Traumatic Brain Injury: A Review and High-Field MRI
Findings in 100 Unarmed Combatants Using
a Literature-Based Checklist Approach
William W. Orrison, Jr.,1,2,3Eric H. Hanson,2,3Tony Alamo,4David Watson,5Mythri Sharma,3
Thomas G. Perkins,6and Richard D. Tandy7
This study reviewed the literature for the extent of neuroimaging findings in boxers, indicative of traumatic
brain injury (TBI) as identified in magnetic resonance imaging (MRI). The study then utilized a systematic
checklist approach to assess 100 unselected consecutive 1.5- and 3.0-Tesla MRI examinations of professional
unarmed combatants to determine the extent of identifiable TBI findings. The percentage of positive findings
and the localization of lesions were quantified using the checklist that included the MRI findings previously
reported in the medical literature. Seventy-six percent of the unarmed combatants had at least one finding that
may be associated with TBI: 59% hippocampal atrophy, 43% cavum septum pellucidum, 32% dilated perivas-
cular spaces, 29% diffuse axonal injury, 24% cerebral atrophy, 19% increased lateral ventricular size, 14%
pituitary gland atrophy, 5% arachnoid cysts, and 2% had contusions. Statistical relationships were found be-
tween number of bouts and lateral ventricular size (tau-b¼0.149, p¼0.0489), with years of fighting correlating
with the presence of dilated perivascular spaces (tau-b¼0.167, p¼0.0388) and diffuse axonal injury
(tau-b¼0.287, p¼0.0013) findings. The improved resolution and increased signal-to-noise ratio on 1.5- and
3.0-Tesla high-field MRI systems defines the range of pathological variations that may occur in professional
unarmed combatants. Additionally, the use of a systematic checklist approach insures evaluation for all possible
TBI-related abnormalities. This knowledge can be used to anticipate the regions of potential brain pathology for
radiologists and emergency medicine physicians, and provides important information for evaluating unarmed
combatants relative to their safety and long-term neurocognitive outcome.
Key Words: boxing; checklist; magnetic resonance imaging; traumatic brain injury; unarmed combatants
fighting with the fists) in the Iliad. Boxing and other forms of
unarmed combat continue to be extremely popular sporting
events. Computed tomography (CT) has traditionally been
utilized to rule out acute conditions commonly associated
with traumatic brain injury (TBI) such as hemorrhagic con-
tusion, subdural and epidural hematomas, and subarachnoid
hemorrhage. Magnetic resonance imaging (MRI) has also
narmed combat is probably as old as the human spe-
cies. Homer made reference to pugilism (i.e., the sport of
demonstrated clinical utility in the acute setting for assessing
TBI (Allkemper et al., 2004; Parizel et al., 2005). CT has been
used as a pre-bout central nervous system (CNS) assessment
tool, but the benefits of such studies must be weighed against
the significant radiation burden of each CT examination, es-
pecially when the imaging is not used for ruling out acute
intheevaluation ofchronicTBIfindingsbecause it has greater
sensitivity in detecting chronic TBI pathology and does not
entail the risk of ionizing radiation associated with CT (Jor-
dan et al., 1990; Jordan, 2000).
1Nevada Imaging Centers, Las Vegas, Nevada.
2Amigenics (Advanced Medical Imaging and Genetics), Inc., Las Vegas, Nevada.
3Touro University Nevada College of Osteopathic Medicine, Henderson, Nevada.
4Alamo Medical Clinic, Henderson, Nevada.
5Nevada State Athletic Commission, Las Vegas, Nevada.
6Philips Healthcare, Cleveland, Ohio.
7Department of Kinesiology, University of Nevada, Las Vegas, Nevada.
JOURNAL OF NEUROTRAUMA 26:1–13 (May 2009)
ª Mary Ann Liebert, Inc.
