The Journal of TRAUMA威 Injury, Infection, and Critical Care

Acute Subdural Hematoma Because of Boxing

Hidehiko Kushi, MD, PhD, Takeshi Saito, MD, Yuichiro Sakagami, MBA, Jyoji Ohtsuki, MD, PhD,
and Katsuhisa Tanjoh, MD, PhD

Background: To identify factors de-
termining the clinical characteristics and
prognosis of acute subdural hematoma
(ASDH) arising from boxing injuries by
comparing with ASDH due to any non-
boxing cause.
Methods: Two groups were selected
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terms of age, the Glasgow Coma Scale at
admission, neurologic findings, cranio-
gram and brain computed tomography
scan findings, operative findings, and prog-
nosis. As potential prognostic indicators
for boxers, the time interval until surgery,
the Glasgow Outcome Scale, hematoma
shift, and their prognosis. The most pecu-
liar clinical presentation of boxers’ ASDH
was that all bleedings were limited from
“bridging veins” or “cortical veins.” The
prognosis of boxers was most closely cor-
related with the site of bleeding (r2 ⴝ 0.81;
p ⴝ 0.0001) and the midline shift (r2 ⴝ

for this study: 10 patients with ASDH be-
cause of boxing injuries and 26 patients
with nonboxer ASDH. All of the patients
underwent neurologic examination by
neurosurgeons. Primary resuscitation and
stabilization as well as operative therapy
were performed to all patients according
to the European Brain Injury Consortium
Guidelines. Two groups were compared in
thickness, midline shift, and the site of
bleeding were analyzed.
Results: The characteristics of pa-
tients because of boxing injuries are that
patients were younger, had lucid interval,
and had no cerebral contusion or con-
tralateral brain injury. There was no sig-
nificant difference in initial Glasgow
Coma Scale, hematoma thickness, midline
0.67; p ⴝ 0.007).
Conclusions: Our study shows that
ASDH because of boxing is characterized
by bleeding from bridging or cortical
veins, and that the site of bleeding is a
significant determinant of their prognosis.
Key Words: Boxing injury, Acute
subdural hematoma, Bridging vein, Cor-
tical vein.
J Trauma. 2009;66:298 –303.

B
oxing is the oldest fighting sport and had its origin in
ancient Greece. Modern rules of competition were es-
tablished in the 19th century, and the goal was often to
cause concussion in the opponent by blows to the head so as
to win the fight. It is, therefore, assumed that intracranial
injuries and facial injuries will occur frequently.
During the latter half of the 20th century, boxing injuries
began to be reported. Chronic brain injury in boxers was
reported for the first time by Martland,1 who called them
“punch drunk.” One study indicated that 37% of boxers who
Submitted for publication May 17, 2007.
Accepted for publication February 28, 2008.
Copyright © 2009 by Lippincott Williams & Wilkins
From the Department of Emergency and Critical Care Medicine (H.K.,
T.S., K.T.), Nihon University School of Medicine, Itabashi-ku, Tokyo, Ja-
pan; Department of Emergency and Critical Care Medicine (H.K., T.S.),
Surugadai Nihon University Hospital, Chiyoda-ku, Tokyo, Japan; CSL Behring
K.K. (Y.S.), Chuou-ku, Tokyo, Japan; and Department of Emergency Medicine
(J.O.), Tokyo Jikeikai Medical University, Minato-ku, Tokyo, Japan.
Dr. Kushi had full access to all of the data in the study and takes
responsibility for the integrity of the data and the accuracy of the data
analysis. Study concept and design was performed by Kushi and Tanjoh.
Acquisition of data was carried out by Kushi, Saito, and Ohtsuki. Analysis
and interpretation of data was done by Kushi and Saito. Drafting of the
manuscript was carried out by Kushi and Sakagami. Statistic analysis was
performed by Saito and Sakagami. Study supervision was done by Kushi.
The authors declare no conflict of interests.
Address for reprints: Hidehiko Kushi, MD, PhD, Department of Emer-
gency and Critical Care Medicine, Nihon University School of Medicine,
30-1 Oyaguchi Kamimachi, Itabashi-ku, Tokyo 173-8610, Japan; email:
hkushi@med.nihon-u.ac.jp.
DOI: 10.1097/TA.0b013e3181715dba
were knocked out in the ring showed abnormal electroen-
cephalographic findings,2 and other reports suggested that the
incidence of chronic brain damage was very high among
boxers.3– 6 Ross et al.7 reported that the detection of cerebral
atrophy and ventricular enlargement on computed tomogra-
phy (CT) scans increased in proportion to the number of
fights, although some researchers found no abnormalities by
magnetic resonance imaging.8,9 Both CT and magnetic reso-
nance imaging have their advantages and disadvantages for
assessment of the brain.10 Lampert and Hardman11 described
in detail the morphologic changes of the brain in boxers,
which had been reported by others between 1928 and 1973,
including subdural hemorrhage, intracerebral hemorrhage,
diffuse axonal injury, cerebral edema, ischemia and her-
niation, cerebral atrophy, enlargement of the ventricles and
septum cavum, cerebellar changes, loss of neurons in the
substantia nigra, and neurofibrillary tangles. The incidence of
chronic encephalopathy is higher among boxers (9%) than
nonboxers (4%);12 autopsy studies have also demonstrated a
higher incidence of encephalopathy among boxers compared
with nonboxers.13 Corsellis et al.14 examined the effect of
boxing on the cerebral parenchyma and reported that “the
average width of the cavum in the boxers was three times that
in the nonboxers,” whereas “cortical scarring on the inferior
surface of the lateral lobes and significant losses of Purkinje’s
cells on the ventral surface” were seen in the cerebellum.
Rodriguez et al.15 examined the effect on cerebral blood
flow and detected a severe decline of regional cerebral blood
flow in professional boxers. They reported that this observation
was correlated with electroencephalographic data and CT findings.

