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Brain Injury
ISSN: 0269-9052 (Print) 1362-301X (Online) Journal homepage: http://www.tandfonline.com/loi/ibij20
Longitudinal changes in diffusion tensor imaging
parameters of the corpus callosum between 6 and
12 months after diffuse axonal injury
Johan Ljungqvist, Daniel Nilsson, Maria Ljungberg, Eva Esbjörnsson,
Catherine Eriksson-Ritzén & Thomas Skoglund
To cite this article: Johan Ljungqvist, Daniel Nilsson, Maria Ljungberg, Eva Esbjörnsson,
Catherine Eriksson-Ritzén & Thomas Skoglund (2017): Longitudinal changes in diffusion tensor
imaging parameters of the corpus callosum between 6 and 12 months after diffuse axonal
injury, Brain Injury, DOI: 10.1080/02699052.2016.1256500
To link to this article: http://dx.doi.org/10.1080/02699052.2016.1256500
Published online: 27 Jan 2017.
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ORIGINAL ARTICLE
Longitudinal changes in diffusion tensor imaging parameters of the corpus callosum
between 6 and 12 months after diffuse axonal injury
Johan Ljungqvist
a
, Daniel Nilsson
a
, Maria Ljungberg
b
, Eva Esbjörnsson
c
, Catherine Eriksson-Ritzén
a
,
and Thomas Skoglund
a
a
Department of Neurosurgery;
b
Department of Medical Physics and Biomedical Engineering;
c
Department of Clinical Neuroscience and
Rehabilitation, Sahlgrenska University Hospital, Goteborg, Sweden
ABSTRACT
Background: Magnetic resonance diffusion tensor imaging (MR-DTI) is used increasingly to detect diffuse
axonal injury (DAI) after traumatic brain injury (TBI).
Primary objective: To investigate changes in the diffusion tensor imaging parameters of the corpus
callosum 6 and 12 months after TBI, to optimize the timing of follow-up DTI investigations. A secondary
goal was to study the relationship between DTI parameters and outcome.
Research design: Longitudinal prospective study.
Methods and procedures: MR-DTI was performed in 15 patients with suspected DAI, 6 and 12 months
post-injury. Sixteen controls were also examined. Fractional anisotropy (FA) and diffusivity (trace) in the
corpus callosum were analysed. The outcome measures were the extended Glasgow Outcome Scale and
the Barrow Neurological Institute Screen for Higher Cerebral Functions, assessed at 6 and 12 months.
Main outcomes and results: FA decreased and trace increased at 6 and 12 months compared to controls. Trace
continued to increase even further between 6 and 12 months, while FA remained unchanged. Patients with the
worst outcomes had lower FA and higher trace compared to patients with better outcomes.
Conclusions: DTI parameters have not reached a stable level at 6 months after DAI, but continue to
change, probably reflecting an incessant microstructural alteration of the white matter.
ARTICLE HISTORY
Received 3 February 2016
Revised 4 September 2016
Accepted 31 October 2016
KEYWORDS
Traumatic brain injury;
axonal injury; MRI; outcome
measures
Introduction
Diffuse axonal injury (DAI) is a distinct manifestation of primary
traumatic brain injury (TBI), often leading to poor clinical out-
come including physical as well as cognitive impairment [1,2].
The stretching and shearing of white matter fibres in the brain,
due to the rapid inertial forces of acceleration and deceleration, is
considered to be the cause of DAI, as it initiates a progressive
process that leads to axonal failure and disconnection [3,4].
Conventional neuroimaging such as computerized tomography
(CT) is considered inadequate for the evaluation of DAI and it
has been suggested that conventional magnetic resonance ima-
ging (MRI) under-estimates the extent of injury [5].
Diffusion tensor imaging (DTI) is a magnetic resonance
technique that can indirectly evaluate the integrity of white
matter tracts by measuring water diffusion (expressed as trace
or mean diffusivity), its directionality in three dimensions,
and the diffusion anisotropy (often expressed as fractional
anisotropy, FA) [6]. In white matter regions with a regular
parallel fibre arrangement, such as the corpus callosum, the
diffusion of water molecules in the direction of the fibre is
high compared to the water diffusivity in the perpendicular
direction (high anisotropy), whereas in less coherent struc-
tures, such as in regions where fibres of different bundles
merge, the anisotropy is low [7].
