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Boxing-Related Head Injuries

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Abstract and Figures

Fatalities in boxing are most often due to traumatic brain injury that occurs in the ring. In the past 30 years, significant improvements in ringside and medical equipment, safety, and regulations have resulted in a dramatic reduction in the fatality rate. Nonetheless, the rate of boxing-related head injuries, particularly concussions, remains unknown, due in large part to its variability in clinical presentation. Furthermore, the significance of repeat concussions sustained when boxing is just now being understood. In this article, we identify the clinical manifestations, pathophysiology, and management of boxing-related head injuries, and discuss preventive strategies to reduce head injuries sustained by boxers.
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CLINICAL FOCUS: NEUROLOGY, REHABILITATION MEDICINE, CARDIOMETABOLIC HEALTH
Introducon
From 1732 to November 2007, 1465 boxing-related deaths were recorded worldwide. About 70% of these
fatalities occurred in professional boxers.1 Although the number of fatalities has decreased considerably
since 1960, it still averages about 77 deaths per decade.1 Many of these fatalities occur because of
progression of, or not identifying, cognitive impairments, as well as serious concussions and injuries that
occur during the ght. ere is a large body of evidence demonstrating that boxing-related concussions
alone can result in cognitive impairment.2–10 Although these studies acknowledge the presence of impair-
ment, signicant variance exists with regards to the duration of the impairment and its permanence, if
any. In this article, we identify the various clinical, pathological, and epidemiological aspects of boxing-
related head injuries, their outcomes, and preventive strategies to reduce head injuries when boxing.
Pathophysiology of Brain Injuries in Boxing
ere are 3 types of stresses that occur in the brain when an individual sustains a blow to the head:
compressive, stretching (tensile), and shearing.11 Of these, shearing stresses are the most dangerous
because they can cause direct neuronal injury in proportion to the degree of head acceleration encoun-
tered.10,12,13 Blows to the side of the head (rotational acceleration) produce greater shearing forces than
those directly to the face (translational acceleration), with the exception of those to the chin, which
produce maximal shearing forces.14 ese in turn lead to direct neuronal damage and death, which may
be either focal or diuse depending on the rotational acceleration. e eects of acceleration on the
head can be mitigated by development of greater neck muscle strength, which can absorb the energy
from a blow and reduce the force applied to the brain. A study by Ommaya etal15 determined that a
rotational acceleration of 4500 rad/s2 was required to produce a concussion in an adult, with mild and
moderate diuse axonal injury occurring at 12 500 and 15 500 rad/s2, respectively, and diuse axonal
injury at 18 000 rad/s2. Subsequent studies have demonstrated rotational accelerations during boxing
of up to 13 600 rad/s2, with an average between 1200 and 9000 rad/s2 depending on the boxer’s body
weight.16,17 Diuse axonal injury accounts for a signicant amount of the remainder of traumatic brain
injuries sustained by boxers, along with intracerebral (intraparenchymal contusions) and extracerebral
(subdural and epidural) hemorrhages.
Brain injury caused by a direct blow is oen described as either a coup injury, where the damage
occurs directly under the point of impact, or a contrecoup injury, which occurs opposite to the point
of impact. e point of impact and the underlying skull anatomy oen dictates the severity of coup
and contrecoup injuries. Because of bony prominences in the subfrontal region and the sphenoid wing,
frontal and temporal contusions are the most common examples of coup and contrecoup injuries. Skull
Boxing-Related Head Injuries
Mayur Jayarao, MD, MSc; Lawrence S. Chin, MD, FACS; Robert C. Cantu, MD, MA, FACS, FACSM
Abstract: Fatalies in boxing are most oen due to traumac brain injury that occurs in the ring. In the past 30 years, signicant
improvements in ringside and medical equipment, safety, and regulaons have resulted in a dramac reducon in the fatality rate.
Nonetheless, the rate of boxing-related head injuries, parcularly concussions, remains unknown, due in large part to its variability
in clinical presentaon. Furthermore, the signicance of repeat concussions sustained when boxing is just now being understood. In
this arcle, we idenfy the clinical manifestaons, pathophysiology, and management of boxing-related head injuries, and discuss
prevenve strategies to reduce head injuries sustained by boxers.
