Susanne J van Veluw1, Alessio Fracasso2, Fredy Visser3, Wim G M Spliet4, Peter R Luijten5, Geert Jan Biessels6, Jaco J M Zwanenburg5. 1. Department of Neurology, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, the Netherlands. Electronic address: s.j.veluw-2@umcutrecht.nl. 2. Experimental Psychology, Helmholtz Institute, Utrecht University, Utrecht, the Netherlands. 3. Department of Radiology, University Medical Center Utrecht, Utrecht, the Netherlands; Philips Healthcare, Best, the Netherlands. 4. Department of Pathology, University Medical Center Utrecht, Utrecht, the Netherlands. 5. Department of Radiology, University Medical Center Utrecht, Utrecht, the Netherlands. 6. Department of Neurology, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, the Netherlands.
Abstract
OBJECTIVES: Fluid-attenuated inversion recovery (FLAIR) imaging is an important clinical 'work horse' for brain MRI and has proven to facilitate imaging of both intracortical lesions as well as cortical layers at 7T MRI. A prominent observation on 7T FLAIR images is a hyperintense rim at the cortical surface and around the ventricles. We aimed to clarify the anatomical correlates and underlying contrast mechanisms of this hyperintense rim. MATERIALS AND METHODS: Two experiments with post-mortem human brain tissue were performed. FLAIR and T2-weighted images were obtained at typical in vivo (0.8mm isotropic) and high resolution (0.25mm isotropic). At one location the cortical surface was partly removed, and scanned again. Imaging was followed by histological and immunohistochemical analysis. Additionally, several simulations were performed to evaluate the potential contribution from an artifact due to water diffusion. RESULTS: The hyperintense rim corresponded to the outer - glia rich - layer of the cortex and disappeared upon removal of that layer. At the ventricles, the rim corresponded to the ependymal layer, and was not present at white matter/fluid borders at an artificial cut. The simulations supported the hypothesis that the hyperintense rim reflects the tissue properties in the outer cortical layers (or ependymal layer for the ventricles), and is not merely an artifact, although not all observations were explained by the simulated model of the contrast mechanism. CONCLUSIONS: 7T FLAIR seems to amplify the signal from layers I-III of the cortex and the ependyma around the ventricles. Although diffusion of water from layer I into CSF does contribute to this effect, a long T2 relaxation time constant in layer I, and probably also layer II-III, is most likely the major contributor, since the rim disappears upon removal of that layer. This knowledge can help the interpretation of imaging results in cortical development and in patients with cortical pathology.
OBJECTIVES: Fluid-attenuated inversion recovery (FLAIR) imaging is an important clinical 'work horse' for brain MRI and has proven to facilitate imaging of both intracortical lesions as well as cortical layers at 7T MRI. A prominent observation on 7T FLAIR images is a hyperintense rim at the cortical surface and around the ventricles. We aimed to clarify the anatomical correlates and underlying contrast mechanisms of this hyperintense rim. MATERIALS AND METHODS: Two experiments with post-mortem human brain tissue were performed. FLAIR and T2-weighted images were obtained at typical in vivo (0.8mm isotropic) and high resolution (0.25mm isotropic). At one location the cortical surface was partly removed, and scanned again. Imaging was followed by histological and immunohistochemical analysis. Additionally, several simulations were performed to evaluate the potential contribution from an artifact due to water diffusion. RESULTS: The hyperintense rim corresponded to the outer - glia rich - layer of the cortex and disappeared upon removal of that layer. At the ventricles, the rim corresponded to the ependymal layer, and was not present at white matter/fluid borders at an artificial cut. The simulations supported the hypothesis that the hyperintense rim reflects the tissue properties in the outer cortical layers (or ependymal layer for the ventricles), and is not merely an artifact, although not all observations were explained by the simulated model of the contrast mechanism. CONCLUSIONS: 7T FLAIR seems to amplify the signal from layers I-III of the cortex and the ependyma around the ventricles. Although diffusion of water from layer I into CSF does contribute to this effect, a long T2 relaxation time constant in layer I, and probably also layer II-III, is most likely the major contributor, since the rim disappears upon removal of that layer. This knowledge can help the interpretation of imaging results in cortical development and in patients with cortical pathology.
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