A large number of studies have shown that DTI can be used to
detect alterations in the white matter ultrastructure after TBI (for
a recent review see Studerus-Germann et al. [8]). DTI-studies
have generally shown a reduction of FA and an increase of
diffusivity in the white matter in patients with TBI [8–13].
Studies have also shown correlations between DTI findings and
severity of TBI [14,15], as well as neurocognitive dysfunction
after TBI [10,15–20].
The time difference between the TBI and the DTI scanning is
an important factor because longitudinal studies have also shown
that changes in diffusion properties continue to take place a long
time after the TBI [8,11,19–24]. However, the exact time course
of DTI-related changes after TBI remains largely unknown [9]
and more information is needed on the best time window to scan
patients with TBI with DTI to predict the long-term outcome [8].
The purpose of this longitudinal, prospective investigation was
to examine if a stable state regarding the DTI parameters would be
reached 6 months after TBI or if the DTI parameters continue to
change even after this, thus reflecting a continuous microstructural
alteration of the white matter. A secondary goal was to study the
relationship between DTI parameters and outcome.
Methods
Subjects
This study was approved by the Regional Ethical Review
Board at the University of Gothenburg, and informed consent
was obtained from all participants or their next of kin. All
CONTACT Johan Ljungqvist johan.ljungqvist@vgregion.se Department of Neurosurgery, Sahlgrenska University Hospital, SE-413 45, Goteborg, Sweden.
BRAIN INJURY
http://dx.doi.org/10.1080/02699052.2016.1256500
© 2017 Taylor & Francis Group, LLC
patients were referred to Sahlgrenska University Hospital
during the period June 2006–September 2009 and had sus-
tained TBI. Patients were included consecutively, based on the
criteria that a suspicion of DAI was raised due to impaired
consciousness and/or focal neurological symptoms without an
obvious explanation seen on the computerized tomography
(CT) scan of the brain. MR-DTI was performed at 6 and 12
months post-injury. Sixteen healthy controls, matched to age
and gender (seven women and nine men with a mean age of
34 years; range = 23–62 years) were also recruited. The con-
trol group was only scanned once, as it has been shown that
diffusion properties do not change over a 12-month period in
healthy controls [22].
Diffusion tensor image acquisition
MR-DTI was performed on a Philips Gyroscan Intera 1.5 T,
release 9. The software was upgraded to an Achieva release 1.5
during the study. Before the upgrade, the SENSE head coil
utilized six channels and after the upgrade eight channels. The
DTI method used was HARDI (high angular resolution diffu-
sion imaging; Philips, Eindhoven, the Netherlands).
DTI was performed using a single shot spin-echo echo-
planar imaging (SE-EPI) sequence with SENSE factor of 3.2
and a halfscan factor of 0.712. A b = 0 s mm
–2
and 15
diffusion-sensitizing directions with b = 800 s mm
–2
were
acquired.
For six of the controls and for patient 2, the imaging
parameters were: TE = 69 ms, NSA = 6, BW = 33.8 Hz/
pixel in AP direction, isotropic voxels of 2.2 mm
3
recon-
structedto1.9×1.9×2.2mm
3
resulting in a scan time of 16
minutes. For the remaining 10 controls and for all patients
(except patient 2), the imaging parameters were: TE = 66 ms,
NSA=3,BW=46.8Hz/pixelinAPdirection,isotropic
voxels of 2.5 mm
3
reconstructed to 1.9 × 1.9 × 2.5 mm
3
,
resulting in a scan time of 7.5 minutes.
Data analysis
Post-processing of diffusion tensor metrics and white matter fibre
tracking was carried out using the software DTIStudio V 2.4
(Johns Hopkins Medical Institute, Laboratory of Brain
Anatomical MRI, http://lbam.med.jhmi.edu/)[25]. To minimize
artefacts due to subject motion, all diffusion images were
co-registered to the b = 0 image using the Automated
Image Registration (AIR) included in DTIStudio [26].
Diagonalization of the diffusion tensor yielded three eigen-
vectors that provided the three-dimensional information
about the diffusivity of water molecules per voxel, often
described as the diffusion ellipsoid [6]. From this data,
the three eigenvalues (λmajor, λmedium and λminor), FA
and diffusivity, expressed as trace, can be calculated [6].
The three eigenvalues specify the rate of diffusion along
each of the three orthogonal axes of the diffusion ellipsoid.
