See the corresponding editorial in this issue, pp 1060–1061.

J Neurosurg 116:1062–1069, 2012

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
Samuel S. Shin, Ph.D.,1 Timothy Verstynen, Ph.D., 2 Sudhir Pathak, M.S., 2
Kevin Jarbo, B.S., 2 Allison J. Hricik, M.S.,1 Megan Maserati, R.N., B.S.N.,1
Sue R. Beers, Ph.D., 3 Ava M. Puccio, Ph.D.,1 Fernando E. Boada, Ph.D., 4
David O. Okonkwo, M.D., Ph.D.,1 and Walter Schneider, Ph.D.1,2,4
Departments of 1Neurological Surgery and 4Radiology, University of Pittsburgh Medical Center;
and 3Department of Psychiatry, and 2Learning Research and Development Center,
University of Pittsburgh, Pennsylvania
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.
(http://thejns.org/doi/abs/10.3171/2012.1.JNS111282)

C

Key Words • axonal injury
high-definition fiber tracking

•

diffusion tensor imaging

urrent imaging methods rarely provide definitive
biological indicators of TBI.1 Beyond the identification of mass lesions requiring evacuation, neuroimaging in TBI is generally of low clinical utility. The
absence of a neuroimaging biomarker in TBI is also a major impediment to clinical care and research in the field.
Recent developments in diffusion-weighted imaging have
shown value in identifying axonal injury induced by trauma.4,6–8,11,12 However, the limitations of spatial resolution
of current diffusion imaging methods and their sensitivity
to signal loss from edema and hemorrhage makes it dif-

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

1062

•

traumatic brain injury

•

ficult to visualize the specific locations of axonal injury
and isolate the affected pathways.
We have recently developed a novel white matter
imaging approach, HDFT, which maps fiber pathways
within the brain at a significantly advanced degree of
resolution. We have previously used HDFT for surgical
planning2 and in vivo corticospinal pathway mapping.16
In addition, we have extensively analyzed white matter
damage using the data generated by HDFT. In this paper,
we report our initial application of HDFT in the assessment of TBI.

Case Report

This report centers on 1 patient and compares the results of HDFT in this patient to the results in healthy conJ Neurosurg / Volume 116 / May 2012

High-definition fiber tracking in TBI
trols. Institutional review board approval was obtained
for review of the patient’s medical records and imaging
studies obtained in the patient and healthy volunteers.
This 32-year-old man sustained a severe TBI in an
all-terrain vehicle accident (unhelmeted). The patient had
a postresuscitation Glasgow Coma Scale score of 6 and
had the following injuries: right subcortical intracerebral
hemorrhage, T-8 and T-12 compression fractures, and left
midface fractures. A CT scan of the head showed a 4.7 ×
3.1 × 4–cm acute hemorrhage centered within the right
basal ganglia resulting in local mass effect and 5 mm of
right-to-left midline shift (Fig. 1 left).
After the patient underwent placement of a left external ventricular drain and brain tissue oxygen monitor,
the severe TBI was managed medically. At 7 days postinjury, MRI scans showed a large right-sided basal ganglia
hematoma with associated mass effect (Fig. 1 right). At
3 weeks postinjury, the patient followed commands with
his right upper extremity, but had a dense left hemiparesis. He was subsequently transferred to inpatient TBI
rehabilitation and returned for neurosurgical follow-up at
2 months postinjury.
At follow-up 8 weeks postinjury, the patient continued to have residual left upper- and lower-extremity
weaknesses: hamstrings (3/5), quadriceps (4/5), biceps
(2/5), triceps (3/5), and deltoid (4+/5). The strength at the
wrist and in the hand intrinsic muscle groups was Grade
0 (0/5) according to the British Medical Research Council
grading scale.
Based on the structural images, it might be assumed
that the basal ganglia damage was the primary cause of
the patient’s motor impairments. However, the internal
capsule is a white matter pathway immediately adjacent
to the basal ganglia and contains all the descending corticospinal pathway fibers from the cortical motor areas.
Therefore, at 4 months postinjury, 2 types of diffusionweighted imaging scans were performed to measure
white matter integrity in this descending fiber pathway.
First, a standard 51-direction DTI sequence was acquired.
Next, a novel 257-direction diffusion spectrum imaging
scan was acquired. This second scan allows for the production of HDFT, which we have previously used to track
corticospinal pathways, successfully tracking fibers from
the cortical surface to midbrain with submillimeter resolution.16 The FA map from the 51-direction DTI sequence
(Fig. 2) showed unconstrained diffusion in the basal ganglia, suggesting axonal breakage. Slight signal loss was
also seen in the right anterior limb of the internal capsule that appeared to extend into portions of the posterior
limb. However, the FA map did not provide specific information about which axonal pathway was injured, the degree of the injury, nor the projection field of the pathway.
To better visualize these white matter pathways, we
used fiber tractography, a method that renders the fiber
pathways in a 3D space. Our pilot analysis using DTI for
fiber tracking provided poor-quality visualizations of fiber pathways that had anatomically inconsistent properties, such as false turns, false continuations, and random
fiber trajectories (for example, “looping” [Fig. 3 left]).
We then used HDFT to provide 3D visualization of
fibers. The HDFT data provided accurate mapping of
J Neurosurg / Volume 116 / May 2012

