Psychol. Inj.
and Law (2010) 3:36–49
DOI 10.1007/s12207-010-9064-1
Neuroimaging in Mild Traumatic Brain Injury
Erin D. Bigler
Received: 20 July 2009 / Accepted: 19 December 2009 / Published online: 11 March 2010
# Springer Science+Business Media, LLC 2010
Abstract Neuroimaging in mild traumatic brain injury
(mTBI) is reviewed. While computed tomography remains
the acute standard for neuroimaging of mTBI, it is only
sensitive to gross abnormalities and is typically performed
as a measure to rule out more serious and life-threatening
injury. Magnetic resonance imaging (MRI), especially at
field strength of 3.0 T, is the follow-up neuroimaging
standard for assessing potential underlying structural injury
to the brain. Several MRI sequences are particularly
sensitive to subtle hemorrhagic lesions and signal abnor-
malities in white matter, sensitive enough to detect
pathology when present in mTBI. Clinical correlation of
neuropsychological outcome with neuroimaging findings is
discussed along with the future potential for functional
neuroimaging in evaluating the mTBI patient.
Keywords Mild traumatic brain injury (mTBI) .
Neuroimaging . Neuropsychological outcome . White
matter . Magnetic resonance imaging (MRI) . Computed
tomography (CT) . Functional neuroimaging
E. D. Bigler (*)
Department of Psychology, Brigham Young University,
1001 SWKT,
Provo, UT 84602, USA
e-mail: erin_bigler@byu.edu
E. D. Bigler
Neuroscience Center, Brigham Young University,
1001 SWKT,
Provo, UT 84602, USA
E. D. Bigler
Department of Psychiatry, University of Utah,
Salt Lake, UT, USA
E. D. Bigler
The Brain Institute of Utah, University of Utah,
Salt Lake, UT, USA
A history of positive neuroimaging findings provides
important information that assists the clinician in under-
standing the sequelae and potential effects of a traumatic
brain injury (TBI) on neuropsychological test performance.
Much has been written about neuroimaging methods and
findings in TBI, which are summarized elsewhere (Dubroff
and Newberg 2008; Le and Gean 2009). The focus of this
article is just on neuroimaging findings in mild traumatic
brain injury (mTBI) and how such findings provide
additional context about the likely neuropathology of mTBI
and its relationship to neurocognitive and neurobehavioral
sequelae. This review will be brief and primarily focused
on the clinical information that exists in standard radiolog-
ical reports of mTBI patients and its relevance to neuro-
behavioral and neurocognitive sequelae. Obviously,
psychological and neuropsychological assessments of the
mTBI patient typically occur weeks or months post-injury.
This circumstance requires that any clinician who sees the
patient on follow-up must rely on the medical information,
including clinical neuroimaging that has already been
performed. This also means that the clinician needs to
understand the decision making that takes place in the
emergency department (ED) for how a mTBI is triaged and
when radiological procedures are performed that typically
follow established guidelines (Davis 2007; Jagoda et al.
2008). As such, this review begins with an examination of
the literature on acute neuroimaging and what is typically
performed in the mTBI patient.
Acute Neuroimaging in mTBI
A review of the medical literature on acute neuroimaging of
TBI shows that, when medically indicated, computed
tomography (CT) is typically the first scan performed in
any patient who sustains a TBI, including those who meet
Psychol. Inj. and Law (2010) 3:36–49
the imaging criteria for mTBI (see Jagoda et al. 2008;
Atabaki et al. 2008; Eagles et al. 2008; Davis 2007). When
the trauma has been medically deemed as minor and the
patient clinically shows no significant findings on physical
and neurological examination, such as in a simple sports
concussion (McCrory et al. 2005), including no changes in
mental status, the ED medical decision may be to not scan
at all (Cohen et al. 2009; Kuppermann et al. 2009; Parkin
and Maguire 2009). When performed acutely, CT is fast,
can be done in the presence of life-support equipment, and
expeditiously answers immediate critical care issues with
regards to acute neurological and neurosurgical care and
treatment, as life-threatening complications, although rare,
can occur with mTBI (Jagoda et al. 2008; Stein et al. 2006).
Based on Glasgow Coma Scale (GCS)-rated injury severity,
the majority of moderate-to-severe cases of TBI have
positive CT imaging, in contrast to mTBI where the
majority have no clinically defined visible abnormalities
(see Bigler et al. 2006). Studies that have examined the
frequency of CT abnormalities in all mTBI patients
evaluated in the ED generally report <20% are found to
have any type of abnormality (af Geijerstam and Britton
2005; Belanger et al. 2007; Guzel et al. 2009; Maguire et al.
2009). It should also be noted that, when CT is reported as
abnormal, it is more likely that a medical diagnosis of
mTBI is made (Ryu et al. 2009). Although the majority of
CT imaging studies in mTBI are negative when positive,
the most common findings are linear and skull base
fractures and small contusions and/or petechial hemor-
rhage(s) (Gean 1994; Osborn 1994; Smits et al. 2008a, b).