The largest eigenvalue, λmajor, is equivalent to the diffu-
sivity parallel to the principal axis of the fibres, parallel
diffusivity = λ
║
. The diffusivity perpendicular to the prin-
cipal diffusion direction can be expressed as the perpendi-
cular diffusivity, λ
┴
=(λmedium + λminor)/2. Trace is the
sum of the three eigenvalues (trace = λmajor + λmedium +
λminor) and provides an overall evaluation of the magni-
tude of diffusional motion in a voxel or region. FA repre-
sents the ratio of the anisotropic component of the
diffusion tensor to the whole diffusion tensor [6]. FA values
range from 0–1, where 0 represents maximal isotropic dif-
fusion as in a perfect sphere and 1 represents maximal
anisotropic diffusion. The FA and eigenvectors were used
to calculate colour vector orientation maps.
Analysis of the corpus callosum
The corpus callosum was chosen for study in this investiga-
tion as it is prone to DAI [13,27] and it is anatomically easy to
define using MR-DTI. The mid-sagittal slice through the
corpus callosum was identified on the colour-coded FA
maps. Polygonal regions of interest (ROIs) were manually
placed in the corpus callosum in the two slices immediately
paramedian to the middle slice. Fibre tracking was performed
using the fibre assignment by continuous tracking (FACT)
algorithm in DTIStudio V 2.4 (Johns Hopkins Medical
Institute, Laboratory of Brain Anatomical MRI, http://lbam.
med.jhmi.edu/)[25]. The tracking propagation was termi-
nated when the tract trajectory reached a voxel with an FA
< 0.2 or when the angle between two consecutive steps was >
50°. Only fibres passing through both ROIs were displayed
and used for analysis.
From the data provided in DTIStudio, this study extracted
FA, λmajor, λmedium, λminor and trace for the tracked
voxels in the mid-sagittal section of the whole corpus callo-
sum. From λmajor, λmedium and λminor the parallel and
perpendicular diffusivities were calculated. The procedure was
applied and tested for inter-rater reliability in a previous
investigation [24]. Data was analysed for the 16 controls as
well as for the 15 patients at 6 and 12 months.
Clinical assessment
On admission, the initial level of consciousness was assessed
using the Reaction Level Scale (RLS) [28]. The RLS can be
translated to the Glasgow Coma Scale (GCS) [29] and the
translated GCS is presented here. The mechanism of injury
was also recorded.
The extended Glasgow Outcome Scale (GOSE) [30] was
used for global evaluation of outcome. The assessment of
GOSE scores was based on interviews with the patients or
their next of kin, by a nurse at the time of their follow-up
MR-DTI, i.e. 6 and 12 months post-injury.
The Barrow Neurological Institute Screen for Higher
Cerebral Functions (BNIS) was used for screening of cognitive
function [31]. This instrument was constructed for a neuro-
logical setting to assess patients with verified or suspected
focal, lateralized or diffuse brain damage [32]. BNIS examines
a wide range of different cognitive domains as well as affective
and metacognitive aspects, often neglected in other cognitive
screening methods [33]. Quantitative as well as qualitative
information about the patient’s level of higher cerebral activ-
ity and neuropsychological functioning is gathered. BNIS has
been tested for validity and reliability with good results both
2J. LJUNGQVIST ET AL.
in the US [32,34,35] and in Swedish populations [33,36]. BNIS
has been translated to Swedish and has Swedish manual and
Swedish norms [37]. When establishing reference norms for
BNIS in a Swedish population, good correspondence with US
results was shown by Denvall et al. [36]. In the validation
study by Hofgren et al. [33], the sensitivity of BNIS in differ-
entiating patients with brain damage from controls was 88%
and the specificity was 78% [33].
BNIS starts with a pre-screen of three items to investigate
the level of arousal, communicative ability and co-operative-
ness in order to evaluate whether the person is testable and,
thus, able to participate in the examination. Each item is
scored from 1–3, where a total score of 6 points is a minimum
result for being testable; minimum 2 points on each item.
The screening is composed of seven sub-scales: speech and
language functions, orientation, attention/concentration,
visuospatial and visual problem-solving, memory, affect and
awareness vs performance. Scores are obtained for both the
sub-scales and for the total instrument. In the current study,
the composite score with a maximum of 50 points was used.