Chronic TBI can be a cumulative, long-term neurological
consequence of repetitive concussive and subconcussive head
impact (Jordan, 2000). It occurs with greater incidence in pro-
boxing because of more frequent exposure to repetitive head
trauma, longer bouts, and the lack of protective headgear use
(McCrory, 2002). A review of the medical literature revealed at
least 11 findings that are potentially associated with chronic
diffuse TBI changes: (1) hippocampal atrophy (Baldwin et al.,
1997; Bigler et al., 1997; Smith et al., 1997; Grady et al., 2003;
Tasker et al., 2005; Swartz et al., 2006), (2) cavum septum pel-
lucidum (CSP) (Cabanis et al., 1986; Bogdanoff et al., 1989;
Jordan, 2000; Moseley, 2000; McCrory, 2002), (3) dilated peri-
vascular spaces (DPVS) (Bigler, 2004; Inglese et al., 2005;
Groeschel et al., 2006; Inglese et al., 2006), (4) shearing in-
jury (diffuse axonal injury [DAI]) (Bilaniuk et al., 1984; Gentry
1998; Voller et al., 1999; Paterakis et al., 2000; Hammoud et al.,
cerebral atrophy (Ross et al., 1983; Casson et al., 1984; Cabanis
et al., 1986; Guterman et al., 1987; Ross et al., 1987; Moseley,
2000), (6) increase in lateral ventricular size (Bigler et al., 1993,
1997; Poca et al., 2005), (7) pituitary gland atrophy (Benvenga
et al., 2000; Benvenga, 2005; Schneider et al., 2007), (8) contu-
sions (Bailes et al., 2001), (9) arachnoid cysts (Gosalakkal, 2002;
hemorrhage: subarachnoid, intraventricular, intraparenchy-
mal, subdural, and epidural hemorrhage), and (11) vascular
injury (Rodriguez et al., 1983). In view of this array of potential
TBI imaging abnormalities, a systematic checklist approach
(Table 1), previously demonstrated to improve diagnostic ac-
curacy and to reduce false negative findings (Kinard et al.,
1986), was employed in this study.
This retrospective and anonymized study was performed
with Institutional Review Board (IRB) exemption approval
and was Health Insurance Portability and Accountability Act
(HIPAA) compliant. PubMed was queried to review available
medical literature on the topics of ‘‘pugilists,’’ ‘‘boxing, TBI,’’
‘‘chronic TBI,’’ and combinations of ‘‘boxing’’ and ‘‘magnetic
conducted for the TBI findings on MRI as listed above.
One hundred consecutive unselected MRI scans were per-
mixed martial arts fighters) in two outpatient imaging set-
(Intera NT; Philips Healthcare, Best, The Netherlands), and
25 were imaged on a 3.0-T high-field MRI system (Intera
Achieva; Philips Healthcare). The imaging protocol consisted
of multiple sequences, including (1) a sagittal T1-weighted
three-dimensional (3D) turbo-field-echo (TFE) sequence at 3.0
T (field of view [FOV] 256mm, slice thickness 2.0mm=1.0mm
reconstructed, slice gap 0.0mm=?1.0mmreconstructed, 256?
256 matrix, repetition time msec=echo time msec=inversion
time msec 9.3=4.6=809, number of signals averaged 1), or a
sagittal T1-weighted spin-echo (SE) sequence at 1.5 T (FOV
270mm, slice thickness=slice gap 5.0=1.5mm, 512?512, rep-
etition time msec=echo time msec 450=12, 1); (2) a sagittal
T2-weighted fluid-attenuated inversion recovery (FLAIR)
sequence (turbo factor [TF] 24, FOV 250mm, 3.0=1.0mm,
256?256, 11000=100=2600, 1); (3) an axial T2-weighted gra-
dient and spin echo (GraSE) sequence at 3.0 T (TF 8, echo
planar imaging factor [EPIF] 3, FOV 240, 2.2=0.0mm,
[TSE] sequence at 1.5 T (TF 28, FOV 250mm, 5.0=1.0mm,
512?512, 2887=120, 1); (4) an axial T2-weighted FLAIR se-
11000=100=2600, 1); (5) a coronal T2*-weighted fast-field-echo
(FFE) sequence (FOV 240, 5.0=0.5mm, 512?512, 906=23, 2); (6)
a coronal T2-weighted TSE sequence (TF 21, FOV 250mm,
3.0=1.0mm, 512?512, 10865=120, 3); (7) an oblique coronal T2-
weighted FLAIR sequence (TF 23, FOV 250mm, 4.0=0.4mm,
256?256, 11000=100=2600, 1); and (8) an oblique coronal T2-
5; FOV 240mm, 4.0=0.0mm, 512?512, 930=13=200, 1). All se-
the total data acquisition time, reduce susceptibility artifacts,
and reduce the specific absorption rate (SAR) of the scans.