Other less common findings include epidural hemato-
mas, subdural hematomas, depressed skull fractures, and
subarachnoid hemorrhages (see also Le and Gean 2009). In
a detailed prospective study across four hospitals in the
Netherlands, Smits et al. (2008b) identified almost 7,000
cases of head injury where approximately half met the
criteria for mTBI, but of those, only 312 or <5% had
positive CT findings (i.e., presence of one of the above-
mentioned findings). Only one patient died as a direct
consequence of the mTBI. The review of the literature by
Servadei et al. (2001) showed that, in a mTBI patient with
no loss of consciousness (LOC), no significant posttrau-
matic amnesia (PTA), no vomiting, or no diffuse headache
and a GCS of 15, the patient has an extremely minimal
likelihood for having a neurosurgically treatable trauma-
related intracranial hematoma, reportedly to be 0.1:100.
However, even at a GCS of 15, if the mTBI patient has
positive LOC, PTA, vomiting, and/or diffuse headache, the
likelihood of CT detecting an abnormality requiring
neurosurgical intervention goes up to 1–3:100 and 6–
10:100 if the GCS is 14 and skull fracture is added to the
list of clinical variables. Obviously, the presence of such
lesions indicates a more severe traumatic injury reflective
37
of different severity levels even within the mTBI spectrum.
As reviewed in the study of Servadei et al. (2001), the
majority of CT-detected lesions in mTBI does not require
neurosurgical or other medical interventions (see also Bruns
and Jagoda 2009). CT is capable of detecting small
hemorrhages or petechiae within the brain parenchyma, as
shown in Fig. 1, if thin-cut sections are obtained and if the
hemorrhagic lesion is substantial enough to be distin-
guished from normal-appearing parenchyma (Bee et al.
2009; Smith et al. 2007; Zhu et al. 2009).
During the acute phase of injury, when CT is positive in
a patient meeting the criteria for mTBI, it defines what is
referred to as “complicated mTBI” (Kennedy et al. 2006).
Presence of complicated mTBI is an important clinical
distinction because the presence of acute abnormalities on
CT potentially carries with it greater morbidity (Bruns and
Jagoda 2009; Hessen and Nestvold 2009; Kashluba et al.
2008; Lange et al. 2009; Levin et al. 2008) and will be
discussed more fully later.
The investigation by Smits et al. (2008a, b) mentioned
above also examined the 1-year outcome based on
subjective self-report measures in the cohort of mTBI
patients with positive imaging. Even in the presence of a
history of positive imaging, the majority of mTBI patients
reported good recovery but evidence of parenchymal injury
was found to be an independent factor predictive of poorer
outcome. One possible reason for this observation may be
that the most common areas for brain contusion and
petechial hemorrhage in TBI occur in the frontal and
Fig. 1 From Saatman et al. (2008), depicting a solitary focal acute
hemorrhagic lesion (red arrow) in the left frontal lobe (left is on the
viewer's right). These hemorrhagic lesions are thought to reflect
shearing forces in the brain that result in a focal hemorrhage which
becomes a marker for DAI. Used with permission from the Journal of
Neurotrauma
38
temporal lobes (Bigler 2007, 2008; Levine et al. 2008;
Scheid et al. 2003, 2006), which are critical brain regions
regulating behavior and cognition. Furthermore, petechial
hemorrhages are one potential indicator of diffuse axonal
injury (DAI) and/or traumatic axonal injury (TAI) because
the same strain, deformation, and shearing forces that are
sufficient to damage axons also damage blood vessels and
hence the detection of blood directly by CT imaging based
on the difference in density between congealed blood and
brain parenchyma or blood by-products (i.e., hemosiderin)
as detected by magnetic resonance imaging (MRI) as a
marker of damaged axons (Diaz-Arrastia et al. 2009; Lipton
et al. 2008; Suskauer and Huisman 2009).
At the histological level, postmortem pathological
studies of brain injury have long shown hemorrhagic
lesions associated with axonal injury (Graham and Lantos
2002). However, the first MRI descriptions of hemosiderin
do not occur in the clinical literature until the mid-1980s
(see Hesselink et al. 1986). The early descriptions of
hemosiderin in relationship to DAI/TAI do not occur until
the late 1980s and early1990s (Fobben et al. 1989; Gean
1994; Osborn 1994; Parizel et al. 1998). As stated by
Osborn (1994) “the MRI appearance of DAI depends on the
presence or absence of hemorrhage and age of the lesions”
(p. 214). The presence of hemosiderin in MRI in the mTBI
is considered a marker of DAI/TAI (Besenski 2002; Orrison
et al. 2009; Parizel et al. 1998; Tong et al. 2008).