BNIS is constructed so that healthy persons should get max-
imum or near maximum BNIS scores, hence the distribution
for healthy people is skewed (mean = 47, SD = 2). A cut-off
score < 47 points is recommended, indicating cognitive dys-
function [37]. BNIS assessment was performed by a licensed
neuropsychologist, 6 and 12 months post-injury.
Statistical analysis
Age in the patient group and the control group was compared
using a t-test. For comparison between groups, Fisher’s
non-parametric permutation test [38] was used. For comparison
over time within groups, Fisher’s non-parametric permutation
test for matched pairs [38] was used.
Results
Fifteen patients, seven women and eight men, were included.
The mean age of the patients was 38.1 years (range = 18–69
years), and there was no significant difference in the mean age
of the patients and controls (p= 0.48). The initial GCS scores
of the patients ranged from 3–15, and the outcomes, measured
by the GOSE score at 6 and 12 months, ranged from 3–8. For
BNIS, three patients scored above cut-off level (47) at 6
months, while 10 patients scored below cut-off level, indicating
cognitive dysfunction. Two patients could not be tested due to
the severity of their brain injury. At 12 months, two patients
scored above cut-off level, while 11 patients scored below cut-
off level and two patients could not be tested, indicating still
lower cognitive function. Clinical characteristics and the out-
come scores of the patients are presented in Table I.
For the diffusion parameters, a significant reduction in FA
in the corpus callosum was seen at 6 months and continued to
be decreased at 12 months in the patients compared to the
controls (Table II and Figure 1). No significant difference was
seen between 6 and 12 months regarding the FA values.
Diffusivity, measured as trace, was significantly increased
at 6 months in patients with TBI compared with controls. The
increased diffusivity was caused by rises in both λ
║
and λ
┴
.
The diffusivity then continued to increase with a significantly
higher trace value at 12 months compared to the value at 6
months.
Table I. Clinical characteristics of the patients.
GOSE GOSE BNIS BNIS BNIS
Patient no. Age (years) Gender Mechanism of injury GCS
Intracranial mass lesion
requiring evacuation (6 months) (12 months) (6 months) (12 months) (dev. SD)
1 57 Female Traffic accident 4 Yes 6 6 38 36 –5.7↓
2 25 Male Car accident 3 No 4 5 33 38 –4.7↑
3 48 Female Traffic accident 14 No 7 7 45 44 –1.7↓
4 22 Female Traffic accident 7 No 6 6 43 46 –0.7↑
5 69 Male Fall in steps 6 No 3 3 n.t. n.t. n.t.
6 52 Female Fall in steps 14 No 6 6 50 45 –1.2↓
7 49 Male Traffic accident 6 No 3 3 21 18 –14.7↓
8 20 Female Car accident 5 No 5 7 46 49 0.8↑
9 44 Male Fall from height 15 No 5 6 44 40 –3.2↓
10 61 Female Fall from height 12 No 4 4 36 34 –4.5↓
11 23 Male Car accident 8 No 4 4 n.t. n.t. n.t.
12 19 Male Car accident 5 No 6 6 38 42 –2.5↑
13 18 Male Car accident 6 No 6 6 42 45 –1.2↑
14 23 Female Fall from height 13 No 7 8 49 49 0.8↑↓
15 42 Male Traffic accident 14 No 6 6 49 45 –1.4↓
GCS, Glasgow Coma Scale on admission; GOSE, Glasgow Outcome Scale extended; BNIS, Barrow Neurological Institute Screen for Higher Cerebral Functions (values < 47
points indicate cognitive dysfunction); n.t., not testable; ↑, better cognition; ↓,worsecognition.
Table II. Longitudinal diffusion tensor imaging (DTI) findings in the corpus callosum for controls and for patients 6 and 12 months post-injury.
Patients Patients Differences Differences Differences
Corpus Callosum Controls 6 months 12 months controls /6 months (p-value) controls /12 months (p-value) 6 months /12 months (p-value)
Fractional anisotropy 0.62 (0.04) 0.57 (0.06) 0.56 (0.06) < 0.01 < 0.0001 0.66
Trace 2.28 (0.12) 2.53 (0.28) 2.62 (0.29) < 0.01 < 0.01 0.03
Parallel diffusivity (λ║) 1.36 (0.05) 1.43 (0.10) 1.47 (0.11) 0.02 < 0.01 0.09
Perpendicular diffusivity (λ┴) 0.46 (0.05) 0.55 (0.10) 0.58 (0.10) < 0.01 < 0.01 0.05
λ
║
, parallel diffusivity; λ┴, perpendicular diffusivity.
