.
Conclusion:
Our results suggest that demyelination and axonal degeneration are unlikely to be present in UBOs, which appear to be mainly caused by a shift towards a higher T2-value of the intra- and extracellular water pool. This may arise from altered microstructural compartmentalization, and an increase in 'extracellular-like', intracellular water, possibly due to intramyelinic edema. These findings confirm the added value of combining dMRI and MET2 to characterize the microstructural basis of T2 hyperintensities in vivo.