Petechial hemorrhages and residual hemorrhage from
trauma are often located at the gray–white matter junction
as shown in Fig. 1. Other common regions include the
upper brainstem and corpus callosum (Gean 1994; Graham
and Lantos 2002; Osborn 1994). The corpus callosum
appears to be particularly vulnerable and a common area of
abnormality seen in mTBI (Bazarian et al. 2007; Kumar et
al. 2009a, b; Miles et al. 2008; Rutgers et al. 2008). There
is postmortem confirmation of callosal shearing lesions in
mTBI, including no LOC (Denton and Mileusnic 2003). As
already stated, since most cases of mTBI who undergo CT
do not have positive CT findings, no abnormalities
represent the typical finding on the day of injury and first
evaluation in the ED, as was the case in the mTBI patient to
be discussed in Fig. 2. From the neuropathological
standpoint, Graham and Lantos (2002) offer the following
statement: “… there is now no doubt that a cascade of
pathological events in axons occurs at the moment of injury
and that it is related to shear and tensile strains. The fact
that lesions in the corpus callosum and the dorsolateral
sector(s) in the rostral brainstem are often hemorrhagic,
suggest that these strains can also produce rupture of small
blood vessels. It further seems likely that axonal damage is
the most important single factor contributing to the severity
of brain damage and to the outcome in any patient who
sustains a blunt head injury because it occurs at the moment
Psychol. Inj. and Law (2010) 3:36–49
Fig. 2 3.0 T GRE MRI sequence depicting hemosiderin (red arrow)
in the right frontal WM observed post-acutely following mTBI where
there was positive, brief LOC with PTA <24 h. Initial CT scan was
negative and did not reveal identifiable hemorrhage in the frontal
region. This is a nice demonstration of follow-up MRI providing
useful clinical information that was not available in the day-of-injury
scan. The patient had persistent symptoms of distractibility, reduced
short-term memory function, prominent fatigue with diminished
motivation, and depression
of injury” (p. 867). While much of the initial pathological
effects from a mTBI may be subtle metabolic and
physiological alterations within the brain (Giza and Hovda
2001) given Graham and Lantos' (2002) view that all brain
injury is on a continuum, from the mildest of mild injuries, the
degree that axonal damage can be demonstrated likely relates
to the level and degree of sequelae that occur, if at all. This is
also probably the explanation why the majority of mTBIs
have a positive outcome with no sequelae as they have
minimal to no axonal damage that persists (McCrea 2008).
While still meeting the mTBI criteria, it is nonetheless
important to distinguish between what is referred to as an
uncomplicated mTBI versus a complicated mTBI because this
distinction becomes important for neuropsychological out-
come. Furthermore, the distinction is based on an objective
observation of the presence or absence of neuroimaging
abnormalities. In sports concussion, the most recent consensus
regarding diagnosis requires that “no abnormality on standard
structural neuroimaging” be observed (McCrory et al. 2005,
p. i77). If an abnormality is observed on standard clinical
imaging, it is no longer considered a “sports concussion”
level injury, but a more significant brain injury. “Complicated”
mTBI is, therefore, defined by the presence of a definitive
neuroimaging abnormality, in particular intracranial pathology
(Lange et al. 2009). In both adults (Kashluba et al. 2008) and
children (Fay et al. 2009; Gerrard-Morris et al. 2009),
sustaining a complicated mTBI may be associated with a
greater likelihood for demonstrable sequelae noted on
neuropsychological outcome variables.
This neuroimaging distinction of either positive or negative
neuroimaging findings in the acute to early acute time frame
post-injury becomes an important piece of historical clinical
Psychol. Inj. and Law (2010) 3:36–49
information in evaluating the neuropsychological effects of
the injury. For example, in a university-based mTBI study
performed in Norway, Muller et al. (2009) demonstrated that
a GCS of <15 (but 13 or above) in association with positive
intracranial pathology on CT and presence of serum S100B
(a blood biomarker of brain injury; see Castellani et al. 2009;
Korfias et al. 2009; Unden and Romner 2009) that these
factors “… predicted impaired cognitive performance both at
baseline and after 6 months” (p. 698).
Because sport concussion head injuries are common,
there is another distinction that needs to be made between
sports concussion and the uncomplicated and complicated
mTBI classification and neuroimaging findings. In sports
concussion, the concept of a distinction between “simple”
and “complex” concussions has been made (see Makdissi
2009). A simple concussion refers to a concussion wherein
symptoms last <10 days and, in complex concussion,
symptom duration lasts 10 days or more. Complex
concussions also have features of concussive convulsions,
prolonged LOC, cognitive impairment, and/or multiple
concussions (McCrory et al. 2005). Thus, in sports
concussion, by definition, those who have sustained a
simple concussion recover with the assumption of no
lasting effect of the concussion where the majority will
have never met the criteria for even having neuroimaging.
