45 research outputs found

    In vivo evolution of biopsy-proven inflammatory demyelination quantified by R2t* mapping

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    A 35-year-old man with an enhancing tumefactive brain lesion underwent biopsy, revealing inflammatory demyelination. We used quantitative Gradient-Recalled-Echo (qGRE) MRI to visualize and measure tissue damage in the lesion. Two weeks after biopsy, qGRE showed significant R2t* reduction in the left optic radiation and surrounding tissue, consistent with the histopathological and clinical findings. qGRE was repeated 6 and 14 months later, demonstrating partially recovered optic radiation R2t*, in concert with improvement of the hemianopia to ultimately involve only the lower right visual quadrant. These results support qGRE metrics as in vivo biomarkers for tissue damage and longitudinal monitoring of demyelinating disease

    Modeling the R2* relaxivity of blood at 1.5 Tesla

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    BOLD (Blood Oxygenation Level Dependent) imaging is used in fMRI to show differences in activation of the brain based on the relative changes of the T2* (= 1/R2*) signal of the blood. However, quantification of blood oxygenation level based on the T2* signal has been hindered by the lack of a predictive model which accurately correlates the T2* signal to the oxygenation level of blood. The T2* signal decay in BOLD imaging is generated due to blood containing paramagnetic deoxyhemoglobin (in comparison to diamagnetic oxyhemoglobin). This generates local field inhomogeneities, which cause protons to experience different phase shifts, leading to dephasing and the MR signal decay. The blood T2* signal has been shown to decay with a complex behavior1, termed Non-Lorenztian, and thus is not adequately described by the traditional model of simplemono-exponential decay. Theoretical calculations show that diffusion narrowing substantially affects signal loss in our data. Over the past decade, several theoretical models have been proposed to describe this Non-Lorenztian behavior in the blood T2* signal in BOLD fMRI imaging. The goal of this project was to investigate different models which have been proposed over the years and determine a semi-phenomenological model for the T2* behaviorusing actual MR blood data

    Evaluating brain damage in multiple sclerosis with simultaneous multi-angular-relaxometry of tissue

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    OBJECTIVE: Multiple sclerosis (MS) is a common demyelinating central nervous system disease. MRI methods that can quantify myelin loss are needed for trials of putative remyelinating agents. Quantitative magnetization transfer MRI introduced the macromolecule proton fraction (MPF), which correlates with myelin concentration. We developed an alternative approach, Simultaneous-Multi-Angular-Relaxometry-of-Tissue (SMART) MRI, to generate MPF. Our objective was to test SMART-derived MPF metric as a potential imaging biomarker of demyelination. METHODS: Twenty healthy control (HC), 11 relapsing-remitting MS (RRMS), 22 progressive MS (PMS), and one subject with a biopsied tumefactive demyelinating lesion were scanned at 3T using SMART MRI. SMART-derived MPF metric was determined in normal-appearing cortical gray matter (NAGM), normal-appearing subcortical white matter (NAWM), and demyelinating lesions. MPF metric was evaluated for correlations with physical and cognitive test scores. Comparisons were made between HC and MS and between MS subtypes. Furthermore, correlations were determined between MPF and neuropathology in the biopsied person. RESULTS: SMART-derived MPF in NAGM and NAWM were lower in MS than HC (p \u3c 0.001). MPF in NAGM, NAWM and lesions differentiated RRMS from PMS (p \u3c 0.01, p \u3c 0.001, p \u3c 0.001, respectively), whereas lesion volumes did not. MPF in NAGM, NAWM and lesions correlated with the Expanded Disability Status Scale (p \u3c 0.01, p \u3c 0.001, p \u3c 0.001, respectively) and nine-hole peg test (p \u3c 0.001, p \u3c 0.001, p \u3c 0.01, respectively). MPF was lower in the histopathologically confirmed inflammatory demyelinating lesion than the contralateral NAWM and increased in the biopsied lesion over time, mirroring improved clinical performance. INTERPRETATION: SMART-derived MPF metric holds potential as a quantitative imaging biomarker of demyelination and remyelination
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