JOURNAL OF NEUROTRAUMA 25:1049–1056 (September 2008)

© Mary Ann Liebert, Inc.

DOI: 10.1089/neu.2008.0566

Focal Lesions in Acute Mild Traumatic Brain Injury

and Neurocognitive Outcome: CT versus 3T MRI

Hana Lee,1,2 Max Wintermark,2,3 Alisa D. Gean,2,3 Jamshid Ghajar,4,5

Geoffrey T. Manley,1,2 and Pratik Mukherjee2,3

Abstract

Mild traumatic brain injury (mTBI) is associated with long-term cognitive deficits. This study compared the de-
tection rate of acute post-traumatic focal lesions on computed tomography (CT) and 3T (Tesla) magnetic reso-
nance (MR) imaging with neurocognitive outcomes. Adults (n  36; age range, 19—52 years) with a single
episode of mTBI (Glasgow Coma Scale 13—15, as well as loss of consciousness and post-traumatic amnesia)
were prospectively enrolled and had CT within 24 h of injury and 3T MR within 2 weeks of injury. The CT and
MR scans were reviewed by two neuroradiologists who were blinded to clinical information. Twenty-eight of
these mTBI subjects and 18 matched healthy volunteers also underwent serial neurocognitive testing. Of the 36
mTBI cases, intraparenchymal lesions were detected in 18 CT and 27 acute MR exams, consisting of hemor-
rhagic traumatic axonal injury (TAI) (eight CT, 17 MR), non-hemorrhagic TAI (zero CT, four MR), and cerebral
contusions (13 CT, 21 MR). Mild TBI patients had significantly worse performance on working memory tasks
than matched controls at the acute time point (2 weeks), and at 1 month and at 1 year post-injury; yet there
was no significant correlation of imaging findings with working memory impairment. In conclusion, 3T MR
detected parenchymal lesions in 75% of this mTBI cohort with loss of consciousness and post-traumatic am-
nesia, a much higher rate than CT. However, the CT and 3T MR imaging findings did not account for cogni-
tive impairment, suggesting that newer imaging techniques such as diffusion tensor imaging are needed to pro-
vide biomarkers for neurocognitive and functional outcome in mTBI.

Key words: computerized tomography; high-field magnetic resonance imaging; mild traumatic brain injury;
neurocognitive outcome; traumatic axonal injury

Introduction 13—15, loss of consciousness (LOC) lasting less than 30 min,

and posttraumatic amnesia (PTA) of less than 24 h.

T RAUMATIC BRAIN INJURY (TBI) is the leading cause of death

and disability in Americans under the age of 45 in the
United States. Each year, approximately 1.4 million people
sustain traumatic brain injury and seek emergency care as a
result of falls, traffic related motor vehicle accidents, assaults
and other mechanisms (CDC, 2003). Of these reported TBI
cases, approximately 85% are classified as mild traumatic
brain injury (mTBI) (Bazarian et al., 2005). However, case de-
finitions are varied in the literature with different classifica-
tions of concussions and mTBI (Carroll et al., 2004; Bigler,
2008). Furthermore, mTBI is widely heterogeneous in clini-
cal presentation and functional outcome (Kushner, 1998; Tel-
lier et al., 1999). For the purposes of the current study, mild
TBI is defined as an initial Glasgow Coma Score (GCS) of
In emergency care, computed tomography (CT) is the first-
line imaging modality for assessing TBI, and 1.5-Tesla (1.5T)
magnetic resonance (MR) imaging is occasionally used for
further assessment. CT is comprehensive in detecting frac-
tures, hemorrhage, and mass effect in the acute phase after
injury and is faster, allowing for better patient compliance
and decreased movement artifacts. However, it has been es-
tablished that high field MR is more sensitive than CT in de-
tecting traumatic lesions during the acute phase of the in-
jury (Paterakis et al., 2000; Mittl et al., 1994). Even mTBI can
lead to considerable traumatic axonal injury (TAI), some-
times referred to as diffuse axonal injury (DAI), that is not
appreciated in CT (Mittl et al., 1994). TAI results from shear-
ing forces during acceleration, deceleration and rotation

1Neurological Surgery, 2Brain and Spinal Injury Center, and 3Radiology, University of California, San Francisco, California.
4Neurological Surgery, Weill Cornell Medical College and 5Brain Trauma Foundation, New York, New York.

