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Proton MR Spectroscopy and MRI-Volumetry in Mild Traumatic Brain Injury

B.A. Cohena, M. Inglesea, H. Rusineka, J.S. Babba, R.I. Grossmana and O. Gonena

a From the Department of Radiology, New York University School of Medicine, New York, NY


Figure 1
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Fig 1. Segmentation performance. T1-weighted sagittal images were used to construct a whole-brain (WB) mask, subdivided here into GM and WM masks, using a threshold halfway between their respective signal intensities. Our partial volume technique enables better, subpixel, precision. CSF masks were created from T2-weighted MR imaging.


Figure 2
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Fig 2. Whole-head 1H spectra, left patient 9, right (matched) control subject 5 in Tables 1 and 2. The hatched regions indicate the peak-areas used to obtain QNAA of Eq 1. Note the excellent lipid suppression. Also note that localization relies on knowledge that NAA, unlike the other metabolites (eg, choline, creatine, etc), is exclusive to neuronal cells.


Figure 3
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Fig 3. Box plots of 1st, 2nd (median), 3rd quartiles (box), ± 95% (whiskers) and outliers (*) for WBNAA, PBV, PGM, and PWM in patients (hatched) and control subjects. Note the significant WBNAA deficit in patients (arrow), reflecting diffuse neuronal injury. Although PBV and PGM did not significantly differ between patients and control subjects, the wide range of the lower half of the patient distributions suggests a subset suffered global and GM atrophy.


Figure 4
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Fig 4. Scatter plot of WBNAA versus age for mild TBI patients and their matched control subjects. Note that WBNAA deficits increased with age, indicating greater neuronal injury after mild trauma, which may help explain part of their generally worse prognosis.


Figure 5
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Fig 5. Scatter plots of WBNAA, PBV, and PGM versus time from TBI. Although WBNAA remained statistically stable, volumetric measures revealed global atrophy, localized mostly to GM, suggesting that the eventual pathologic outcome of mild TBI is loss of cortical neurons. Stable WBNAA suggests that this loss, measured by QNAA, continued well after the initial traumatic insult but at the same pace as global atrophy.