Keywords: boxing; sports injury; concussion; postconcussive syndrome; chronic traumac encephalopathy; second-impact syndrome
Mayur Jayarao, MD, MSc1
Lawrence S. Chin, MD, FACS1,2,
Robert C. Cantu, MD,
MA, FACS, FACSM3–6
1Department of Neurosurgery,
Boston Medical Center,
Boston, MA; 2Department of
Neurosurgery, Boston University
School of Medicine, Boston,
MA; 3Center for the Study of
Traumatic Encephalopathy, Boston
University Medical Center,
Boston, MA; 4Neurological
Sports Injury Center, Brigham
and Women’s Hospital, Boston,
MA; 5Department of Exercise
and Sports Science, University
of North Carolina, Chapel Hill,
NC; 6Department of Surgery,
Emerson Hospital, Concord, MA
Correspondence:
Robert C. Cantu, MD, MA, FACS, FACSM,
131 Old Rd to Nine Acre Corner
John Cumming Building, Suite 820
Concord, MA 01742.
Tel: 978-369-1386
E-mail: rcantu@emersonhosp.org
Jayarao et al
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fractures can also inuence the severity of the underlying brain
injury. A skull fracture may dissipate energy, reducing the
impact of the blow, or the fracture could lacerate the brain or
artery, resulting in a hematoma, thus potentiating the severity
of a coincidental brain injury.
Acute Brain Injuries in Boxing
Acute brain injuries in boxing include concussions, intracranial
hemorrhage, and second-impact syndrome (malignant brain
edema syndrome).
Concussion
Concussions are the most common head injury in all sports,
including boxing.1 8 As outlined at the 3rd International
Conference on Concussion in Sport held in November 2008,19
concussion is dened as a complex pathophysiological process
that aects the brain and is induced by traumatic biomechanical
forces. Several common features that incorporate clinical,
pathologic, and biomechanical injury constructs that may be
used to dene the nature of a concussive head injury include:
1. Concussion may be caused by a direct blow to the head,
face, neck, or elsewhere on the body, with an “impulsive”
force transmitted to the head.
2. Concussion typically results in the rapid onset of short-lived
impa ir ment of neurolog ic fu nction that re solves
spontaneously.
3. Concussion may result in neuropathologic changes, but
the acute clinical symptoms largely reect a functional
disturbance rather than a structural injury.
4. Concussion results in a graded set of clinical symptoms that
may or may not involve loss of consciousness. Resolution
of the clinical and cognitive symptoms typically follows a
sequential course; however, it is important to note that in
a small percentage of cases, postconcussive symptoms may
be prolonged.
5. No abnormality on standard structural neuroimaging
studies is seen in concussion.
Clinical Diagnosis and Evaluaon
e diagnosis of acute concussions involves many domains,
including clinical (somatic, cognitive, emotional), physical
(loss of consciousness, amnesia), behavioral (irritability), sleep
(drowsiness), and cognition (slowed reaction).
If any athlete demonstrates any of these features, the
consensus for on-site evaluation states that:19
1. e player should be medically evaluated on-site using
standard emergency manag em ent pr in ciples , an d
particular attention should be given to excluding a cervical
spine injury.
2. The appropriate disposition of the player must be
determined by the treating health care provider in a timely
manner. If no health care provider is available, the player
should be safely removed from practice or play, and urgent
referral to a physician should be arranged.
3. Once the rst aid issues are addressed, then an assessment
of the concussive injury should be made using the SCAT220
or a similar tool.
4. e player should not be le alone following the injury,
and serial monitoring for deterioration is essential over
the initial few hours following injury.
5. A player with diagnosed concussion should not be allowed
to return to play on the day of injury. Occasionally, in adult
athletes, there may be return to play on the same day as
the injury if appropriate medical expertise and resources
are immediately available.
There should be adequate time for assessment, and
facilities should be available. For on-site evaluations, brief
neuropsychological batteries, such as those by Maddocks21
and the Standardized Assessment of Concussion (SAC),22 have
been eective and reliable. Standard orientation questions
(eg, time, place, and person) have not been demonstrated
as being reliable. Formal evaluations by medical personnel
in appropriate settings, such as the hospital or emergency
department, should also include: comprehensive history and
detailed neurological examinations, determination regarding
the clinical status of the patient, and determination regarding
the need for neuroimaging.