298 February 2009


Other symptoms specific to boxers include isolated
growth hormone deficiency because of hypopituitarism,16
human Kluver-Bucy syndrome after removal of acute sub-
dural hematoma,17 and changes of various structures, such as
the orbital arch, conjunctiva, iris, and retina.18
The most frequent sequelae of acute brain injury in
boxers are concussion, postconcussion, and memory
impairment.19 Intracranial hemorrhage because of boxing in-
juries usually requires emergency surgery and has only been
documented in case reports, so no studies have been based on
a sufficient number of patients. In Japan, 32 boxing deaths
were reported between 1930 and 1996, and the incidence
(4.5/10,000 boxers per year) appeared to be higher than in
other countries.20 The major cause of boxing death was acute
subdural hematoma.
To prevent such injuries in the future, the Japan Boxing
Association, the Japan Boxing Commission, and a commis-
sion of doctors took the initiative to examine methods for
ensuring the safety of boxers.
Our hospital is located near a boxing stadium, so injured
boxers are brought to us while being managed by a boxing
commission doctor. As a result, we have treated 10 patients
with acute subdural hematoma (ASDH) because of boxing. In
this study, we examined the features of ASDH that resulted in
a fatal outcome, as well as identifying differences in the
features of ASDH between boxers and nonboxers.
PATIENTS AND METHODS
Subjects
The present study was approved by the Surugadai Nihon
University Hospital Human Subject Review Committee, and
written informed consent was obtained from each participant
or from the patient’s family when appropriate. This study was
undertaken at a university intensive care unit from January
1997 to December 2004. The study group consisted of 10
patients with head injuries because of boxing. Among the 10
patients, 6 patients developed intracranial hemorrhage during
a boxing event. At admission, they had already undergone
endotracheal intubation for ventilation by a commission doc-
tor at the ringside. Their level of consciousness was ⱕ8
points according to the Glasgow Coma Scale (GCS). Three
patients developed disturbance of consciousness while spar-
ring and were brought to our hospital by ambulance while on
oxygen therapy. The remaining one patient was brought to
our hospital by ambulance because of severe headache after a
fight. His consciousness remained clear.
The control group (i.e., the nonboxers) consisted of 26
patients who were diagnosed as having ASDH because of
nonboxing traumatic brain injury and underwent emergency
surgery.
Patient Management and Operative Therapy
After admission to the intensive care unit, all of the
patients in both groups underwent neurologic examination by
a neurosurgeon. Then, primary resuscitation and stabilization
Volume 66 • Number 2
Acute Subdural Hematoma Because of Boxing
as well as operative therapy were performed according to the
European Brain Injury Consortium Guidelines for manage-
ment of severe head injury.21
All patients underwent axial cranial computed tomogra-
phy. Cranial computed tomography scans were obtained at
admission, after surgical decompression, routinely 24 hours
after admission. Subsequent scans were obtained if they were
considered necessary for clinical management of the patient,
e.g., because of increased intracranial pressure (ICP) or neu-
rologic deterioration. The operation was performed as soon as
possible, in principle.
Decompressive surgery22–24 was begun with a large,
unilateral, curvilinear incision in the frontotemporoparieto-
occipital region, including a duraplasty, was performed. Spe-
cial care was taken to remove the temporal bone down to the
base of the cranium. This was followed by preparation of a
myocutaneous flap and craniectomy with elevation of a free
frontotemporoparietal-occipital bone flap. The dura was then
opened, and beginning at the temporal base of the opening in
the dura, the hematoma was gently removed. After the re-
moval of hematoma via a large decompressive craniectomy,
the site of bleeding was carefully identified. In both surgical
groups, bone flaps were removed. A device to monitor ICP
(Camino 3000, Integra NeuroSciences, San Diego, CA) was
placed into the lateral ventricle.
Excluding one patient with a boxing injury whose con-
sciousness was clear at admission, the patients were treated in
accordance with the principles described in the American
Association of Neurologic Surgeons guidelines for the man-
agement of severe head injury.25
If the ICP remained elevated (⬎20 mm Hg for ⬎10
minutes), an intravenous bolus of 20% mannitol was admin-
istered over 10 minutes to 15 minutes (0.5–1 g/kg). Cortico-
steroids were not used. The following physiologic parameters
were continuously monitored (Hewlett Packard, Boblingen,
Germany): arterial blood pressure via a radial artery catheter,
arterial oxygen saturation by pulse oximetry, body tempera-
ture via a rectal temperature probe, cardiac rhythm, and
respiratory rate. All parameters were recorded in a comput-
erized database. Plasma glucose, blood gas, and serum elec-
trode values were measured regularly and kept within the
respective normal ranges.
Assessment of Neurologic Outcome
A specialist in physical medicine and rehabilitation who
was unaware of the patients’ treatment assignments deter-
mined the neurologic outcome at 6 months after head injury.
The neurologic outcome was scored according to the Glas-
gow Outcome Scale (GOS)26 as follows: (1) death; (2) per-
sistent vegetative state with inability to interact with the
environment; (3) severe disability with inability to live inde-
pendently but the ability to follow commands; (4) moderate
disability with the ability to live independently but inability to
return to work or school; and (5) good recovery with the
ability to return to work or school.
299
 The Journal of TRAUMA威 Injury, Infection, and Critical Care