In complex concussion, recovery occurs over a more
protracted time period, but does generally occur where the
athlete ultimately returns to baseline level of function (Lau
et al. 2009). However, in neither simple nor complex sports
concussions are intracranial abnormalities present on
standard structural neuroimaging studies. So the “complex”
classification is not the same as complicated mTBI.
Complicated mTBI is likely a more significant mild injury
than either simple or complex sports concussion.
One limitation of CT is that it is less sensitive in
detecting hemorrhage than is MRI (Kidwell and Hsia
2006). Therefore, negative CT in the acute period under-
estimates the number and location of hemorrhagic lesions
compared to MRI. The case presented in Fig. 2 demon-
strates this point where this patient had a negative CT on
admission following a mTBI, but because of persisting
PTA was rescanned wherein the MRI demonstrated
frontal petechial hemorrhages. Thus, the absence of
identifiable CT abnormalities does not mean that under-
lying parenchymal injury has not occurred or that
petechial hemorrhages are not present, but merely their
presence may simply be under the threshold of detection.
This has been shown in a case with negative CT but
positive postmortem histological analysis of the brain
following an mTBI (see Bigler 2004).
As already mentioned, when the radiological report(s) of
acute neuroimaging studies in an mTBI patient reflect
intracranial pathology, the important issue for psychology is
39
that a complicated mTBI has a greater likelihood of being
associated with cognitive and emotional sequelae (Hessen
et al. 2008; Hessen and Nestvold 2009; Kashluba et al.
2008). As indicated previously in this review, the presence
of petechial hemorrhage is considered a marker for axonal
injury (Giugni et al. 2005; Graham and Lantos 2002; Li and
Feng 2009) and presence of petechia in the acute CT imaging
represents intracranial pathology. As such, presence of
petechia in the acute imaging provide objective information
about DAI/TAI being present in the mTBI patient and such
findings represent an objective distinction for the clinician
where sequelae in emotional, memory, and attentional
functioning become more likely (Kraus et al. 2007).
Just as with conventional CT, conventional MRI findings
in uncomplicated mTBI are often negative both in the acute
as well as chronic stage (Bruns and Jagoda 2009; Le and
Gean 2009). However, with MRI, there are many more
methods of image analysis that can be applied, especially
those that are specific to detecting white matter (WM)
integrity like the fluid-attenuated inversion recovery
(FLAIR) sequence, diffusion tensor imaging (DTI), and
MRI measures that directly assess the biochemical compo-
sition of the brain via magnetic resonance spectroscopy
(MRS; Gasparovic et al. 2009; Topal et al. 2008; Yeo et al.
2006). There has also been a recent MRI improvement in
detecting hemosiderin using what is referred to as suscep-
tibility weighted imaging (SWI; Tong et al. 2008). Iron is a
composition of blood, and iron, of course, has paramagnetic
properties which, if in sufficient concentration, can be
detected by MRI. As a result of stretching beyond normal
tensile strength tolerance and/or shearing forces that breech
blood vessel integrity, microhemorrhages occur within
brain parenchyma. Blood in brain parenchyma quickly
degrades and, acutely, the gelled blood becomes concen-
trated where the iron deposition can be readily detected by
MRI, as was shown in Fig. 2.
The hemosiderin detected in the case shown in Fig. 2
was with standard gradient-recalled echo (GRE). MRI–
SWI may be twice as effective in detecting hemosiderin as
the standard GRE sequence (Tong et al. 2004). This
patient was a college student who was struck by a car and
sustained a brief LOC, as documented by eyewitnesses.
The patient had several hours of PTA and spent the night
in the hospital for observation. The patient was a graduate
student at the time of injury and required accommodations
within the graduate program to be able to continue with
her education and training. As seen in Fig. 1, hemosiderin
is clearly identified and, therefore, DAI/TAI is likely
present in the right frontal area. Neuropsychologically,
The patient’s primary performance problems were in
working memory and executive function and, subjectively,
she complained of problems with attention/concentration
with an inability to sustain focus, diminished motivation,
40
fatigue, and disrupted sleep. The presence of demonstrable
pathology in the frontal lobe likely correlates with the
objective neuropsychological deficits observed in this
mTBI patient as well as subjective symptoms. Scheid et
al. (2006) have shown that the presence of hemosiderin
primarily within frontotemporal regions, as a reflection of
prior trauma-related microhemorrhages, was associated
with cognitive symptoms and sequelae, offering further
confirmation of the likely link between the MRI-identified
abnormalities in this mTBI patient and her neuropsycho-
logical sequelae.