1049
1050
forces during impact which cause focal injury to the white
matter tracts (Gennarelli and Graham, 1998). CT scans of
mTBI patients underestimate these lesions, which have been
reported as a major predictor of poor outcome (Medana and
Esiri, 2003), including cognitive impairment and disability
(Fork et al., 2005). Studies have shown that even mTBI sub-
jects have persistent deficits in attention, working memory,
and executive functions (Arcia and Gualtieri, 1994; Suh et al.,
2006; Kurca et al., 2006).
Yanagawa et al. (2000) reported that T2*-weighted gradi-
ent-echo imaging at 1.5T was positively correlated with LOC
and Glasgow Outcome Scale (GOS) and could be useful for
evaluating clinical symptoms of head injury during the acute
phase. Other studies have also reported use of T2*-weighted
gradient-echo imaging at 3 Tesla (3T) to be superior to 1.5T
at detecting hemorrhagic and non-hemorrhagic TAI in the
chronic phase of TBI (Scheid et al., 2007).
However, previous imaging studies of CT and MR have
predominantly focused on moderate and severe brain injury
or mTBI during chronic stages of injury (Scheid et al., 2003).
There are no prior studies examining 3T MR for the detec-
tion of focal parenchymal lesions in the early stages of TBI,
and these prior 3T studies did not focus on mild TBI. Hence,
it is not yet known how frequently focal lesions can be de-
tected at 3T in mTBI, and how this compares to findings on
initial head CT evaluation. Additionally, there have been no
previous studies that followed an mTBI cohort serially to as-
sess neurocognitive deficits and functional outcome.
This study compared the detection rate of post-traumatic
focal lesions such as contusions and TAI on CT performed
on the day of mTBI and on 3T MR within two weeks of the
injury. The results were correlated with performance on the
California Verbal Learning Test-Second Edition (CVLT-II)
(Delis et al., 2000) administered within 2 weeks, 1 month,
and 1 year post-mTBI. We hypothesized that 3T MR would
detect more focal lesions, including more TAI lesions, than
CT. We also postulated that patients with more focal lesions
would have worse verbal memory performance as detected
by the CVLT.
Methods
Participants
Thirty-six subjects (29 male, seven female) with blunt and
isolated mTBI were prospectively enrolled. The mean age of
the subjects was 30 years (30.2 SD  8.0 years; range 19—52
years). The mechanisms of injury consisted of 25 cases of mo-
tor-vehicle related accidents (69%), seven cases of assaults
(19%), and four cases of falls (11%). These mild TBI subjects
were identified by Emergency Department (ED) staff in San
Francisco General Hospital (SFGH), and all of the subjects
received CT scans within 24 h of injury as part of routine
clinical care in the ED. The mTBI subjects presented with
Glasgow Coma Score (GCS) of 13—15 in the field; and in the
ED, 24 (66%) mTBI patients had GCS of 15, 10 patients (27%)
had GCS of 14, and two patients (6%) presented with GCS
of 13. These mTBI subjects all had witnessed loss of con-
sciousness of less than 30 min and presence of post-traumatic
amnesia as part of the study inclusion criteria. The mTBI sub-
jects did not report any prior history of brain injuries or other
neurological or psychiatric diagnosis, including substance or