Table 1 Acute Subdural Hematoma in Boxers and Statistical Analysis

Results are expressed as the mean ⫾ SD. The Mann-
Nonboxers
Whitney U test was used to examine between-group differ-
Boxers (n ⫽ 10) Control (n ⫽ 26) p ences of age, initial GCS score, hematoma thickness, midline
Age 23 ⫾ 3.6 58 ⫾ 15.4 ⬍0.0001 shift, and physiologic parameters, whereas Fisher’s exact test
Initial GCS 6 ⫾ 3.4 6 ⫾ 2.6 0.8137 was used to examine between-group differences in the site of
Hematoma thickness 17 ⫾ 2.9 15 ⫾ 7.6 0.8044
bleeding, presence of skull fracture, presence of cerebral
(mm)
Midline shift (mm) 21 ⫾ 3.1 19 ⫾ 6.5 0.8536 contusion, presence of contralateral brain injury, and outcome
Time interval until 117 ⫾ 38.5 128 ⫾ 40.5 0.4251 according to the GOS. Correlation coefficients were obtained
surgery (min) with Spearman’s method (because there were not enough
Physiological cases, we could not perform multivariate analysis). Probabil-
parameters
ity ( p) values of less than 0.05 were considered statistically
Systemic blood 160 ⫾ 44.3 165 ⫾ 44.2 0.7406
pressure (mm Hg) significant.
Pulse rate 68 ⫾ 19.5 83 ⫾ 18.6 0.017
(beats/min) RESULTS
Respiratory rate 18 ⫾ 9.3 18 ⫾ 4.5 0.9747
(beats/min)
Twelve patients in the control group were injured be-
Plasma sugar 244 ⫾ 74.7 181 ⫾ 44.2 0.0027 cause of falling injuries, and 14 patients were traffic crashes.
(mg/dL) Among them, nine patients were intoxicated. As shown in
White blood cell 13,820 ⫾ 4,746 14,714 ⫾ 4,185 0.5303 Table 1, significant differences between the two groups were
(counts/␮L) detected in terms of age, pulse rate, plasma sugar, presence of
Cerebral contusion 0/10 24/26 ⬍0.0001
Skull fracture 0/10 23/26 ⬍0.0001
contralateral brain injury, presence of cerebral contusion,
Contralateral brain 0/10 14/26 0.0146 bleeding from the brain surface, presence of skull fracture,
injury and presence of drinking.
Lucid interval 9/10 2/26 ⬍0.0001 Table 2 shows the clinical characteristics of ASDH be-
Alcohol 0/10 9/26 0.0394 cause of boxing. The mean age of the 10 patients with boxing
Prognosis
Poor outcome/good 4/6 15/11 0.4631
injuries was 23 years ⫾ 3.6 years (range, 17–27 years), and
outcome the mean GCS score at admission was 6 points ⫾ 3.4 points.
ASDH occurred during a fight in seven patients and while
Poor outcome: severe disability, vegetative state, and death;
good outcome: good recovery, moderate disability. sparring in three patients. A lucid intervals of ⱕ15 minutes
The Mann-Whitney U test was used for analysis of age, initial was noted in nine patients.
GCS, hematoma thickness, midline shift, time interval until surgery, Pupillary symptoms, anisocoria, and mydriasis were seen
and physiological parameters, whereas Fisher’s exact test was used in six and three patients, respectively, whereas the remaining
for analysis of the other variables.
one patient showed normal pupillary reflexes. The light reflex