Fig. 1. 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.

white matter pathways in healthy controls (Fig. 3 right)
and in our patient (Fig. 4). Using HDFT, we were able to
map several major pathways with specificity and quantify
the degree of loss of connectivity as a result of axonal
fiber damage. We reconstructed the corona radiata, cingulum, and superior longitudinal fasciculus. The HDFT
data were then analyzed by comparing right and left fiber
tracks, as well as by comparing the injured patient’s fiber
tracks to those of healthy controls.
Our first analysis mapped the corona radiata pathway,
which contains fibers that pass through the anterior and
posterior limbs of the internal capsule. Since fiber tracking involves a stochastic seeding process that has been reported to produce unstable results, 5 we seeded the tracks
4 times using 70,000, 90,000, 110,000, and 130,000 random seeds to estimate the variability and significance of
the method across random reseedings. The resampling
variance was small (corona radiata SD 1.6%, cingulum
SD 6.1%, and superior longitudinal fasciculus SD 6.4%).
The volume estimates showed a 59.6 ± 4.3 cm3 loss on
the left side compared with the right. There was a 62.8%
± 1.6% difference (z score 38.3, p < 0.0001) between the
left and right sides (Table 1, Video 1).
Video 1. Comparison of the left and right sides of the
corona radiata showing losses in the right side, with significant
loss at the level of the midbrain. Click here to view with Media
Player. Click here to view with Quicktime.

In contrast, volumetric analysis of the cingulum and superior longitudinal fasciculus found no significant differences (p > 0.1) between the left and right sides. Additional
repeat reliability analysis performed by reseeding the corona radiata 10 times showed a similar mean volume loss
of 67.4% ± 0.3% (Table 2). The repeat analysis confirmed
low variance (SD 0.3) and reliability of this method (z
score > 200, p < 0.0001), and both methods produced
nearly the same proportion of loss (62.8% volume, 67.4%
track counts).
After identification of the volumetric loss in the corona radiata, further analysis was performed by computing
the number of fiber termination points, locations where
diffusion signals for fiber tracks end. Fiber termination
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S. S. Shin et al.