MRI in the Subacute and Chronic Phase of mTBI
Because of the higher sensitivity of MRI procedures in
detecting subtle pathology associated with mTBI, review of
current literature on this topic shows that MRI is the
radiological method of choice for evaluating the mTBI
patient in the post-acute phase of assessment (see Jagoda et
al. 2008; Le and Gean 2009). The standard clinical MRI
sequences that are routinely performed in mTBI are the
following five procedures: (1) the anatomical sequence or
T1, which can also be done as a thin-slice three-
dimensional volume that permits quantitative measurements
of brain structures (quantification methods for T1 and other
sequences reviewed by Brewer 2009; Brewer et al. 2009;
Filippi and Agosta 2009; Holdsworth and Bammer 2008;
Pagani et al. 2008); (2) the T2 sequence that highlights
cerebrospinal fluid (CSF), where increased CSF may be an
indication of atrophy (MacKenzie et al. 2002; Trivedi et al.
2007); (3) the FLAIR sequence that is particularly sensitive
to WM signal abnormalities (Akhtar et al. 2003; Ding et al.
2008; Sigmund et al. 2007; Topal et al. 2008); (4) the GRE
or SWI sequences that are sensitive to hemorrhagic lesions
(Chastain et al. 2009; Hammoud and Wasserman 2002; Tong
et al. 2003; Topal et al. 2008); and (5) the DTI where various
metrics can assess WM integrity (Singh et al. 2009).
Figure 3, from Levine et al. (2008), shows the
application of quantitative neuroimaging to assess the
overall structural integrity of the brain following injury
and shows the effect of TBI injury severity on atrophic
changes (brain volume loss) that occur, including those
associated with mTBI. Brain atrophy occurs in some cases
of mTBI (see Cohen et al. 2007; Inglese et al. 2005, 2006;
MacKenzie et al. 2002) because, even in mTBI, cell death
or injury that results in cellular damage may result as a
consequence of the trauma, as shown in animal and human
studies (Dikranian et al. 2008; Tashlykov et al. 2009; Teresa
et al. 2009; (Blumbergs et al. 1994; Veevers et al. 2009;
Viano et al. 2009).
As inferred from Fig. 3, a somewhat linear relationship
between injury severity and presence of cerebral atrophy
Psychol. Inj. and Law (2010) 3:36–49
occurs but atrophic brain changes take weeks to months
post-injury to develop (Blatter et al. 1997) and may take
weeks post-injury to document. These kinds of changes can
be demonstrated by performing quantitative MRI analyses a
month or more post-injury (Bigler et al. 2006; Ghosh et al.
2009; Wilde et al. 2006) where the duration of PTA is a
better predictor than GCS of whether atrophy occurs or not.
Having an early baseline scan of either CT or MRI and
comparing follow-up scans, particularly in terms of a
whole-brain CSF measures, is a straightforward method
for assessing cerebral atrophy related to TBI (see MacKenzie
et al. 2002). Voxel-based morphometry involving either
structural or DTI scans have also been used to quantify
changes in suspected mTBI (Adams et al. 2007; Chappell et
al. 2008; Gale et al. 2005).
Sensitivity of MRI in Detecting mTBI-Related
Abnormalities
As of this writing, there is no large-scale, prospective
study that can provide the proper reference to calculate
actual sensitivity and specificity for incident abnormal
MRI findings following mTBI in the subacute or chronic
phase. However, some inferences can be made from
existing clinical investigations, indicating the usefulness
of follow-up MRI in mTBI in the patient that remains
symptomatic. Using a 3.0-T scanner, Lee et al. (2008)
examined 36 mTBI patients, all with positive LOC and
PTA, so each patient had clearly sustained a significant
mTBI requiring clinical assessment within a university-
based ED, and all subjects had CT and a follow-up MRI
within 2 weeks of injury. Fifty percent of the subjects had
identifiable CT abnormalities, but 75% had identifiable
MRI abnormalities. The breakdown of abnormalities was
as follows: hemorrhagic TAI (eight out of 36 CT, 17 out of
36 MRI), nonhemorrhagic TAI (zero out of 36 CT, four
out of 36 MRI), and cerebral contusions (13 CT, 21 MRI).
Scheid et al. (2007) have shown the increased sensitivity
of higher field strength of a 3.0-T MRI over a 1.5-T scan,
yet the most common clinical scan in the United States
remains a 1.5-T MRI. Unless a 3.0-T MRI is performed
and, at a minimum, the five sequences indicated above
examined, abnormalities as a result of mTBI may be
missed or overlooked based on the studies of Lee et al.
(2008) and Scheid et al. (2007).