alcohol abuse. Twenty-eight of these mTBI subjects (23 male,
LEE ET AL.
five female; mean age 30.3 SD  8.6 years) also underwent
neurocognitive testing within 2 weeks of injury, and again
at 1 month and at 1 year post-trauma.
Eighteen healthy volunteers (15 male, 3 female, mean age
34.3 SD  8.9) were matched to the patients by gender, age,
levels of education, and handedness (Table 1). All of the
healthy volunteers completed neurocognitive testing and re-
ceived 3T MR examinations which were reported as normal
by a board-certified neuroradiologist.
All subjects and controls were selected for English as the
native primary language to ensure language was not a bar-
rier in neurocognitive testing. The subjects and controls were
all capable of self-consent and signed a written informed con-
sent prior to participation. The magnetic resonance imaging
and other study protocols were approved by the Committee
on Human Research at University of California, San Fran-
cisco.
Image acquisition
Admission CT scans were obtained from the radiology de-
partment of SFGH. These were contiguous axial CT images
of the head at 5-mm collimation and 5-mm intervals.
The MR scans were acquired using 3T GE EXCITE scan-
ner (GE Healthcare, Milwaukee, WI) equipped with an eight-
channel head coil and performed at University of California,
San Francisco. The following conventional 3T MR sequences
were acquired: (1) axial three-dimensional (3D) inversion re-
covery fast spoiled gradient-recalled echo (FSPGR) T1-
weighted images (TE  1.5 msec, TR  6.3 msec, TI  400
msec, flip angle of 15 degrees) with 230 mm FOV, 156 1.0-
mm contiguous partitions at a 256  256 matrix; (2) axial T2-
weighted fluid-attenuated inversion recovery (FLAIR) im-
ages (TE  126 msec, TR  10 sec, TI  2200 msec) with 220
mm FOV, 47—48 3.0-mm contiguous slices at a 256  256
matrix; and (3) axial magnetization prepared gradient echo
(MPGR) T2*-weighted images (TE  15 msec, TR  500
msec, flip angle of 20 degrees) with 220  170 mm FOV, 47—
48 3.0-mm contiguous slices at a 256  192 matrix.
The CT and MR scans were independently reviewed by
two attending neuroradiologists certified by the American
Board of Radiology and with extensive prior experience in
assessing TBI (M.W., A.G.). They were blinded to the de-
mographic and clinical information while reviewing the
scans. Image characteristics were reported and characterized
categorically by presence of the following: (1) any abnor-
malities, (2) traumatic subarachnoid hemorrhage (SAH), (3)
intraventricular blood, (4) basal cisterns (normal, com-
pressed, or absent), (5) midline shift (1—5 mm, 6—10 mm,
10 mm), (6) extra-axial lesions such as epidural hematoma
(EDH) and subdural hematoma (SDH), (7) hemorrhagic TAI,
(8) non-hemorrhagic TAI, and (9) contusions (hemorrhagic,
non-hemorrhagic). Additionally, all of the CT scans were as-
signed a Marshall CT classification and a Rotterdam score
(Maas et al., 2005). A consensus meeting was held with a
third board-certified neuroradiologist (P.M.) after the initial
review to resolve points of disagreement.
Neurocognitive assessment
The California Verbal Learning Test, 2nd ed. (Delis et al.,
2000) is a word list learning task which is used to examine
verbal learning and memory. It requires reproduction of 16
CT VERSUS 3T MRI OF ACUTE MILD TBI 1051