Fig. 2. 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.

points are presumed to be where axonal fiber bundles
terminate (such as the cortex or nuclei), and these were
identified along the length of the corona radiata in the
posterior to anterior direction (Fig. 5 upper left). The right
corona radiata fibers projecting to the central sulcus and
precentral gyrus showed a 54% reduction in termination
points compared with the left corona radiata. Also, the
right corona radiata fibers projecting to the anterior areas, including premotor areas (that is, the supplementary
motor area, presupplementary motor area, and cingulated motor area), showed a 97% reduction in termination
points compared with the contralateral hemisphere. In
1064

comparison, the corona radiata of an uninjured individual
showed a relatively similar number of termination points
in the left and right hemispheres (Fig. 5 upper right).
Since our goal was to determine if the etiology of the
patient’s motor deficits was damage to the motor pathways
adjacent to the basal ganglia lesion, we focused on the
subset of fibers that contribute to the corona radiata and
directly project to spinal motor neurons: the corticospinal pathway. We tracked the corticospinal pathway fibers
descending from the motor areas such as the precentral
gyrus and central sulcus through the internal capsule and
the midbrain (Fig. 6). In the standard clinical structural
J Neurosurg / Volume 116 / May 2012

High-definition fiber tracking in TBI

Fig. 3. 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.

Fig. 4. 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.

J Neurosurg / Volume 116 / May 2012

scans (CT and T1- and T2-weighted MRI), most of the
damage was visible in the basal ganglia, and no specific
damage was apparent in the posterior limb of the internal
capsule where the corticospinal pathway fibers traverse
(Figs. 1 and 2B and C). Yet, large areas of fiber breaks
were detected in the posterior limb of the internal capsule by HDFT (Fig. 6B). The corticospinal pathway fiber
tracks of 6 healthy age- and sex-matched controls were
analyzed and compared with corticospinal pathway fiber
tracks of the TBI patient at 4 and 10 months postinjury
(Fig. 6C). As expected, the TBI patient exhibited a decreased ratio of fibers at each level analyzed: precentral
gyrus, internal capsule, and midbrain. In contrast, the ratios of right and left corticospinal pathway fiber tracks in
the controls were close to 1 at these regions. At 4 months,
the z scores of the patient’s left/right ratio for precentral gyrus, internal capsule, and midbrain were 2.65 (p
≤ 0.01), 3.58 (p ≤ 0.001), and 2.74 (p ≤ 0.01), respectively,
relative to the control values. At 10 months, the z scores
of the patient’s left/right ratio for the precentral gyrus,
internal capsule, and midbrain were 3.39 (p ≤ 0.01), 3.60
(p ≤ 0.001), and 3.55 (p ≤ 0.01).
Physical examination correlated with the corticospinal pathway deficits. At follow-up 6 months postinjury,
the patient had normal left lower-extremity strength but
weakness of the left upper extremity. There was near paralysis of the left hand intrinsic muscles (1/5) and weakness of the biceps (2/5), triceps (2/5), and deltoid (2/5).

Discussion

We report the initial use of HDFT and quantification
1065

S. S. Shin et al.
TABLE 1: Percent volumetric fiber track difference of right side compared to left*
Structure

Left (cm3)

Right (cm3)

% Difference

z Score

p Value

corona radiata
cingulum
superior longitudinal fasciculus

94.9 ± 4.5
47.9 ± 2.9
68.1 ± 3.4

35.3 ± 0.2
51.5 ± 3
71.7 ± 1.4

62.8 ± 1.6
6.9 ± 6.1
6.3 ± 6.4

38.3
1.1
1

<0.0001
0.13
0.16

* Mean values ± SD are displayed for volume and percentage differences.