Table 2 Clinical Characteristics of Acute Subdural Hematoma Because of Boxing

Hematoma Midline
Age Boxing Lucid Interval Until
Case GCS Pupils Thickness Shift Site of Bleeding Shock GOS
(yr) Incident Interval Surgery (min)
(mm) (mm)

1 21 4 Sparring Anisocoria Yes 14 19 150 Bridging vein, No GR

temporal
2 27 4 5R TKO Anisocoria Yes 15 17 120 Cortical vein No GR
3 21 4 3R TKO Mydriasis Yes 18 23 95 Bridging vein, No D
SSS post
4 17 5 4R TKO Anisocoria Yes 13 21 205 Bridging vein, No MD
SSS ant
5 22 7 10R down Anisocoria Yes 18 22 85 Bridging vein, No MD
temporal
6 25 5 Sparring Anisocoria Yes 18 23 95 Bridging vein, Yes D
SSS post
7 25 4 4R TKO Mydriasis Yes 21 24 90 Bridging vein, No D
SSS post
8 24 4 5R TKO Mydriasis Yes 18 22 100 Cortical vein No GR
9 21 15 6R down Isocoria No 12 15 105 Cortical vein No GR
10 23 5 Sparring Anisocoria Yes 19 24 115 Bridging vein, No SD
temporal
TKO, technical knockout; SSS, superior sagittal sinus; post, posterior; ant, anterior; GR, good recovery; MD, moderately disabled; SD,
severely disable; D, dead.