Diffusion Tensor Imaging
DTI was first discussed in the mid-1990s (see Basser
1995), but because of technical and magnetic field
strength issues, it really took about a decade for DTI
research to become mainstream, with evolving clinical
applications (Dong et al. 2004; Sundgren et al. 2004). At
Psychol. Inj. and Law (2010) 3:36–49
Fig. 3 From Levine et al. (2008). Top left group pattern associated
with the latent variable, expressed as correlations of group member-
ship (coded as 1 or 0) with the pattern of volume changes. Error bars
represent 99% confidence intervals. Group differences are indicated
by non-overlapping error bars. Remaining panels regional plots of
bootstrap ratios indicating pattern of CSF (top right), WM (bottom
left), and gray matter (bottom right). The color bar indicates the
coding scheme according to the level of the bootstrap ratio, interpreted
similar to a Z score. CSF values are positive, indicating volume
the time of writing this article, as listed in the National
Library of Medicine (http://www.pubmed.gov), the num-
ber of mTBI DTI articles is now approaching 30, all
demonstrating a subset of mTBI patients with positive
findings. The most recent studies clearly demonstrate that
DTI is sensitive in detecting WM abnormalities in mTBI,
even in the mildest form of mTBI, and that DTI-identified
abnormality, when observed in the mTBI patient, tends to
be in the frontal and temporal lobes and corpus callosum
(for example, as a partial listing, see Huang et al. 2009;
Kumar et al. 2009a, b; Lipton et al. 2008, 2009; Lo et al.
2009; Rutgers et al. 2008).
Higher field strength and the number of directions in
creating the tensor maps greatly improve the sensitivity of
detecting abnormalities (Alexander et al. 2006). Aggregate
WM tracts can be identified with DTI and discontinuity
within these tracts can be shown in some mTBI patients as
41
increases associated with TBI severity, whereas gray matter and WM
values are negative, indicating volume loss associated with TBI
severity. Images were thresholded at a bootstrap ratio of 3.0,
corresponding approximately to p=0.001. Axial images are displayed
in radiologic convention (right hemisphere displayed on left side of the
image). The right cingulate volume is displayed on the right side of
the images and the left cingulate volume is displayed on the left side of
the images. Reproduced by permission from the American Academy
of Neurology from Levine et al. 2008
presented in Fig. 4 from Rutgers et al. (2008). Niogi et al.
(2008a, b) have used a similar approach but also correlated
neuropsychological performance with WM microstructural
abnormalities. What is especially important about the
approach of Niogi et al. is that it shows what may be
particularly important in mTBI is not the total burden of
WM damage in mTBI, but linking specific tracts with
function. For example, the integrity of the uncinate
fasciculus, a WM tract that links the temporal and frontal
regions, is associated with impaired short-term memory
performance. WM integrity of longer tracts like fronto-
occipital and corpus callosum relate to speed of processing
and executive functioning (Kumar et al. 2009a, b; Lipton et
al. 2009; Singh et al. 2009).
DTI studies also help address the question of whether
mTBI has a distinctly different pathological basis than more
severe TBI. This actually represents a rather intense debate
42 Psychol. Inj. and Law (2010) 3:36–49

Fig. 4 From Rutgers et al.

(2008), showing discontinuity
in the frontal WM forceps
associated with frontal projec-
tions with the anterior aspect
of the corpus callosum in a
49-year-old mTBI patient.
Upper left FLAIR sequence that
showed no abnormalities. Top
middle axial plane color-coded
FA map, with a region of
reduced FA identified in the
left frontal lobe. This region of
interest (ROI) is identified in
the T2-weighted image (upper
right), with the DTI fiber
tracking superimposed on the
T2 image (lower left) and
without the ROI (lower right)
which highlights the
discontinuity noted in this
region. Reproduced with per-
mission from American Society
of Neuroradiology

in the literature (see Hoge et al. 2009). However, DTI
studies suggest that mTBI is, as the classification implies,
simply a milder form of TBI resulting in some diffuse, but
subtle changes (Singh et al. 2009). Several converging lines
of evidence support this view. For example, in both child
and adult TBI, the relationship between generalized
cerebral atrophy and severity of injury is generally linear
(Ghosh et al. 2009; Wilde et al. 2006; Levine et al. 2008)
and mild, generalized, and nonspecific cerebral atrophy has
been documented in prospective, longitudinal follow-up
cases of mTBI as already mentioned (MacKenzie et al.
2002) and as shown in Fig. 3. The distribution of pathology
shown in both acute (Chu et al. 2009; Wilde et al. 2008),
subacute (Lipton et al. 2008, 2009) and more chronic injury
effects (Singh et al. 2009) favors some degree of diffuse
injury with a frontotemporal focus, just as the case in more
severe TBI. Recently, Lipton et al. (2008, 2009) examined a
group of mTBI patients within 2 weeks of injury who they
describe had very mild TBI (GCS = 15) where DTI
abnormalities within the dorsal lateral prefrontal cortex
were related to impaired performance on executive function
measures. Lo et al. (2009) have shown subtle but chronic
DTI changes in the genu of the corpus callosum and this
related to cognitive impairments. Despite these excellent
and promising advances in imaging underlying pathology
observed in some mTBI patients, DTI is still best considered
a research tool at this time, but standardized protocols tested
on a broad sample of mTBI subjects are the subject of
ongoing research.