of left/right asymmetries to identify white matter damage following TBI. This novel approach successfully detected, visualized, and quantified damage when previous
methods (CT, structural MRI, and DTI) did not provide
these details. With HDFT, we identified a specific lesion
of the corticospinal pathway in the corona radiata that
was directly associated with the functional deficits in our
TBI patient. The volumetric losses as well as the number
of fibers projecting from the motor cortices were reduced
in the injured side, correlating with the left upper-extremity weakness. The other methods focused on describing
the basal ganglia hemorrhage, but the patient’s hemiplegia (left-sided weakness) could not be solely explained
by basal ganglia damage. With HDFT, we could specify
lesions to the corticospinal pathway adjacent to the basal
ganglia and quantify their extent beyond the capabilities
of current neuroimaging modalities.
At 6 months’ follow-up, only left upper-extremity
weakness was present, and the lower-limb weakness had
resolved. Basal ganglia hemorrhage was apparent on the
standard clinical imaging methods (CT, structural MRI,
and DTI), but the corticospinal pathway damage correlating with the patient’s functional deficit (left-sided weakness) was not. Standard clinical structural imaging suggested damage in the posterior limb of the internal capsule
but did not convey the spatial specificity and degree of
damage to the descending motor pathways as HDFT did
(Table 3). High-definition fiber tracking showed a reduction in the number of fibers descending from the motor
areas of the cortex. Using HDFT, we were able to visualize the specific location and quantify the degree of white
matter injury responsible for the patient’s persistent motor
deficits. The decrease in fiber detection was specific to
the injured hemisphere and correlated with the left upperextremity weakness.
After the identification of losses in the corticospinal section of the corona radiata, we performed a second
analysis looking specifically at the entire corticospinal
pathway projections. With this analysis, we were able to
locate the specific area of damage as the fiber tracks descended from the cortex. These areas of fiber damage can
be clearly visualized (Fig. 6A and B) and quantified (Fig.
6C). The major fiber breakage was localized to the region
between the internal capsule and the midbrain, shown by
the sudden decrease in the ratio of right and left corticospinal fibers. As depicted in Fig. 6, the surviving fibers of
the right corticospinal pathway are from the dorsomedial
area of the primary motor cortex, which is responsible
for lower-extremity control. However, major fiber losses
are seen in fibers projecting from the ventrolateral area,
which contains neurons controlling the upper extrem1066

ity. The locations of fiber breaks are consistent with the
clinical symptoms showing normal left lower-extremity
function and severe left upper-extremity weakness at 6
months’ follow-up.
Throughout the analysis, the ratios of fiber tracks
between the left and right sides were used for each individual (patient or healthy control). This method was used
to reduce the variability due to interindividual white matter differences and scanning data quality differences. Although the right corticospinal pathway and corona radiata
exhibited the most pronounced damage in our patient, it
is possible that the corticospinal pathway on the left side
also had some degree of damage due to contra coup injury. Thus, a limitation of our analysis is the fact that the
degree of axonal damage may be even more severe than
detected by our current methods.
Due to the concern that edema and hemorrhage in
the basal ganglia following injury may artificially impact
the fiber tracking (Fig. 2B), the data from a second MRI
study performed at 10 months following injury were analyzed using HDFT. Edema and hemorrhage in the basal
ganglia (Fig. 2C) had resolved at 10 months, but the corticospinal pathway damage was still apparent (Fig. 6C).
In fact, the loss of fiber tracks was more pronounced at
the 10-month time point compared with the 4-month time
point, possibly due to chronic axonal Wallerian degeneration following injury. Similarly, the loss of fiber tracks in
the left anterior corona radiata was found (Fig. 2I) at 10
months, possibly due to chronic degeneration. Although
the anterior corona radiata has previously been described
to have an important role in attentional control,14 we focus
TABLE 2: Repeat reliability test of corona radiata tractography*
Sample
No.

Left Corona
Radiata

Right Corona
Radiata

Ratio (L/R) × 100%†

1
2
3
4
5
6
7
8
9
10

13,940
14,093
14,016
14,013
14,001
13,941
14,015
13,933
13,975
14,069

4,644
4,597
4,573
4,536
4,539
4,546
4,516
4,600
4,556
4,543

33.3%
32.6%
32.6%
32.4%
32.4%
32.6%
32.2%
33.0%
32.6%
32.3%

* All raw values are fiber track counts.
† Mean 32.6% ± 0.3%.