TABLE 1. DEMOGRAPHIC DATA AND CLINICAL

CHARACTERISTICS OF CONTROLS AND MTBI SUBJECTS

mTBI

Control Imaging only Imaging and CVLT

N 18 36 28
Age (years) 34.3  8.9 30.2  8.0 30.3  8.6
Gender
Male 15 29 23
Female 3 7 5
Handedness
Right 16 34 27
Left 2 1 0
Ambidextrous 0 1 1
Years of education 15.8  2.3 15.3  2.7 15.4  2.8
Injury mechanism
Traffic 25 (69%)
Assault 7 (19%)
Fall 4 (11%)
GCS
15 24 (66%)
14 10 (27%)
13 2 (6%)0
HISC 6.6  3.6
PCS 4.4  2.1
GOS-E 1-year follow-up 7.4  0.81

GCS, Glasgow Coma Scale; GOS-E, Glasgow Outcome Score–Extended; HISC, Head Injury
Symptom Checklist; PCS, Post Concussive Symptom.
The HISC score is the number of symptoms self-reported by the patient at the time of testing. PCS is
a sub-component score of HISC identifying post-concussive symptoms.

words (list A) over five continuous learning trials and the
Total Recall Score of Trials 1—5 reflects the number of ac-
curate recall over all of the five trials. The subjects are then
given a distracter list B, and subsequently asked to recall the
initial list A in the Short Delayed Free Recall (SDFR) task,
and also cued for four semantic categories of the list in the
Short Delay Cued Recall (SDCR) task. Finally, the Long De-
lay Free Recall (LDFR) task and the Long Delay Cued Recall
(LDCR) task are administered after a 20-min delay to assess
verbal memory retention.
The CVLT was administered to controls and in mTBI sub-
jects longitudinally at acute (2 weeks), 1-month, and 1-year
time points post-injury. CVLT scores during the acute stage
of mTBI were compared within the mTBI subjects with imag-
ing findings: (1) normal CT and MR scans, (2) abnormal CT
and/or MR scans, (3) focal parenchymal lesions on MR scans
including TAI, and (4) MR scans with only pure TAI (as de-
fined by findings of traumatic microbleeds on T2*-weighted
gradient-echo images in the absence of other traumatic or
non-traumatic MR abnormalities) (Scheid et al., 2006). Ad-
ditionally, the number of traumatic axonal injury lesions de-
tected by 3T MR was correlated with CVLT measures at acute
(2 weeks), 1-month, and 1-year follow-up.
The subjects completed a self-report questionnaire of the
Head Injury Symptoms Checklist (HISC) to assess global
symptoms after head injury and Post-Concussive Symptoms
(PCS). The mTBI subjects were also assessed using Glasgow
Outcome Scale-Extended (GOS-E) to measure functional out-
come, which includes cognitive impairment, psychological
wellbeing, health status, and social integration factors.
Statistical analysis
The summary statistics of mean and standard deviation
(SD) is reported as mean  SD with standard p-value of less
than 0.05 to identify statistical significance, unless otherwise
noted. The two-tailed Student’s t-tests were used for com-
parisons of CVLT measures between controls and mTBI pa-
tients. Image comparison between two readers was com-
pared using weighted kappa coefficient agreement test. The
inter-rater agreement for number of TAI lesions in each mTBI
was tested using rank correlation ô of Kendall. CVLT mea-
sures were correlated with number of TAI lesions using non-
parametric analysis of Spearman’s rho statistics. All statisti-
cal tests were performed using SPSS v13 (SPSS, Inc., Chicago,
IL).
Results
Imaging results
The overall inter-rater reliability was moderate in overall
detection rate of abnormalities on CT (kappa value 0.60, 95%
confidence interval [0.33—0.87] and high for MR (0.93 [0.80—
1.06]). In particular, agreement for hemorrhagic TAI on CT
was strong (0.72 [0.42—1.02]) but stronger on MR (0.83
[0.64—1.01]). There were too few non-hemorrhagic TAI le-
sions for reliable statistical analysis.
Of the acute imaging examinations in all 36 mTBI subjects,
intraparenchymal lesions were detected in 18 CT (50%) and
27 MR (75%) scans. Traumatic SAH was detected in eight CT
(22%) and two MR (5%) scans. EDH was detected in four CT
1052 LEE ET AL.