Functional Neuroimaging
Functional neuroimaging and neurophysiological measures
have revolutionized cognitive psychology and neuroscience
and such techniques are being applied to the study of mTBI
(Barrett 2009; Hillary and DeLuca 2007). As such, it is also
important in this review to touch on functional imaging and
neurophysiological studies. However, just like DTI, func-
tional neuroimaging of mTBI is still in its developmental
stage with no universal standards or recommendations
published at this time for its clinical use in mTBI. As such,
while providing immensely valuable information about
mTBI, functional neuroimaging techniques are still very
much in development and should not be viewed as stand-
alone assessment techniques (American Academy of Neu-
rology 1996; Granacher 2008; Wortzel et al. 2008).
To be detected in brain parenchyma by standard structural
MRI, a typical minimal size for an abnormality needs to
approximate or exceed a cubic millimeter. Given these
limitations, from a very fundamental neurobiological perspec-
tive where neural elements are measured in microns (1/10,000
of a millimeter), considerable neuropathology is simply below
the threshold of detection by contemporary neuroimaging.
Furthermore, basic structural imaging is just that—an image
of brain structure not directly measuring any function. Given
that the majority of conventional CT and MRI scans
performed on mTBI cases are unremarkable does not mean
absence of underlying abnormality. It may only mean that
underlying pathology, if present, will only be detected by
Psychol. Inj. and Law (2010) 3:36–49
simultaneously assessing structure and function. This has
actually been shown in animal models of mTBI as well as
human studies with normal conventional MRI findings yet
functional neuroimaging or neurobehavioral measures detect-
ing significant differences (Henninger et al. 2007; Lewine et
al. 2007).
Functional imaging has some advantages over traditional
psychological and neuropsychological assessment methods.
Neuropsychological findings can only infer which regions of
the brain are participating in a given function. In contrast,
functional neuroimaging methods now permit a more directly
assessed evaluation of brain activation patterns simultaneous
with cognitive and behavioral functioning. Using computer-
based assessment methods within the MRI environment,
Mayer et al. (2009) have shown that a spatial working
memory/attentional task was particularly sensitive in the
subacute period, distinguishing a disruption in attentional
abilities in mTBI patients. Of particular importance was the
demonstration of how subtle activation differences occur in
multiple brain areas involved in tasks that differentiated the
mTBI group from the controls. This implies a disruption in
underlying connectivity in mTBI (see also Kumar et al.
2009a, b; Suh et al. 2006). These areas included the frontal
and parietal regions, striatum, thalamus, and cerebellum.
Similarly, Smits et al. (2008a) have shown functional
magnetic resonance imaging (fMRI)-based correlates of
disrupted working memory and attention in mTBI, with
such differences not only being shown in the acute but also
chronic phase in those who remain symptomatic following
mTBI (also, see review by Stein and McAllister 2009).
While these studies are research-based and more research is
needed before their use can be applied to clinical practice,
the list of studies showing significant hemodynamic effects
of mTBI on fMRI brain activation continues to grow (Chen
et al. 2008a, b; Ge et al. 2009; Jantzen et al. 2004; Lovell et
al. 2007; Ptito et al. 2007; Suskauer and Huisman 2009).
These studies and others are excellent examples of how a
cognitive probe can be assessed within the functional
neuroimaging setting, providing rich and more direct
information to the clinician about what neural systems are
affected in mTBI. Currently, traditional neuropsychological
measures are being adapted to the fMRI assessment
environment and show considerable promise (Allen et al.
2007; Gountouna et al. 2010; Zakzanis et al. 2005) but as
yet have not been adapted to assessing mTBI. Also, recent
functional neuroimaging studies have been particularly
illuminative about mTBI and recovery of function and
how to use fMRI techniques in sequentially assessing the
effects of mTBI from initial injury to recovery, especially in
sports concussion (Chen et al. 2008a, b).
The functional neuroimaging environment is not con-
strained by the limits of traditional neuropsychological
methods. For example, it is well-known that speed of
43
processing is one of the most common effects of TBI,
including mTBI (Mathias et al. 2004; Mathias and Wheaton
2007) yet most clinical neuropsychological assessments of
speed of processing is an inferred measure with the
clinician using a stopwatch to assess speed while the
patient is performing a task, like the Trail Making Test
(Kashluba et al. 2008). In the functional neuroimaging
environment, the stimuli and the task to be performed can
be computerized and more directly measured. In the future,
this will become much more important in the assessment of
mTBI effects because a variety of measures that are simply
impossible to conduct in the standard clinical neuropsy-
chological assessment will be possible in the functional
neuroimaging environment.
