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Figure 5–8. Detection of microhemorrhage in traumatic brain injury (TBI).This patient sustained a mild TBI, and the computed tomography on the left (A) was interpreted as within normal limits, as was the standard gradient recalled echo (GRE) sequence magnetic resonance image scan (B) also performed on the day of injury. In contrast, the susceptibility- weighted imaging sequence scan shows multiple hemorrhagic lesions (C, arrows; note, again, the frontal location of the small hemorrhagic lesions). This illustrates the greater sensitivity of the GRE in detecting hemorrhagic abnormalities associated with TBI.Source. Bigler 2008. Figure courtesy of Dr. J.V. Hunter, Texas Children'€™s Hospital.

Figure 5–9. Methods of quantitative image analysis.This patient sustained a moderate traumatic brain injury (TBI) in a motor vehicle accident. Axial maps created by statistical parametric mapping (SPM) are shown at top left. As can be readily identified on the gradient recalled echo (GRE) sequence shown at top right, there is hemosiderin in the right frontal region (arrow). The T1 anatomical scan is unimpressive with regard to obvious abnormality, but visually the interhemispheric fissure may be more prominent than what would be expected for a teenager, and likewise some of the frontal sulci are prominent. By applying quantitative analysis (lower right), frontal lobe volume is almost a standard deviation below a control sample of similarly aged individuals, supporting the clinical impression of some frontal atrophy. Voxel-based morphology (VBM) analyses clearly demonstrate that the extent of atrophic change in both white matter (WM) and gray matter (GM) concentration in and around the hemosiderin-defined shear lesion is actually considerably greater than that shown on the GRE sequence where just the hemosiderin deposit can be visualized. The VBM map superimposes the location of the WM and GM abnormalities on a standard 3-D surface magnetic resonance imaging brain reconstruction.

Figure 5–10. Diffusion tensor imaging (DTI) of the corpus callosum.The left images show DTI tractography (upper left) of the corpus callosum superimposed on the T1 image of a traumatic brain injury patient who suffered a severe injury. Note, in comparison with the age-matched individual on the right without a history of brain injury, that the tractography demonstrates a significant reduction in the number of aggregate white matter tracts that can be identified coursing across the corpus callosum and projecting into the left hemisphere. The lower images show the midsagittal plane of the DTI color maps. The arrow in the lower left panel points to the corpus callosum highlighted in red, because DTI is sensitive to the directionality of the fiber tracts; red denotes lateral back-and-forth direction, whereas green reflects anterior-posterior and blue indicates vertical. The arrow in the upper left points to a corpus callosum tract coming out of the forceps minor projection system and is shown here to give the reader orientation for interpreting Figure 5–11.

Figure 5–11. White matter damage in traumatic brain injury (TBI).(A) The top 3-D image shows a cutaway with the left hemisphere diffusion tensor imaging (DTI) tractography findings from a child who sustained a severe TBI. Note the thinning out of tracts, similar to that observed in the case depicted in Figure 5–10. The arrow points to the location of the forceps minor region of white matter projection in the frontal lobe where the mild TBI case presented below shows discontinuity of the tracts in this region. Whereas the disruption of white matter tracts may be substantial in moderate to severe TBI, DTI findings when present in mild TBI are quite subtle and typically much less dramatic. (B) Fluid-attenuated inversion recovery (FLAIR) scan, fractional anisotropy (FA) map, and fiber tracking in a 49-year-old patient with TBI who was imaged 16 months after the initial trauma. The FLAIR image shows no abnormalities (top left). After analysis of the color-coded FA map (top middle), a region with reduced FA was identified in the WM of the left frontal lobe. This region of interest (ROI), illustrated in the top right T2-weighted image, included forceps minor and fronto-temporo-occipital fibers (bottom left), superior oblique view; the ROI is red and located centrally; the fibers are superimposed on an axial T2-weighted scan. At the level of the ROI, the respective fibers are discontinuous (arrow, bottom right; the ROI is left out in this image).Source. Panel (B) images reprinted from Rutgers DR, Toulgoat F, Cazejust J, et al: "White Matter Abnormalities in Mild Traumatic Brain Injury: A Diffusion Tensor Imaging Study." American Journal of Neuroradiology 29:514–519, 2008. Used with permission of the American Society of Neuroradiology.

Figure 5–12. Magnetic resonance spectroscopy of traumatic brain injury.(A) Position of the spectroscopic imaging voxel of interest (VOI), as viewed in the axial and sagittal planes. On the axial image, the outlined sections inside the VOI depict voxels typically selected for the four regions of interest, and the pattern surrounding the VOI is the area covered by the eight multiple regional saturation technique pulses for saturating lipid signals from the scalp. (B) Average spectra obtained from the left frontal lobe of a patient versus that of a control subject demonstrate a decrease in N-acetyl aspartate (NAA) after traumatic brain injury. Cho = choline; Cre = creatine; ppm = parts per million.Source. Reprinted from Hunter JV, Thornton RJ, Wang ZJ, et al: "Late Proton MR Spectroscopy in Children After Traumatic Brain Injury: Correlation With Cognitive Outcomes." American Journal of Neuroradiology 26:482–488, 2005. Used with permission of the American Society of Neuroradiology.


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