Table 1. Systematic Checklist Approach for Identifying TBI-Associated Findings on MRI
Cavum septum pellucidum
Increased lateral ventricle size
Dilated perivascular spaces
Shearing injury (DAI)
Pituitary gland atrophy
Grade I &
Grade II &
Grade III &
TBI, traumatic brain injury; MRI, magnetic resonance imaging; CSP, cavum septum pellucidum; DPVS, dilated perivascular spaces; DAI,
diffuse axonal injury.
Table 2. Subject Characteristics
combatants Age (years)
combatNumber of bouts
2 ORRISON ET AL.
Table 3. Overall Percentage of Eleven Findings Associated with Chronic TBI in 100 Consecutive
Unselected Unarmed Combatants
Pathology Normal or absent
grade III Percent positive
DPVS (none, grade I, grade II, or grade III)
PathologyAbsent PresentPercent positive
Pituitary gland atrophy
For definitions of abbreviations, see Table 1.
Hippocampal atrophy. (A) Normal. (B) Mild atrophy. (C) Moderate atrophy. (D) Severe unilateral (right) atrophy.
For 85 of the 100 unarmed combatants, complete data was
available regarding their number of years of fighting and
number of bouts as a professional athlete. The unarmed com-
batants ranged in age from 19 to 42 years (mean¼27.3, SD¼5
years), had participated inthesport for 1–19years (mean¼5.1,
SD¼12.3 bouts; Table 2). The percentages of athletes found to
have the 11 TBI-associated findings are shown in Table 3. Chi-
square test of independence was used to determine if signifi-
cant differences existed in the number of TBI findings on 3.0-T
compared to 1.5-T imaging. Kendall’s tau-b correlation tech-
nique was used to determine the relationship between the
number of bouts to number of years of fighting and the extent
due to the ordinal level variables and large number of tied
values in the data. The Kendall’s tau-b correlation methodol-
ogy is described elsewhere (Howell, 1997).
Grading of the findings was performed by a board certified
neuroradiologist (W.W.O.) using the following grading scale,
atrophy was graded as mild, moderate, or severe based upon
the size of the temporal horns as illustrated in Figure 1. CSP
was defined as the presence of a fluid-filled space separating
laminae of the septum pellucidum (McCrory, 2002). CSP was
graded as mild, moderate, or severe as illustrated in Figure 2.
DPVS was graded I, II, or III based on a modified grading
scale presented by Heier et al. in 1989 (Fig. 3). Mild or grade I
DPVS were at least 2mm in diameter and 1cm in length.
Moderate or grade II DPVS were 2–3mm in diameter and
1–2cm in length, and severe or grade III spaces were >3mm
in diameter and >2cm in length (Heier et al., 1989). DAI was
FLAIR and T2-weighted sequences, measuring up to 5mm in
maximum diameter, and located at the gray matter=white
matter interface or within or adjacent to the corpus callosum.
Examples of DAI are presented in Figure 4. Cerebral atrophy
the cortical sulci as illustrated in Figure 5. Enlargement of the
lateral ventricles was graded as mild, moderate, or severe,
based upon the size of the lateral ventricles as illustrated in
Figure 6. Pituitary gland atrophy (Fig. 7) was defined as a sig-
nificant decrease in the size of the pituitary gland with an as-
sociated increase in cerebrospinal fluid (CSF) signal intensity
within the sella turcica (e.g., empty or partially empty sella).
Pituitary atrophy was noted as present or absent. Arachnoid
cysts (Fig. 8) were defined as collections of fluid within an
arachnoidmembrane (Gosalakkal,2002).Priorcontusions were
defined as an area of damage located within the brain cortex or
subcortical white matter and measuring ?6mm in diameter,
demonstrating an increase in signal intensity on FLAIR and
T2-weighted sequences (Fig. 9), and consisting of prior hem-
orrhage, infarction, necrosis, or edema (Bailes et al., 2001).
Although abnormalities were better visualized on the 3.0-T
than on the 1.5-T MRI examinations, there was not a statisti-
cally significant difference between the numbers of TBI find-
ings on 3.0- and 1.5-T imaging (p>0.05 for all cases).