For example, using a neurophysiological measure,
Heitger et al. (2008) have shown that eye movement
abnormalities determined in the subacute time frame and
not neuropsychological performance were predictors of
mTBI outcome. The reason why eye movement may be so
sensitive is that the response is partially reflexively driven
and requires integration across a number of elaborate WM
pathways that engage the upper brainstem, frontal eye
fields, and motor execution. These types of techniques can
be adapted to the functional neuroimaging environment and
simply are not something that can be assessed with
traditional neuropsychological techniques. Furthermore,
returning to the study discussed by Mayer et al. (2009)
above, the neural processing of a memory/attentional task
distinguished mTBI from controls occurred at about 200 ms
after stimulus presentation and, obviously, such processing
speed differences cannot be detected with traditional
neuropsychological techniques.
As another example of this principle, but using positron
emission tomography (PET) or single photon emission
computed tomography (SPECT) imaging, is the difference
between resting metabolic functioning of the brain, which
may show no difference between subjects with mTBI and
controls versus a cognitively challenging task (see Belanger
et al. 2007; Gross et al. 1996; Mehr and Gerdes 2001;
Metting et al. 2007; Umile et al. 2002). For example,
Hattori et al. (2009) use SPECT in assessing mTBI patients
at rest and during the Paced Auditory Serial Addition Test
(PASAT) where, during the PASAT, mTBI patients' perfor-
mance was different but not at rest. Another interesting
technique that can only be done via neuroimaging using
SPECT or PET is ligand receptor uptake studies. For
example, Hashimoto and Abo (2009) have shown distinct
differences in frontal lobe benzodiazepam receptor uptake
in those subjects with mTBI. Finally, magnetoencephalog-
raphy has been applied to assessing mTBI, with consider-
able promise (Huang et al. 2009; Lewine et al. 2007),
mainly because of the fine-tuned analyses that can be
performed. MRS studies done in the acute phase of sports
44
concussion clearly show acute changes (Henry et al. 2009).
MRS findings in mTBI have also been documented in the
subacute (Gasparovic et al. 2009) and chronic phase
(Mamere et al. 2009).
Clinical MRI at 3.0 T is Superior in Detecting Subtle
Pathology Associated with mTBI
As already stated, higher field strength is superior to lower
field strength in detecting subtle abnormalities (Scarabino
et al. 2003) and MRI is superior to CT (Lee et al. 2008). By
definition, when neuroimaging abnormalities are observed
in the mTBI patient, they tend to be subtle (Le and Gean
2009). CT imaging in the acute phase is not done to detect
subtle neuropathology, but rather to emergently detect
medically treatable pathology (Jagoda et al. 2008; Coles
2007). However, in the chronic stage, the objective of
neuroimaging is not for acute medical management, but to
identify any pathology that can assist the clinician in
understanding the effects of the brain injury.
Several studies have compared 1.5 and 3.0 T MRI, with
the higher magnetic field strength being superior in
detecting more subtle abnormalities (Le and Gean 2009)
and, therefore, if the goal is to best understand the potential
neurobehavioral and neurocognitive sequelae of mTBI,
then performing MRI at field strength <3.0 T may lack
sensitivity and specificity in identifying pathological
changes associated with trauma. Because of its improved
sensitivity in detecting pathology associated with mTBI,
particularly the SWI and DTI techniques in detecting subtle
hemorrhagic lesions and WM lesions (Barnes and Haacke
2009; Bosnell et al. 2008) and the increased availability of
3.0 T MRI, it will likely become the standard in assessing
brain injury (Fischbach et al. 2008; Heidemann et al. 2006;
Sicotte et al. 2003).
General Conclusions
In mTBI patients who undergo acute neuroimaging as part of
their initial evaluation, the day-of-injury CT scan findings
provide important baseline information. Presence of any CT
intracranial abnormality during the acute stage is a marker for
“complicated mTBI,” and complicated mTBI carries with it
greater likelihood for neuropsychological morbidity. Follow-
up MRI within the first few days to weeks is primarily done
to determine if structural indicators of trauma such as
presence of hemosiderin as residual indicia of subtle cortical
contusions and/or underlying shear lesions indicative of DAI
and/or TAI are present on FLAIR and/or GRE/SWI sequen-
ces or WM FLAIR signal abnormalities are present, reflective
of WM abnormalities. DTI studies have the potential to show
subtle pathology associated with mTBI and objective stand-
Psychol. Inj. and Law (2010) 3:36–49
ards are likely forthcoming in evaluating the mTBI patient.
Functional neuroimaging studies in the clinical assessment of
mTBI remain a work in progress. MRI done 3 months or
more post-injury may also identify chronic lesions as well as
establish whether any atrophic changes have occurred,
particularly reflected in reduced size of the corpus callosum,
increased ventricular size, or greater prominence of cortical
sulci than expected for age, which can all be determined
through quantitative analyses (Bigler 2001). When possible,
follow-up MRI done at a 3.0-T field strength likely has
greater sensitivity in detecting abnormalities associated with
mTBI. Most recently Metting et al. (2009) have shown that
disturbed CT perfusion in mTBI patients with normal
noncontrast CT correlated with outcome.
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