High-definition fiber tracking for assessment of neurological deficit in a case of traumatic brain injury: finding, visualizing, and interpreting small sites of damage

Case report

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For patients with traumatic brain injury (TBI), current clinical imaging methods generally do not provide highly detailed information about the location of axonal injury, severity of injury, or expected recovery. In a case of severe TBI, the authors applied a novel high-definition fiber tracking (HDFT) to directly visualize and quantify the degree of axonal fiber damage and predict functional deficits due to traumatic axonal injury and loss of cortical projections.

This 32-year-old man sustained a severe TBI. Computed tomography and MRI revealed an area of hemorrhage in the basal ganglia with mass effect, but no specific information on the location of axonal injury could be obtained from these studies. Examinations of the patient at Week 3 and Week 8 after TBI revealed motor weaknesses of the left extremities. Four months postinjury, 257-direction diffusion spectrum imaging and HDFT analysis was performed to evaluate the degree of axonal damage in the motor pathway and quantify asymmetries in the left and right axonal pathways. High-definition fiber tracking was used to follow corticospinal and corona radiata pathways from the cortical surface to the midbrain and quantify projections from motor areas. Axonal damage was then localized by assessing the number of descending fibers at the level of the cortex, internal capsule, and midbrain. The motor deficit apparent in the clinical examinations correlated with the axonal losses visualized using HDFT. Fiber loss estimates at 4 months postinjury accurately predicted the nature of the motor deficits (severe, focal left-hand weakness) when other standard clinical imaging modalities did not. A repeat scan at 10 months postinjury, when edema and hemorrhage had receded, replicated the fiber loss.

Using HDFT, the authors accurately identified the presence and location of damage to the underlying white matter in this patient with TBI. Detailed information of injury provided by this novel technique holds future potential for precise neuroimaging assessment of TBI.

Abbreviations used in this paper:DTI = diffusion tensor imaging; FA = fractional anisotropy; HDFT = high-definition fiber tracking; TBI = traumatic brain injury.

Article Information

Address correspondence to: David O. Okonkwo, M.D., Department of Neurological Surgery, University of Pittsburgh Medical Center, UPMC Presbyterian, Suite B-400, 200 Lothrop Street, Pittsburgh, Pennsylvania 15213. email: okonkwodo@upmc.edu.

Please include this information when citing this paper: published online March 2, 2012; DOI: 10.3171/2012.1.JNS111282.

© AANS, except where prohibited by US copyright law.



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    Axial CT scan (left) obtained 5 days after severe TBI and T2-weighted FLAIR MR image (right) obtained 7 days after the injury showing acute hemorrhage in the basal ganglia with mass effect.

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    Axial T1-weighted MR images (A–C), DTI FA maps (D–F), and HDFT fiber tracks (G–I) obtained in a healthy volunteer (A, D, and G), our TBI patient at 4 months postinjury (B, E, and H), and our patient at 10 months postinjury (C, F, and I). The T1-weighted MR image obtained 4 months postinjury (B) shows hyperintensity in the right basal ganglia, demonstrating edema and hemorrhage. The DTI FA map (E) from the same time point also shows loss of white matter pathways passing through the basal ganglia. Fiber streamlines obtained using HDFT (H) show major loss of the right anterior corona radiata at 4 months. A T1-weighted MR image obtained at 10 months post-TBI (C) demonstrates clearance of edema and hematoma, and specific damage to the same region is demonstrated by HDFT (I). The standard clinical scans at 10 months show subtle changes that are difficult to interpret in the structural images (C) and DTI FA images (F). In contrast, the loss of left corona radiata fibers (I) clearly demonstrates substantial loss of innervation to the motor cortex, predicting the observed functional deficit.

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    Left: Corona radiata fibers in a healthy control mapped using DTI. Fibers are shown in the coronal plane as viewed from the front of the brain. This image contains fiber shapes and trajectories that are inconsistent with known anatomy, including false turns (fibers that deviate from the underlying pathway), false continuations (fibers that cross the midline), and “looping” (fibers that wander in arbitrary directions). Right: Fiber tracking of the corona radiata with HDFT does not show the same errors. These fibers match a priori anatomical expectations.

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    Diffusion tensor imaging fiber tracking (upper) and HDFT (lower) in the TBI patient at 17 weeks postinjury. The DTI fiber tracking shows inaccurate fiber directions and termination points (white circle), whereas the HDFT scan shows accurate details of damaged areas of the right anterior corona radiata without false turns or false continuations.

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    Number of fiber termination points along the corona radiata in the TBI patient (left) and a healthy control (right). Major losses are noticeable for fibers terminating in the right central sulcus, precentral gyrus, and premotor areas of the injured patient. However, the healthy control does not have major differences between the corona radiata of left and right hemispheres. Dashed white lines show the central sulcus (border of the primary motor cortex) in the axial view images (bottom row).

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    Corticospinal fibers descending from the precentral gyrus imaged by HDFT. A: The right corticospinal pathway with significant damage is shown in red, and the left corticospinal pathway is shown in green. The yellow dotted outline shows the range of missing fibers detected at the cortical level in the right hemisphere. Ext. = extremity. B: A close-up view of the rectangular area in panel A shows fibers terminating in thalamic and subthalamic regions (solid lines), as well as regions of major fiber damage (dotted lines). C: Graph showing the ratios of left and right corticospinal fibers descending from the cortex for 6 healthy controls (mean ± SD), the TBI patient at 4 months postinjury, and the TBI patient at 10 months postinjury. The ratios for the patient are decreased at all 3 levels at both time points. Positions of measurements are shown on the left hemisphere in panel A.


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