In this study, 76% of the unarmed combatants had at least
one finding that may be associated with TBI: 59% had hip-
pocampal atrophy; 43% had CSP; 32% had DPVS; 29% had
DAI; 24% had cerebral atrophy; 19% had an increase in lateral
ventricular size; 14% had pituitary gland atrophy; 5% had
arachnoid cysts; and 2% had contusions. A summary of these
findings including the grading of each finding is shown in
Table 3. Figures 1–9 demonstrate typical images for each
finding. None of the subjects had evidence of hemosiderin
deposition that would suggest prior hemorrhage.
lesions were counted and identified according to location and
size. The locations included left frontal (23 of 100 unarmed
combatants, 50 total lesions), right frontal (18 of 100 unarmed
of 100 unarmed combatants, four total lesions), and parietal
(one of 100 unarmed combatants, one lesion). Bilateral frontal
DAI lesions were present in 12 of 100 unarmed combatants
and ranged from 1 to 12 lesions per unarmed combatant.
Moderate. No severe CSP was observed.
Cavum septum pellucidum (CSP). (A) Mild. (B)
4 ORRISON ET AL.
Magnetic resonance angiography (MRA) was negative for
of the unarmed combatants in this study.
finding most prominently in the parietal subcortical white
matter (Fig. 3). Benign DPVS were not included as abnor-
malities and were defined as focal round areas of CSF signal
intensity commonly seen as normal variations on MRI studies
impact syndrome and chronic TBI) and the risk of these lead-
ing to long-term behavioral or cognitive problems in athletes
has been a subject of concern (Bailes et al., 2001; Koh et al.,
2003). Head injury in athletes appears to be in part dependent
upon the sport. Boxers experience impacts with a shorter du-
ration of acceleration, increased rotational acceleration, and
increased neck loads compared to those experienced by pro-
fessional football players, while professional football players
experience increased translational acceleration, longer dura-
tion of acceleration, higher effective ‘‘punch’’ mass, and higher
blows in training and professional bouts than mixed martial
artists (T. Alamo, unpublished data).
In a systematic review of the literature from 1985 to 2000,
levels of head trauma observed in boxing to that reported for
American football, boxing, ice hockey, martial arts (judo,
karate, and taekwondo), rugby, and soccer. Overall, boxing
was associated with the highest frequency of concussion in
athletes of all ages regardless of competitive levels. In a recent
study of 427 professional boxers, the authors found 107 in-
juries, of which 89.8% were head, neck, and face injuries, and
15.9% were concussions (Zazryn et al., 2003).
Dilated perivascular spaces. (A) Normal. (B) Grade I. (C) Grade II. (D) Grade III.
REVIEW OF MRI FINDINGS IN TBI5
The ability of high-field MRI to show improved tissue
et al., 1991) has made it a valuable diagnostic tool for deter-
mining the extent of chronic TBI. In previous studies of box-
ers, MRI has been used to identify atrophy, focal or diffuse
nonspecific white matter lesions, hemorrhage, infarcts, and
demyelination (Casson et al., 1984). In a prevalence study
from 1969, it was estimated that approximately 17% of 224
retired professional boxers exhibited clinical findings consis-
tent with chronic TBI (Casson et al., 1984; Jordan, 2000). In a
more recent study, 18 former and active professional boxers
underwent neurological examination, electroencephalography
(EEG), CT scans, and neuropsychological tests. Eighty-seven
percent of these boxers had findings that were indicative of
brain damage, including CSP and cerebral atrophy (Casson
et al., 1984). However, technical comparison limitations, espe-
cially use of lower field strength MRI units in studies prior to
1985, are likely to limit the generalizability of conclusions ob-
tained from these earlier studies.
In the study reported here the data revealed that the
number of bouts fought by the athletes was significantly re-
lated to an increase in lateral ventricle size (tau-b¼0.149,
p¼0.0489) and DAI (tau-b¼0.234, p¼0.0051). The relation-
ship of the number of bouts and DPVS approached statistical
significance (tau-b¼0.145, p¼0.0540), while years of fighting
was positively correlated with both DPVS (tau-b¼0.167,
p¼0.0388) and DAI (tau-b¼0.287, p¼0.0013). These results
are to be expected, as the number of years of fighting and the
The findings included in the checklist approach used in this
study are well documented in the medical literature and are
briefly reviewed below.
Head trauma may produce white matter loss associated
with increased temporal horn size and sulcal CSF volumes, as
well as substantial hippocampal atrophy related to memory
impairment (Bigler et al., 2002). Temporal horn dilatation of
the lateral ventricles often accompanies TBI. (Bigler et al.,
1993; Gale et al., 1995; Bigler et al., 1997).