(11%) and three MR (8%) scans. SDH was detected in six CT 0.007). Additionally, there was a difference between mTBI
scans (16%) and in 11 (31%) MR scans. Hemorrhagic TAI was and healthy controls in LDCR at 1-year follow-up (11.4  3.3
detected in eight CT (22%) and 17 MR (47%) scans (Table 2, vs. 13.4  2.6, p  0.031), and there were other trends of im-
Fig. 1). There was no non-hemorrhagic TAI detected on CT, paired verbal memory between mTBI and healthy controls
but this was found in four MR (11%) scans. Cerebral contu- at 1-month and 1-year follow-up in SDFR, SDCR, and LDFR,
sions were detected in total of 13 CT (36%) and 21 MR (58%) but these did not reach a significant difference.
examinations (Table 2, Fig. 2). The CVLT results in controls and acute mTBI patients
Inter-rater agreement for number of TAI lesions detected were compared with specific imaging findings. Compared
on 3T MR showed significant correlation (  0.987, p  to the controls, the mTBI subjects with normal CT and MR
0.001). scans had significant deficits across all measures of CVLT
(Fig. 3). Mild TBI subjects with abnormal CT and/or MR
Neurocognitive results scans also showed significant verbal memory impairment
on all CVLT measures compared to controls, but were not
There were significant differences between healthy con-
significantly different in performance from those mTBI pa-
trols and mTBI subjects across all CVLT measures: Total Re-
tients with normal CT and MR scans. Similarly, mTBI pa-
call Trials 1—5, SDFR, SDCR, LDFR, and LDCR during the
tients with TAI lesions on MR also performed significantly
acute testing (Table 3). The mild TBI subjects showed im-
worse than controls, but were not significantly different
paired verbal memory compared to the healthy controls in
from the other mTBI groups categorized by imaging find-
Total Recall Trials 1—5 during the acute testing (47.1  9.8
ings, including those with normal scans. When controls
vs. 56.4  8.1, p  0.001), at 1-month (48.9  10.2 vs. 56.4 
were compared to the patients with pure TAI, there were
8.1, p  0.008), and at 1-year (48.0  10.7 vs. 56.4  8.1, p 
trends toward lower scores in the patients but these were
not significant (p0.05).
Correlation between number of TAI lesions and CVLT
TABLE 2. IMAGING FINDINGS IN MTBI SUBJECTS measures at the acute time point were largely negative. SDFR
at the acute time point did show a weak significant inverse
CT 3T MRI correlation with TAI (r  0.40, p  0.030). However, there
was no significant relationship with Total Recall on Trials
Normal 13 9 1—5 (r  0.32, p  0.092), SDCR (r  0.24, p  0.218),
Abnormal 23 27
LDFR (r  0.24, p  0.201), or LDCR (r  0.24, p  0.219).
Extraparenchymal abnormalities (total) 12 11
Traumatic SAH 8 2 Moreover, there was no significant correlation between num-
Intraventricular bleed 1 0 ber of TAI lesions and any of the CVLT scores at the 1-month
Basal cisterns and 1-year follow-up time points (p  0.05)
Compressed 1 0
Absent 0 0 Discussion
Midline shift
1–5 mm 2 0 Computed tomography versus 3T magnetic resonance
6–10 mm 0 0 imaging comparison
10 mm 0 0 Mild TBI is heterogeneous in clinical presentation and
Lesions
brain imaging. Previous study by Tellier et al. (1999) showed
EDH 4 3
SDH 6 11 that mTBI subjects with lower GCS had higher percentages
Intraparenchymal abnormalities (total) 18 27 of abnormalities in CT. In our study, which was a cohort of
TAI mTBI predominantly of GCS 14 and 15 but with LOC and
Hemorrhagic TAI (microhemorrhages) 8 17 PTA, 50% of patients had focal intraparenchymal brain le-
Non-hemorrhagic TAI 0 4 sions on CT. However, CT underestimates the true extent of
Contusions focal lesions in this patient population (Mittl et al., 1994).
Hemorrhagic 12 17 Consistent with our first hypothesis, we show that 75% of
Non-hemorrhagic 1 4 mTBI patients with no prior history of injury had traumatic
Marshall CT classification intraparenchymal brain lesions on acute 3T MR imaging, in-
I 15
cluding half of the patients without visible intraparenchy-
II 21
III 0 mal lesions on acute CT (Table 2, Figs. 1 and 2). Most of these
IV 0 lesions missed by CT were microhemorrhages due to TAI,
V 0 although some small contusions were also not detected.
VI 0 Marshall CT classification (p  0.05) and Rotterdam CT
Rotterdam CT score scores (p  0.05) showed little variation in our cohort, which
1 0 is not surprising since they were not designed for evaluat-
2 23 ing mTBI. The Marshall CT classification and Rotterdam CT
3 13 scores were therefore not predictive of long-term neurocog-
4 0 nitive deficits (p  0.05). While 3T MR imaging showed more
5 0
intracranial abnormalities than CT, for extra-axial lesions
6 0
they were almost equivalent (12 cases for CT vs. 11 cases for
EDH, epidural hematoma; SAH, subarachnoid hemorrhage; SDH, MR). In particular, CT detected many more cases of sub-
subdural hematoma; TAI, traumatic axonal injury. arachnoid hemorrhage (11 vs. 6), which can be explained by
CT VERSUS 3T MRI OF ACUTE MILD TBI 1053