J Neurosurg / Volume 116 / May 2012

High-definition fiber tracking in TBI

Fig. 5. 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).

on motor deficits for the scope of this case report. The
replication of corticospinal pathway deficit at 10 months
indicates that the damage visualized by HDFT is not an
artifact of edema and hematoma.
Our results suggest that high-resolution white matter
imaging and comparisons of left/right fiber tractography
may provide valuable diagnostic information in characterizing the nature of motor pathologies. Previous studies
using similar white matter imaging techniques, such as
DTI, have been able to detect axonal damages induced
by TBI.1,4,9–13,15 Due to its sensitivity in detection of white
matter microstructure, DTI is reported by many authors
as a sensitive technique to detect axonal damage in TBI.
While DTI provides a sensitive detection of white matter
pathology, HDFT can provide a complementary advantage in the detection of white matter injury. Whereas DTI
has a limited ability to resolve crossing of fibers within
a voxel,3 HDFT analysis utilizes diffusion spectrum imaging, which has a high angular resolution that allows
tractography to navigate complex fiber crossings. Thus,
HDFT provides high-resolution details of axonal pathways and projection fields that allow detection of specific
location and degree of damage.
Traditional ways to quantify white matter integrity,
such as DTI-based estimates of voxel FA (Fig. 2), have
several limitations. These measures have a limited spatial resolution at the level of individual voxel, their values are difficult to interpret, and they cannot identify the
specificity of the cortical origins of damaged fibers (for
example, selective damage to upper-body fibers). In addiJ Neurosurg / Volume 116 / May 2012

tion, DTI FA measurement is compromised by interstitial
fluid content.3,5,17,18 The DTI measurement becomes ambiguous in the presence of hemorrhage and edema (FA
decreases when there is an increase in interstitial fluid
or loss of axons). In contrast, our high angular resolution
tracking technique, HDFT, has the ability to both localize and quantify axonal damage at the level of detail
necessary for clinical purposes and is robust to changes
in white matter pathway shape, interstitial fluid, and stochastic reseeding of the fiber tracks. This technique may
have a valuable clinical diagnostic role that can augment
current diagnostic imaging studies in the evaluation and
management of TBI. The high spatial resolution of HDFT
provides a better potential to link observed clinical symptoms with white matter damage. For example, we were
able to show that the fibers affected by the midbrain lesion were primarily innervating upper-body areas of the
motor cortex and this is in accordance with the contralateral, upper-extremity deficits reported in the clinical examination. Taking the limitations of current clinical imaging into account, tractography-based approaches in the
clinical evaluation process may have significant potential
for optimizing diagnosis.
The limitation of the current study is that we have
only focused on motor deficits as a symptom of TBI. Given that there is damage to the corona radiata and possibly
other pathways, various functional losses are expected.
However, cognitive deficits such as memory, language
function, and informational processing speed were not
analyzed since such analysis was beyond the scope of
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S. S. Shin et al.
TABLE 3: Summary of imaging findings by modality
Imaging Modality

Diagnostic Summary

CT

Large intraparenchymal hemorrhage in the right
basal ganglia affecting the anterior limb of the internal capsule. Degree of damage in posterior
limb of the right internal capsule is difficult to assess. (Day 5, 4 mos)
FLAIR
Mild compression of posterior limb of the internal
capsule (Day 7). No compression of posterior
limb of the internal capsule (4 mos).
T1-weighted MRI Intraparenchymal hemorrhage in the right basal
ganglia. Specific degree and location of damage
in the right internal capsule is difficult to assess.
(4 mos)
DTI (FA)
Significant loss of FA in the right basal ganglia.
Slight signal loss of the anterior limb of the internal capsule extending into portions of the posterior limb, suggesting partial damage of motor
tracts. (4 & 10 mos)
HDFT
Localized decrease in fibers of the motor areas of
the corona radiata; substantial loss of axon volume in the motor (54%) and premotor areas
(97%); 79% volume loss at the midbrain in the
right corona radiata; focal fiber breaks in the corticospinal pathway in ventral aspects of right internal capsule that indicated reduced projection
to left-hand M1, suggesting likely reduction of
function; intact fiber projections from the lowerextremity areas of the motor cortex. (4 & 10
mos). The observations of 10 mos replicate the
findings observed at 4 mos with a small increase
in fiber loss at the level of the midbrain.