300 February 2009


was lost in nine patients, but was retained for both eyes in one
patient.
The time interval before surgery ranged between 85
minutes and 205 minutes, with a mean delay of 117 min-
utes ⫾ 38.5 minutes. CT scans revealed loss of the basal
cistern in nine patients. The midline shift ranged between 15
mm and 24 mm, with a mean shift of 21 mm ⫾ 3.1 mm. The
thickness of the hematoma ranged between 12 mm and 21
mm, with a mean thickness of 17 mm ⫾ 2.9 mm. The midline
shift appeared to be quite large relative to the hematoma
thickness.
All of the boxers had a unilateral ASDH without asso-
ciated cerebral contusion. One patient developed shock dur-
ing surgery. The site of bleeding was a bridging vein in three
patients, a cortical vein adherent to an enlarged arachnoid
granulation on the sylvian fissure in three patients, a bridging
vein at the anterior region of the superior sagittal sinus in one
patient, or a bridging vein at the posterior region of the
superior sagittal sinus in three patients. Three patients with
bleeding from a bridging vein in the posterior region of the
superior sagittal sinus developed severe cerebral edema dur-
ing surgery and died when ICP could not be controlled. The
outcome after 6 months according to the GOS was good
recovery in four patients, moderate disability in two patients,
severe disability in one patient, and death in three patients.
According to Spearman’s rank correlation analysis, the
coefficient of determination (r2) with respect to the influence
on the prognosis was 0.26 for the age ( p ⫽ 0.13), 0.31 for the
time interval until surgery ( p ⫽ 0.12), 0.04 for the GCS score
at admission ( p ⫽ 0.52), 0.003 for the pupillary findings
( p ⫽ 0.90), 0.36 for the hematoma thickness ( p ⫽ 0.09), 0.67
for midline shift ( p ⫽ 0.007), and 0.81 for the site of bleeding
( p ⫽ 0.0001). Therefore, the prognosis was most closely
correlated with the site of bleeding, followed by the extent of
midline shift.
On the other hand, the control group was examined as
0.20 for the age ( p ⫽ 0.017), 0.20 for the time interval until
surgery ( p ⫽ 0.014), 0.28 for the GCS score at admission
( p ⫽ 0.003), 0.40 for the pupillary findings ( p ⫽ 0.001), 0.18
for the hematoma thickness ( p ⫽ 0.017), 0.24 for midline
shift ( p ⫽ 0.06), 0.07 for the site of bleeding ( p ⫽ 0.109),
and 0.12 for the contralateral brain injury (p ⫽ 0.047) (Table 3).
DISCUSSION
Physiologic Parameters
Compared with the control group, the pulse rate was
deteriorated significantly in the boxing group. There seemed
to be two reasons: one was that the patients in the boxing
group were younger and the other is that the cardiac output
was higher in the boxing group because of their physical
trainings. On the other hand, the value of plasma sugar in the
boxing group was significantly high because they had phys-
ical stress before their head injuries by weight loss and their
strain of exfoliation nervous system by matches of boxing
and sparring.
Volume 66 • Number 2
Acute Subdural Hematoma Because of Boxing
Table 3 Spearman’s Rank Correlation Analysis, the
Coefficient of Determination (r) With Respect to the
Influence on the Prognosis
Boxer Controls
Age r2⫽0.26; p ⫽0.13 r2 ⫽ 0.20; p ⫽ 0.017
Time interval r2⫽0.31; p ⫽0.12 r2 ⫽ 0.20; p ⫽ 0.014
until surgery
GCS score at r2⫽0.04; p ⫽0.52 r2 ⫽ 0.28; p ⫽ 0.003
admission
Pupillary findings r2⫽0.003; p⫽0.90 r2 ⫽ 0.40; p ⫽ 0.001
Hematoma r2⫽0.36; p ⫽0.09 r2 ⫽ 0.18; p ⫽ 0.017
thickness
Midline shift r2⫽0.67; p ⬍0.01 r2 ⫽ 0.24; p ⫽ 0.006
Site of bleeding r2⫽0.81; p ⬍0.01 r2 ⫽ 0.07; p ⫽ 0.109
Contralateral r2 ⫽ 0.12; p ⫽ 0.047
brain injury
r, Spearman’s rank correlation coefficient.
Mechanism of Subdural Hematoma in Boxers
Transmission of an external force to the brain occurs
because of translational (linear) acceleration or rotational
acceleration, and the latter type of acceleration is known to
induce brain damage more frequently than the former.27,28
Rotational acceleration leads to cerebral concussion
when the extent and duration of acceleration reach a thresh-
old, although it causes no injury if mild.2 This is because
neuronal function is temporarily interrupted by cephalogyric
stress on the brain tissue.
As the extent and duration of rotational acceleration
increase, the gap between the skull and the brain surface that
is most affected by centrifugal force becomes larger, resulting
in the stretching of bridging veins that run between the
cranium and the cerebral surface. ASDH occurs when a
bridging vein is ruptured. The effect of centrifugal force is
more pronounced on the cerebral parenchyma than at the
surface of the brain. It interferes with long nerve fiber tracts
and fine intracerebral vessels, leading to diffuse axonal
injury.29 The occurrence of ASDH or diffuse axonal injury is
related to the extent and duration of rotational acceleration.
Because boxing trauma involves relatively mild rotational
acceleration, either ASDH or diffuse axonal injury may oc-
cur. Autopsy of boxers with ASDH has revealed bleeding
from the basal ganglia and brain stem as well as a crushed
wound,11,30 indicating that boxing may result in diffuse brain
injuries.
Lucid Interval
ASDH is classified according to whether or not it is
accompanied by cerebral contusion. In patients with ASDH
accompanied by cerebral contusion, a lucid interval is rela-