FIG. 1. (Top row) Negative CT of a mild TBI patient on ED admission (24 h of injury). (Bottom row) 3T MR gradient
echo T2*-weighted images showing several hemorrhagic TAI lesions at less than 2 weeks post-injury.

the earlier timing of the CT scans, since traumatic SAH re-
solves quickly. Conversely, the later timing of MR imaging
might have increased its sensitivity relative to CT for contu-
sions (13 vs. 21), which are known to often blossom late. Per-
haps, surprisingly, more cases of subdural hematoma were
detected by MR than by CT (11 vs. 6). One advantage of MR
imaging for detecting small subdural hemorrhages is the ab-
sence of beam hardening artifact seen on CT adjacent to ir-
regular contours of the calvarium. However, as with the con-
tusions, the fact that the MR exam was obtained later than

FIG. 2. (Left) CT of a mild TBI patient on ED admission (24 h of injury) showing no intraparenchymal lesions. (Right)
3T MR FLAIR T2-weighted image showing a small nonhemorrhagic right temporal cortical surface contusion not detected
on the CT.
1054 LEE ET AL.

TABLE 3. CVLT COMPARISON OF CONTROLS AND MTBI SUBJECTS

mTBI

CVLT Control Acute 1 Month 1 Year

Total trials 1–5 56.4  8.1 47.1  9.8 0.001** 48.9  10.2 0.008** 48.0  10.7 0.007**
SDFR 12.3  2.8 9.5  2.7 0.001** 11.0  3.0 0.124 10.6  2.8 0.053
SDCR 12.9  2.5 10.1  3.0 0.002** 11.7  3.0 0.148 11.1  3.4 0.064
LDFR 12.8  2.9 9.7  3.2 0.002** 11.3  3.2 0.107 11.0  3.2 0.066
LDCR 13.4  2.6 10.0  3.0 0.000** 11.8  3.1 0.058 11.4  3.3 0.031*

California Verbal Learning Test (CVLT) comparison for controls and mild traumatic brain injury (mTBI) subjects at acute phase (2
weeks), 1 month follow-up, and 1-year follow-up post-injury.
*p-values  0.05, **p-values  0.01 for significant difference between controls and mTBI groups.

the CT exam may also partially explain this difference, and
represents a confounding factor for comparing the sensitiv-
ities of the two modalities.
Neurocognitive and functional outcome testing
In neurocognitive testing, mTBI patients performed worse
than controls matched for age, gender, handedness and ed-
ucational levels. The mTBI subjects showed significant
deficits in working memory on all measures of the CVLT
during the acute phase after injury. These results demon-
strate that acute mTBI patients have impairment of learning,
encoding and retrieval for verbal memory. Those differences
were greatest at the acute time point. There was evidence of
recovery between the acute and 1-month time points that
persisted with no significant changes at the 1-year time point.
By the 1-year time point, only some measures (Total Recall
1—5 and LDCR) were significantly abnormal, with trends
towards poorer performance shown on the other CVLT mea-
sures compared to the control subjects.
GOS-E was not a useful measure of outcome even at 1 year
after injury, which was uniformly high for mTBI patients
(range 5—8, 7.4  0.81). Although the GOS-E takes into ac-
count cognitive deficits such as memory failures and con-
centration problems as part of the sub-score of return to nor-
mal life (Levin et al., 2001), it may not be as sensitive to
neurocognitive deficits in specific domains as more special-
ized tests such as the CVLT.
Correlation of imaging findings
with neurocognitive function
Contrary to our second hypothesis, CT and conventional
3T MR imaging findings did not predict neurocognitive func-