Cavum septum pellucidum
CSP is formed by the separation of the bilaminar glial
membrane (septum pellucidum) of the lateral ventricles
(Guterman et al., 1987). It has been postulated to be a sign of
boxer’s encephalopathy and is commonly reported in asso-
ciation with chronic TBI (Bogdanoff et al., 1989; Jordan, 2000;
McCrory, 2002). Some authors have suggested that CSP is an
anatomical variant of no clinical significance (Moseley, 2000).
Prior imaging studies of boxers report the incidence of CSP to
be between 0.7% and 37%. (Cabanis et al., 1986). We found
CSP in 42% of our subjects probably in part due to the im-
proved resolution of the higher field strength MRI systems
Dilated perivascular (Virchow-Robin) spaces
Dilated perivascular (Virchow-Robin) spaces (DPVS), also
known as dilated Virchow-Robin spaces (VRS), have been
described in the literature since the mid-1800s: in 1849 by
Pestalozzi; in 1851 by Virchow; and in 1859 by Robin. DPVS
are typically confined to the deep white matter or basal gan-
glia and were previously considered of limited significance
(Groeschel et al., 2006). More recently the scientific literature
has documented the connection between DPVS and TBI (Ing-
leseet al., 2005). Ithas also been suggestedthat ‘‘ajudgment on
whether dilated VRS in an individual patient is a normal var-
iant or part of a disease process can be made by taking into
account the appearance of the adjacent tissue on MRI and the
VRS in patients with TBI has been shown to be significantly
may result from shear-strain injury (Inglese et al., 2006). In our
study, we measured both the width and length of the DPVS,
excluding round benign-appearing DPVS (enlarged VRS) as a
(A–F) Typical diffuse axonal injury (DAI). DAI indicated by arrow.
6 ORRISON ET AL.
1% had grade I DPVS, 31% had grade II DPVS, and none had
severe (grade III) DPVS. The number of years fighting and the
number of bouts were both significantly correlated with the
presence of this finding.
It is of interest that most of the DPVS in our study was
located in the parietal subcortical white matter while most of
the DAI were located in the frontal subcortical white matter.
This ‘‘coup-contrecoup’’ pattern of DAI coupled with DPVS
supports the view that some DPVS represents a form of DAI
in head trauma victims (Inglese et al., 2006).
Shearing or diffuse axonal injury
The term ‘‘shearing injury’’ is often used interchangeably
with ‘‘diffuse axonal injury’’ (DAI) and is presumed to rep-
resent the causative forces of injury, although this remains a
abundant regarding the presence of DAI following head
trauma (Gentry et al., 1988a,b; Gentry, 1994; Parizel et al.,
1998;Voller et al.,1999;Paterakis et al.,2000;Hammoud et al.,
2002; Scheid et al., 2003; Parizel et al., 2005). When portions of
the accelerating and rotating brain lag behind adjacent faster
moving areas, shear and=or tensile strains develop between
tissues. The axons are stretched and subsequently disconnect,
leading to the formation of axonal retraction balls, which
represent deathofthedistal axonal segment(Fitzpatrick et al.,
1998). DAI lesions may occur in any area of the brain, but are
more commonly found in the hemispheric subcortical white
matter, centrum semiovale, corpus callosum, basal ganglia,
brainstem, and cerebellum (Parizel et al., 1998). There was
Cerebral atrophy. (A) Normal. (B) Mild. (C) Moderate. No severe cerebral atrophy was observed.
REVIEW OF MRI FINDINGS IN TBI7
a statistically significant correlation between DAI lesions and
years of professional competition (tau-b¼0.287, p¼0.0013),
as well as between DAI lesions and the total number of bouts
Radiographic changes indicating brain atrophy have fre-
moderate to severe cerebral atrophy in approximately 15% of
boxers examined with a 0.15-T scanner (Cabanis et al., 1986;
our study population had mild atrophy, and 3% had mod-
erate cerebralatrophy.Some studies haveshown thatcerebral
atrophy appears to be more frequent in boxers who have
fought in the greatest numbers of bouts (Ross et al., 1983;
Casson et al., 1984; Guterman et al., 1987). In our study,
however, we found only a weak (nonsignificant) correlation
between the number of bouts fought and extent of cerebral
atrophy (tau-b¼0.098, p¼0.136).