tively less common because the primary disturbance of con-
sciousness persists for longer. In contrast, a lucid interval
usually occurs in patients who have ASDH without cerebral
contusion because the primary disturbance of consciousness
is only temporary.
301
 The Journal of TRAUMA威 Injury, Infection, and Critical Care
Similar to some earlier case reports on boxing
injuries,11,30 –32 our 10 boxers all had ASDH without cerebral
contusion and a lucid interval of ⱕ15 minutes was noted.
This observation seems to indicate that ASDH because of
boxing occurs when a bridging vein is ruptured by relatively
mild rotational acceleration.
Interval From Onset to Surgery
Seeling et al.33 reported that the mortality rate of
common ASDH may be as low as 57% if craniotomy is
performed to remove hematoma within 4 hours after the
onset. Koyama et al.34 reported that the mortality rate of
boxers with ASDH was 33% when craniotomy was done
within 2 hours after the onset.
All 10 boxers treated at our hospital underwent extensive
decompressive craniectomy within 4 hours of injury, and the
mortality rate was 30%. Because the pathology (including the
site of bleeding) of ASDH because of boxing is different from
that of common acute subdural hematoma, it is difficult to
predict or discuss the prognosis based on the time interval
until surgery.
Surgical Procedures, Operative Findings, and
Prognosis
Although surgery was performed according to the
same procedures used for common acute subdural hema-
toma, our patients all underwent extensive decompressive
craniectomy23 targeting the bridging veins in the frontopari-
etal lobe and tip of the temporal region so as to remove
hematoma for decompression and control bleeding from the
bridging veins after removal of the hematoma. Horizontal and
vertical tissue shifts and ventricular and vascular compression
by massive ASDH are relieved by removal of the bone flap.
However, there are no reports confirming that decompressive
craniectomy improves the outcome. Jiang et al.24 found that
decompressive surgery could improve the outcome and sup-
press the development of delayed hematoma in a prospective
comparative multicenter trial. We consider that our approach
to decompressive surgery, which is similar to Jiang’s and
involves making a large craniectomy down to the base of the
cranium, is clinically appropriate in that it prevents brain
stem and temporal lobe compression.
During the operation, the patient was positioned with the
upper part of the body forward 30 degrees, the head turned
backward 30 degrees to 40 degrees, and the top of the head
slightly lowered toward the surgeon to facilitate treatment of
the bridging vein.
Bleeding from a cortical vein is characteristic of boxing
injuries. It has already been reported that the source of bleed-
ing in patients with ASDH because of boxing was a bridging
vein.11,30 –32 However, 3 of the 10 patients in our series had
bleeding from a cortical vein in the temporal lobe, which was
involved by thickened arachnoid granulations in the sylvian
fissure that were adherent to the dura mater. Malignancy,
infections, inflammation, reactive processes, and chemical
302
factors are considered to be related to enlargement [hyper-
trophy] of the arachnoid granulations.35 In the case of boxing
injuries, repeated blows to the head seem to induce enlarge-
ment [hypertrophy] of the arachnoid granulations, which ad-
here to the dura mater and the surface of the brain and thus
traps a cortical vein.
Although ASDH because of mild injury or idiopathic
acute subdural hematoma36 are known to be accompanied by
the rupture of a cortical branch of the middle cerebral artery,
there has been no previous report of ASDH associated with
enlarged arachnoid granulations. Because there are no reports
of acute subdural bleeding from a cortical vein involved by
enlarged arachnoid granulations, it seems that this condition
may be a specific boxing injury.
Because the range of cortical venous perfusion is limited,
obliteration of a cortical vein does not seriously interfere with
venous perfusion, resulting in a good prognosis. In contrast,
the territory of the bridging veins is wide, so ligation of a
bridging vein causes impaired venous perfusion and de-
creases cerebral blood flow (venous ischemia), leading to
severe cerebral swelling and death.
Under the nonboxing acute subdural hematoma, cerebral
contusions were frequently triggered, and the midline shift
seemed to become stronger than hematoma thickness.
On the other hand, under the ASDH by boxing injury,
although there was no cerebral contusion, the cerebral swell-
ing occurred because venous perfusion was damaged. As a
result, it is thought that the midline shift became stronger than
the hematoma thickness.
CONCLUSIONS
ASDH because of boxing is characteristically unaccom-
panied by skull fracture, contralateral brain injury, or cerebral
contusion. The source of bleeding is either a bridging vein or
a cortical vein. The extent of the territory of the source vein
will determine the prognosis.
The sample size of the present study was limited. Because
boxing injuries occur under special condition, it is not easy to
collect a large group of patients with ASDH because of boxing,
so this study was performed with the available data.
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