FIG. 3. California Verbal Learning Test (CVLT) comparison by imaging findings in mild traumatic brain injury (mTBI)
subjects and healthy controls at the acute time point. (a) Total Recall Trial 1—5. (b) SDFR, SDCR, LDFR, LDCR. *p-value 
0.05; **p-value  0.01 for significant difference between controls and mTBI groups.
CT VERSUS 3T MRI OF ACUTE MILD TBI
tion at any stage of mTBI, nor did it predict functional out-
come at 1-year post injury. Patients with normal CT and 3T
MR imaging did not perform significantly better on the
CVLT or score significantly higher on the GOS-E than pa-
tients with intraparenchymal lesions such as contusions and
TAI (Fig. 3). The performance of subjects with pure TAI
could not be reliably distinguished from the controls; how-
ever, this may be due to insufficient statistical power given
the relatively small number of subjects with pure TAI.
Moreover, the regression analysis of number of TAI le-
sions on 3T MR imaging also failed to correlate with neu-
rocognitive function or predict functional outcome at 1 year,
consistent with our prior results in chronic mTBI patients
(Niogi et al., 2008). Hence, it does not appear that findings
on conventional neuroimaging, as performed routinely for
clinical diagnosis, were relevant to verbal memory as tested
by the CVLT in the mild TBI population. This could be be-
cause the abnormalities shown by conventional neuroimag-
ing do not represent the pathology which occurs in mTBI
that is important for neurocognitive outcome (Hughes et al.,
2004; Scheid et al., 2003; Scheid et al., 2006). Perhaps the rel-
evant pathology is at the microstructural level, and is better
assessed by newer imaging techniques such as diffusion ten-
sor imaging (DTI) (Niogi et al., 2008; Kraus et al., 2007). It is
also possible that imaging findings may impact other aspects
of neurocognitive function not tested in this study which
may be affected in mTBI patients. Alternatively, because it
was not possible to obtain neurocognitive measures before
the injury, we cannot fully exclude the possibility that these
mTBI patients may have had poorer premorbid verbal mem-
ory compared to the controls, even though we controlled for
factors such as age, gender, handedness, and level of edu-
cation. However, we would not expect this to be the domi-
nant factor in explaining the neurocognitive results, since the
CVLT scores of the mTBI patients did improve over time
during the first year after trauma.
In conclusion, acute 3T MR imaging detects many more in-
tra-axial lesions, especially hemorrhagic TAI, than CT in mild
TBI patients with LOC and PTA. Indeed, 75% of these mild
TBI patients with no prior history of brain injury showed ev-
idence of focal post-traumatic intraparenchymal brain lesions
on 3T MR imaging. This cohort of patients showed poorer ver-
bal memory at acute, 1-month and 1-year follow-up compared
to matched controls. However, imaging findings on CT and
on conventional 3T MR imaging did not correlate with acute
neurocognitive status nor did it predict 1-year neurocognitive
or functional outcome. Newer MR imaging techniques such
as DTI may provide better biomarkers for mild TBI than cur-
rent clinical neuroimaging methods.
Acknowledgments
This research was supported by a collaborative grant from
the James S. McDonnell Foundation to the Brain Trauma
Foundation for the Cognitive and Neurobiological Research
Consortium (CNRC) in Traumatic Brain Injury, and by the
UCSF Academic Senate and UCSF Brain and Spinal Injury
Center.
Author Disclosure Statement
No conflicting financial interests exist.
1055
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Address reprint requests to:
Pratik Mukherjee, M.D.
Department of Radiology
University of California, San Francisco
505 Parnassus Avenue, L-358
San Francisco, CA 94143
E-mail: pratik@radiology.ucsf.edu