Increase in lateral ventricle size
In a 2005 study of 95 patients with TBI, Poca et al. (2005)
found post-traumatic ventriculomegaly in 39% of patients
with severe TBI and in 27% with moderate TBI. The authors
concluded that post-traumatic ventriculomegaly is a frequent
and early finding in patients with moderate or severe TBI.
Moreover, a study of long-term rehabilitation following TBI
has shown that the presence of dilated ventricles in the
(Note cavum septum pellucidum [CSP] in A and C.)
Lateral ventricle size. (A) Normal. (B) Mild. (C) Moderate. No severe lateral ventricle enlargement was observed.
8 ORRISON ET AL.
absence of obstructive hydrocephalus provides the worst
prognosis for independent living (Timming et al., 1982).
In our study, based on the resultant Kendall’s tau-b, this
finding demonstrated statistically significant correlation with
the number of bouts (p<0.05).
Pituitary gland atrophy
In a 2000 review article, Benvenga et al. reported identify-
ing 367 cases of post head trauma hypopituitarism in the lit-
erature. The types of anatomic lesions found in the pituitary
gland and stalk and hypothalamus were highly varied, and
the timing of onset of symptoms (e.g., lack of menses, erectile
dysfunction) and signs (e.g., diabetes insipidus, generalized
years (Benvenga et al., 2000).
Although the atrophy observed in this study is possibly
secondary to trauma, there is also the possibility that an un-
known proportion of these changes are in part related to illicit
steroid use or other etiologies.
Due to linear translational, rotational, and angular accel-
eration forces, the brain can undergo deformation and dis-
tortion depending on the site of impact of traumatizing force,
severity of the traumatizing force, and tissue resistance of the
brain (Besenski, 2002). DAI and cortical contusions are com-
monly identified traumatic brain lesions and are associated
with significant morbidity (Brandstack et al., 2006). Contu-
sions mostly occur due to rapid acceleration-deceleration
mechanisms, resulting in compression of the brain against the
skull and a coup-contrecoup injury (Bailes et al., 2001).
There are some predilections for areas of the brain where
contusions tend to occur (e.g., bases and the tips of the frontal
lobes, and bases and lateral surfaces of the temporal lobes due
to brain gliding upon the uneven (rough) surface of the skull
base). At 4–6 months after trauma, the lesion may become
cystic (encephalomacia) (Besenski, 2002). Only 2% of the un-
armed combatants in this study had findings considered ce-
rebral contusions based upon the size of the lesions (greater
than 5mm) and location (the cortex or subcortical white
surface area provided by boxing gloves, and the mobility of
the unrestrained head, which cushions direct blows, resulting
in a much greater incidence of DAI than contusions.
Arachnoid cysts are relatively rare, accounting for ap-
proximately 0.23–1% of space-occupying lesions (Gosalakkal,
2002; Eskandary et al., 2005), and have been reported more
frequently in males and on the left side (Wester, 1992;
Eskandary et al., 2005). While true arachnoid cysts are con-
genital and are usually identified as incidental findings, sec-
ondary arachnoid cysts may result from post-inflammatory
accumulation of CSF in the subarachnoid space in patients
with head injury, intracranial hemorrhage, or infection.
In our study, 5% of unarmed combatants had single
arachnoid cysts located in the left frontal, right frontal, left
anterior temporal, and left temporal lobes, and in the poste-
rior fossa. It is not clear if the increased incidence of asymp-
tomatic arachnoid cysts found in our study was influenced by
the chronic head trauma experienced by the athletes.
Although hemosiderin deposition is well established as an
MR marker of prior hemorrhage and, when using CT, the
finding of blood products is considered the most reliable in-
dicator of DAI, the current literature suggests that hemosid-
erin deposition is infrequently present in DAI on MRI studies.
(Gentry et al., 1988a,b; Gentry, 1994; Mittl et al., 1994; Kampfl
et al., 1998; Pierallini et al., 2000). In one study involving
24 patients with mild TBI, no foci of microhemorrhage were
identified (Inglese et al., 2005). In unarmed combatants, he-
mosiderin deposition may indicate the presence of prior
Pituitary gland atrophy. (A) Normal. (B) Atrophy.