BRAIN INJURY 3
When dichotomizing the patients into two groups based on
their outcome at 6 months, eight patients had a good outcome,
defined as a resumption of most of their pre-TBI activities
(GOSE 6–8), and seven patients had an unfavourable outcome
(GOSE 3–5). The mean FA value in patients with unfavourable
outcome was 0.54 ± 0.06 and was significantly lower (p<0.05)
compared to patients with favourable outcome (0.59 ± 0.03).
The trace value was significantly higher (p< 0.0001) in patients
with unfavourable outcome (2.77 ± 0.22) compared to those
with favourable outcome (2.32 ± 0.10). Using the same dichot-
omizing at 12 months, 10 patients had a favourable outcome,
while five patients had an unfavourable outcome. The differ-
ence in mean FA was not significant (0.53 ± 0.07 vs 0.58 ±
0.04), while the patients with unfavourable outcome had a
significantly higher (p= 0.01) trace (2.88 ± 0.22) compared to
patients with favourable outcome (2.49 ± 0.22).
However, when analysing the diffusion properties on an
individual patient basis it becomes apparent that there is an
overlap between the groups. Neither the FA value nor the
trace value totally discriminates between the controls and the
patients or between the patients with favourable vs unfavour-
able outcome. In Figure 2, the trace value is plotted vs the FA
value for each of the patients. The figure shows that most
patients with a favourable outcome are located in the lower
right part of the diagram, i.e. with high FA and low trace
values, and most patients with unfavourable outcome in the
upper left corner. Still, single patients with unfavourable out-
come can be found in the lower right part of the diagram.
Discussion
The current report presents the results from a prospective
longitudinal study of 15 patients with TBI, using MR-DTI of
the corpus callosum 6 and 12 months post-injury. It was
found that FA decreased at 6 months post-injury and con-
tinued to be decreased at the same level at 12 months.
Diffusivity, expressed as trace, was increased at 6 months
but had not reached a stable level, and a significant further
increase could be detected at 12 months. On group level,
Figure 1. Diagram showing the diffusion tensor imaging (DTI) parameters for the controls and the patients. Whisker bars represent range of data; top and bottom of
boxes represent first and third quartile, respectively; midline through box represents median. NS = non-significant.
Figure 2. The trace plotted vs the fractional anisotropy for each of the patients at (a) 6 months post-injury and (b) 12 months post-injury. Each dot represents the
diffusion parameters for one patient and the figure adjacent to the dot represents the GOSE value for the patient. Note that the patients with the worst outcomes
(low values) are situated in the upper left corner of the graph, representing a decrease in FA and an increase in trace. Trace expressed as ×10
-3
mm
2
/s.
4J. LJUNGQVIST ET AL.
patients with unfavourable outcomes had lower FA and
higher trace compared to patients with better outcomes.
This investigation found that FA decreased and trace
increased in the corpus callosum at 6 and 12 months after
traumatic brain injury compared to controls. This is in line
with a number of other studies. Kumar et al. [11]founda
persistent significant decrease in FA of the whole corpus callo-
sum 6 months after injury and a significant increase in diffu-
sivity in patients classified as having non-haemorrhagic DAI.
Sidaros et al. [10] examined patients with TBI in the sub-acute
stage (i.e. at 8 weeks) and at 12 months post-injury. They found
a decrease in FA in the posterior corpus callosum in the sub-
acute stage. At 12 months, they noticed a further reduction in
FA and increased diffusivity, including both parallel and per-
pendicular diffusivities. Wang et al. [12] studied patients in the
acutephase(within9days)and6–14 months post-injury and
found a decrease in FA and an increase in diffusivity in the
acute phase compared to controls and further progression of
these changes in the chronic phase. Earlier work from this
group found a significant reduction in FA in the corpus callo-
sum in the acute phase (within 11 days post-injury). There was
no significant change in the parallel or perpendicular eigenva-
lues or trace. At 6 months, a significant reduction in FA and a
significant increase in trace and perpendicular eigenvalues were
noticed compared to controls [24].
The present report could also find a relation between the
alterations in the DTI parameters and the outcome of the
patients; FA was lower and trace was higher in the group of
patients with unfavourable outcomes. The relation between
DTI parameters of the corpus callosum and clinical outcome
has also been investigated by a number of other groups.