Fig. 6. 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.

this paper. A future study analyzing white matter pathway damage in multiple patients with varying degrees of
injury and areas of damage is needed to further demonstrate that HDFT findings also correlate with cognitive
1068

deficits. A prospective clinical trial in individuals with a
high likelihood of TBI, such as athletes or soldiers, may
provide additional support for the utility of HDFT if preinjury and postinjury data can be compared. There is also
a need to verify that the observed breaks in fiber streamlines that we visualized do in fact represent loss of axons.
In a previous case report, we have shown that HDFT can
identify the location of surgical cuts.2 Future work will
use presurgical and postsurgical scans in neurosurgery
cases to segment and track microscopic fiber changes. In
addition, animal studies can validate the use of fiber tractography in identifying axonal injury.
We present a case of severe TBI wherein a novel
HDFT method provided clinically useful diagnostic information. The routine clinical imaging in this case, CT
scanning, structural MRI, and diffusion imaging, revealed the presence of an intracerebral hematoma without
any specificity to the effect on axonal tracks. High-definition fiber tracking allowed for the quantification of the
axon volume loss and fiber loss far from the hematoma.
In addition, this technique localized and visualized the
fiber breaks and loss of projections to the premotor and
motor cortices. The visualization and quantification of
the losses of motor pathways correlated with the motor
deficits observed in the patient. Although future studies
J Neurosurg / Volume 116 / May 2012

High-definition fiber tracking in TBI
are needed to confirm the utility of this technique, HDFT
may potentially provide clinically useful characterization
of axonal losses following TBI.
Disclosure
Funding for this study was provided through a Defense
Ad­
vanced Research Projects Agency (DARPA) contract
(D09PC75271). The views, opinions, and/or findings contained
in this paper are those of the authors and should not be interpreted
as representing the of­ficial views or policies, either expressed or
implied, of DARPA or the United States Department of Defense.
The authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this
paper.
Author contributions to the study and manuscript preparation
include the following. Conception and design: Boada, Okonkwo,
Schneider. Acquisition of data: Shin, Pathak, Jarbo, Maserati.
Analysis and in­ter­pretation of data: Shin, Verstynen, Pathak, Jarbo,
Beers, Schnei­der. Drafting the article: Shin, Verstynen. Critically
revising the ar­ticle: all authors. Reviewed submitted version of
manuscript: all authors. Approved the final version of the manuscript on behalf of all authors: Okonkwo. Statistical analysis: Shin,
Verstynen, Pathak, Jar­­bo. Administrative/technical/material support:
Hricik, Maserati, Puc­cio. Study supervision: Beers, Puccio, Boada.
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Manuscript submitted August 1, 2011.
Accepted January 11, 2012.
Supplemental online information:
Video: http://mfile.akamai.com/21490/wmv/digitalwbc.download.
akamai.com/21492/wm.digitalsource-na-regional/jns11-1282_
video_new.asx (Media Player).
http://mfile.akamai.com/21488/mov/digitalwbc.download.
akamai.com/21492/qt.digitalsource-global/jns11-1282_video_new.
mov (Quicktime).
Please include this information when citing this paper: published online March 2, 2012; DOI: 10.3171/2012.1.JNS111282.
Address correspondence to: David O. Okonkwo, M.D., De­­
partment of Neurological Surgery, University of Pittsburgh Med­i­
cal Center, UPMC Presbyterian, Suite B-400, 200 Lothrop Street,
Pittsburgh, Pennsylvania 15213. email: okonkwodo@upmc.edu.

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