REVIEW OF MRI FINDINGS IN TBI9
significant hemorrhagic head trauma. We did not identify
any evidence of hemosiderin deposition in any of the athletes
in our study population.
The regional cerebral blood flow in 14 professional and
amateur boxers compared to non-boxing, age-matched con-
trols demonstrated that the values for amateurs were within
normal range whereas the professional boxers’ flow values
were significantly below normal. This study shows that some
boxers may face an increased risk of vascular lesions (Ro-
driguez et al., 1983).
The finding of an aneurysm or arteriovenous malformation
in unarmed combatants would raise the possibility that these
lesions are post-traumatic. In addition, consideration must be
given to the potential increased risk of cerebral trauma during
future competition when a vascular lesion is identified. In our
study, the MR angiography performed in each boxer did not
demonstrate abnormal vascular changes.
The limitations of the present study include the possibility
that the chronic TBI findings are not related to unarmed com-
batant activities, although the young age of these athletes and
ongoing occupational exposure as a source of induced trauma
would indicate that this is unlikely. It would also be preferable
to correlate the chronic TBI findings with total years of boxing
andmixed martialarts(rather thanjustprofessionalyears)and
total round experience (i.e.,sparring bouts,amateur bouts,and
professional bouts) as well as the number and severity of cra-
nial blows. However, these data were not available.
Arachnoid cysts. (A) Anterior temporal. (B) Frontal. (C) Posterior fossa.
10 ORRISON ET AL.
The improved tissue clarity and definition of pathology on
1.5- and 3.0-T high-field MRI reveals a wide range of abnor-
malities that may occur in unarmed combatants. The obser-
vations in the unarmed combatants reported here are similar
tothose found duringourreview oftheliteratureand support
a current policy requiring the use of 1.5-T or higher field
strength MRI and MRA as screening modalities for unarmed
combatants (NAC, 2007).
We found the checklist approach to the interpretation of
MRI examinations in unarmed combatants further enhanced
the utility of higher field MRI by insuring that less commonly
reported findings are not overlooked. This checklist serves as
a means to provide safety to these athletes, not only by in-
creasing the number of findings being reported, but by also
allowing for the creation of a database that can be correlated
with long-term outcomes.
As additional data become available from MR imaging
techniques such as diffusion tensor imaging with fiber track-
ing (Huisman et al., 2004; Naganawa et al., 2004; Sundgren
et al., 2004; Ducreux et al., 2005; Gupta et al., 2005; Inglese
2006; Tisserand et al., 2006; Wilde et al., 2006a,b), and func-
tional MRI (McAllister et al., 1999; Christodoulou et al., 2001;
Adriani et al., 2003; Lidzba et al., 2006), the checklist can be
incremental diagnostic information. Expanding athletic com-
mission databases in the future can serve to further enhance
the safety monitoring of these athletes. Ultimately, correlating
chronic TBI findings from multimodality MR technologies
inflammation (Jordan et al., 1997; Marciano et al., 2002; Dash
et al., 2004) present in each athlete will help determine which
athletes may have increased susceptibility to CNS damage.
These methods are currently being studied in unarmed com-
batant populations and the application of these sophisticated
approaches to chronic TBI will allow for individualized
monitoring and development of future neuroprotective and
neurorestorative therapeutic options.
We would like to acknowledge the support and the efforts
of the Nevada State Athletic Commission during the time
of the study: Chairman Tony Alamo, M.D., Commissioner
Raymond Avansino Esq., Commissioner John R. Bailey Esq.,
Commissioner Joe W. Brown Esq., Commissioner T.J. Day,
Executive Director Keith Kizer Esq., and also the Ring Side
Physicians during the time of the study: David Watson, M.D.,
Jeff Davidson, M.D., Al Capanna, M.D., Bill Berliner, M.D.,
James Game, M.D., Rodney Courson, M.D., Anthony Rug-
geroli, M.D., James Dettling, M.D., Steve Brown, M.D., Todd
Zapman, M.D., and Damon Zavala, M.D. We would also like
to acknowledge the technical expertise provided by Timothy
Mueller, Jon Gibson RT, Evelyn Roberston RT, and Susan
Haas who facilitated the completion of this manuscript.
Author Disclosure Statement
Philips Healthcare provided an unrestricted medical grant
(no applicable grant number) for a portion of this article to
Eric H. Hanson. Thomas G. Perkins is a full-time employee of
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