Håberg et al. [39] analysed DTI-parameters in 49 moderate-
to-severe survivors of TBI, acquired more than 1 year post-
injury. They found a correlation between the GOSE scores
and decreased FA in the corpus callosum and increased trace
in the thalamus. Dennis et al. [40] examined 32 children with
moderate-to-severe TBI at 1–5 months post-injury and
assessed the corpus callosum by measuring inter-hemispheric
transfer time. Patients with slow inter-hemispheric transfer
time demonstrated lower FA and higher trace in the corpus
callosum and poorer neurocognitive functioning. Arenth et al.
[41] studied 12 patients with complicated mild-to-severe TBI
in the chronic phase (mean = 1.7 years) with both DTI-
parameters of the corpus callosum and neuropsychologic test-
ing. FA was significantly higher and radial diffusivity was
significantly lower compared to controls and results from
cognitive tasks and reaction times were impaired in the TBI
group.
An interesting finding in the current report was the signifi-
cant increase of trace at 12 months compared to 6 months post-
injury. This result shows that the diffusion parameters have not
reached a stable level 6 months post-injury, but continue to
deteriorate. There is a relative paucity in reports about the long-
itudinal long-term development of DTI parameters after TBI.
Farbota et al. [20] examined patients with TBI, three times over a
4-year period. FA in the corpus callosum decreased between the
first (2 months post-injury) and the third (3 years post-injury)
visits, due to an increase in perpendicular diffusivity, but there
were no significant changes between the second (1 year post-
injury) and third visits [20]. Moen et al. [42] examined 57
patients at 7 days, 3 and 12 months after TBI using DTI. They
found a gradual increase of the mean trace during the 12-month
follow-up. The results from Farbota et al. [20], Moen et al. [42]
and the current study indicate thata stable or chronic level of the
DTI properties has not been reached 6 months post-injury, but
changes continue to take place at least until 12 months. These
changes are probably due to a progressive white matter dete-
rioration, which continues for a long time post-injury, perhaps
for several years. Moen et al. [42] hypothesized that the pro-
longed changes in diffusion parameters could be the result of loss
of myelin sheaths. This is a phenomenon that has been found to
continue for 1–2 years post-injury by neuropathological exam-
inations (see also Meythaler et al. [3]).
Although this study tried to include only patients with
pure DAI, the patients constitute a heterogeneous group of
TBI ranging from severe-to-mild (GCS range = 3–15). Despite
the lack of findings on the CT scans that could explain the
patients’impaired consciousness and/or focal neurological
symptoms, there was probably a mixture of different patterns
of brain injury, for example, axonal disruption and intra- and
extra-cellular oedema.
Another limitation of the present study, besides the hetero-
geneity of the patients, is the small sample size. For example, a
trend was noted toward decreased FA values between 6–12
months, which might have reached statistical significance with
a larger sample size. A larger sample size might also make it
possible to analyse the different sub-domains in the cognitive
screening.
To optimize the timing of follow-up investigations of
patients with DAI, one must consider both the structural
changes as they are interpreted from the MR DTI and the
clinical course. A longitudinal study of the neuropsycholo-
gical outcomes of a sub-set of the patients included in the
present investigation showed ’that recovery occurred in
most cognitive functions for the majority during the first
6 months, but that there was then a reversion, which
seemed to appear between 6–12 months, where cognition
and reaction speed deteriorated in more than half the
group’[43]. Björkdahl et al. [44] also studied a sub-group
of the patients included in the present investgation and
found that the decline in cognitive function did not neces-
sarily imply a corresponding decline in ability to perform
activities. To determine the optimal timing for DTI after
DAI for prognostication, patients must be followed longer
than in the current study. The exact time course of DTI-
related changes after TBI still remains unknown [9], but it
is believed that the current study contributes to a growing
literature supporting the hypothesis that TBI should be
viewed not as an isolated incident, but as a prolonged
disease state [20]. Further studies with even longer post-
injury follow-up are needed in order to establish how long
DTI properties continue to change after TBI.
Acknowledgements
We would like to thank Nils-Gunnar Pehrsson and Anton Mårtensson
for their support in the statistical analysis.
BRAIN INJURY 5
Declaration of interest
The authors report no conflicts of interest. This work was supported by
grants from the Health and Medical Care Committee of Västra Götaland,
and the Foundation for Medical Imaging in Memory of Erik Lysholm.
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