Invesgaons
In nearly all cases of concussion, conventional structural
neuroimaging, such as computed tomography (CT) and
magnetic resonance imaging (MRI) is normal. Nevertheless,
if a concussion is suspected, either of these modalities
should be considered. Other MRI modalities such as
gradient echocardiography, perfusion, functional MRI
(fMRI), diusion tensor imaging (DTI), positron emission
tomography (PET), and magnetic resonance spectroscopy
(MRS), are being evaluated. Recent data by Zhang etal,23,24
Kumar etal,25 and Chappell etal26 revealed alterations in diu-
sion constants (increase) and anisotropy (decrease) in the cor-
Boxing-Related Head Injuries
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pus callosum and internal capsule on DTI when compared with
nonconcussed individuals. e studies and data suggest that
DTI may be considered to identify those with early evidence
of neural injury, while simultaneously maintaining that further
study would be required.
Balance testing or posturography using sophisticated force
plate technology (eg, Sensory Organization Test [SOT] on the
NeuroCom® Smart Balance Master®) and less sophisticated
clinical balance tests (eg, Balance Error Scoring System27) have
identied postural stability decits that typically last up to
72hours aer a sports-related concussion. ese decits were
most evident when subjects were standing on either foam or
moving (tilting) surfaces.27–31 Postural stability testing allows
objective motor assessment and is considered a reliable valid
assessment in athletes who sustain a concussion.19
Neuropsychological and neurocognitive screening is
increasingly being implemented to individually monitor con-
cussed athletes.32–34 Consequently, numerous computerized
tests, such as the Automated Neuropsychological Assessment
Metrics (ANAM; US Department of Defense, Washington
DC),35 CogSport (CogState Ltd., Melbourne, Australia),36
HeadMinder™ (HeadMinder Inc., New York),37 and ImPACT™
(ImPACT Inc., Pittsburgh, PA)38 tests, have been used to
compare the athlete’s recovery, especially his or her pre-injury
level of cognitive function. Its utility, implementation, and
reliability have been demonstrated.39–44 However, it must be
emphasized that neuropsychological assessments require spe-
cialized neuropsychologists, and should not be the sole basis in
return-to-play decision making. In general, neuropsychologi-
cal testing should not be done while the athlete is symptomatic
because it does not add much to determine an athlete’s return
to play, and may also confound the testing results. e current
recommended consensus strategy is to wait for resolution of
clinical symptoms (at rest and following provocative exercise
challenges), and then use the neuropsychological testing as
the nal step in the return-to-play strategy.19,42,45
Finally, genetic testing is being evaluated to identify
concussion risk factors aer studies by Kristman et al46 and
Terrell etal47 demonstrated associations of apolipoprotein
(Apo) E4, ApoE promoter gene, and tau polymerase in athletes
who sustained concussions. Currently, the outcome regarding
genetic testing is unclear and requires further study, while
simultaneously becoming a contentious ethical issue.48 Other
assessment modalities, such as evoked response potential,
cortical magnetic stimulation, and electroencephalography,
have demonstrated abnormalities in postconcussive states,
but their signicance in relation to standard control groups
is unclear.49–54
Management
Concussion management consists of cognitive and physical rest
until symptoms resolve. Following this, a graded program of
exertion is conducted prior to medical clearance and return to
play. A graduated return-to-play protocol19 is recommended by
the consensus on concussion presented at the 3rd International
Conference on Concussion in Sport. e protocol allows the
athlete to proceed to the next level if he or she is asymptomatic
at the previous level. e whole process usually takes about
1week, which (based on multiple studies) is the average time
taken to recover from a concussion.2,4,22,55–57 If postconcussive
symptoms recur, the athlete is to drop back to the previous
asymptomatic grade.
Psychological and pharmacological approaches may be
required as adjuncts, but these are patient-specic and should
be considered only by physicians experienced in concus-
sion management. In addition, other factors such as loss of
consciousness for . 1minute, amnesia (antegrade and ret-
rograde), posturing, or seizures may require modication of
concussion management.
Intracranial Hemorrhage
For all sports, including boxing, intracranial hemorrhage is
the leading cause of death for athletes who sustain serious
head injuries. e 4 types of hemorrhage most frequently
encountered are: epidural hemorrhage, subdural hemorrhage
(SDH), intraparenchymal hemorrhage (IPH) or intracerebral
contusion, and subarachnoid hemorrhage. All 4 can be easily
visualized on CT scan or MRI.
Epidural Hemorrhages
Although epidural hemorrhages are not the most common
injury in boxing, they can be the most rapidly progressive.
ey frequently occur because of middle meningeal artery
rupture resulting from fracture of the overlying temporal
bone. Subsequently, there is accumulation of blood between
the calvarium (skull) and dura mater. Typically, there is a lucid
interval following an initial period of unconsciousness, which
subsequently leads to rapid clinical decline as blood accumu-
lates in the extradural compartment, with resulting compres-
sion of the underlying brain parenchyma. When signicant
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neurological decit or cerebral herniation is encountered,
evacuation via a craniotomy or craniectomy is required.
Subdural Hemorrhages
Acute subdural hemorrhages (Figure1) are the leading cause
of death in boxing-related head injury. ey occur due to
rupture of bridging veins and/or cortical surface arteries, with
resulting accumulation of blood between the dura mater and
brain surface. In boxing, they are associated with prolonged
periods of unconsciousness following a knockout. Due to the
impact force encountered in boxing, SDHs are also associated
with direct axonal injury of the brain parenchyma immediately
adjacent to it. Like an epidural hemorrhage, these also require
evacuation by craniotomy or craniectomy if signicant neuro-
logical decit or evidence of cerebral herniation is present.
Intraparenchymal and Subarachnoid Hemorrhages
In tra par enc hym al he morr hag es an d sub arac hno id
hemorrhages are encountered less frequently in boxing. An
IPH occurs within the brain parenchyma itself and may be
associated with extremely rapid neurological deterioration
without a lucid interval. Subarachnoid hemorrhages occur
between the arachnoid and pia mater, and can be diuse. When
diuse, it can lead to signicant surrounding perihemorrhagic
edema that can cause gradual, progressive neurological decline.
Both IPH and SAH may then require decompression via a
craniotomy or craniectomy. In some cases, evacuation of the
intraparenchymal hemorrhage may also be necessary.
Second-Impact Syndrome
Second-impact syndrome was rst described by Schneider58
in 1973, although the term itself was introduced in 1984
by Saunders and Harbaugh.5 9 Even the mildest grade of
concussion can lead to second-impact syndrome, and the
condition is oen fatal (50%) if not severely debilitating
(100%). e syndrome occurs when an athlete sustains a
recurrent head injury before the symptoms associated with an
initial head injury have resolved.60,61 e second impact may
be minor and not even occur directly to the head. It may occur
elsewhere (eg, the thorax) but because of transmitted forces
cause an “indirect” head injury. As a result, the athlete may
initially appear stunned and may even continue to compete
without any immediate loss of consciousness. However, loss
of consciousness eventually occurs in the ensuing minutes,
usually in a dramatic manner. e athlete usually collapses
to the ground, comatose or semicomatose, with neurological
and hemodynamic features suggestive of cerebral herniation.
Although most cases of second-impact syndrome involve
athletes aged , 18 years, it has also been seen in others,62,63
and is likely frequently missed in boxers who have had severe
head injuries.
e pathophysiology of second-impact syndrome remains
controversial. e current theory postulates that it occurs
to cerebrovascular dysregulation, which leads to hyperemic
cerebral edema, elevated intracranial pressure, and subse-
quent cerebral herniation (frequently uncal and tonsillar)
with brain stem compression, and ultimately death within
minutes of injury. Research in animal models has revealed
that vascular engorgement following even mild traumatic
brain injury can sometimes be extremely dicult to con-
trol.64–67 Although intracranial hemorrhage is not always
present, there have been recent reports by the senior author
(RC) and others of second-impact syndrome associated with
a thin SDH.62,63
A diagnosis of second-impact syndrome is usually made
from a unique history as well as CT and MRI ndings. Treat-
Figure 1. Non-contrast computed tomography image demonstrating subdural hemor-
rhage in a boxer.
A 33-year-old male boxer was admitted to the emergency department after losing
consciousness following a blow to the head during a practice session. At the scene, the
patients Glasgow Coma Score (GCS) was 11 (Eyes-3, Verbal-3, Motor-5). On route, in
the ambulance, his neurological status declined, and on evaluation at the emergency
department was found to have a GCS of 6 (Eyes-1, Verbal-1, Motor-3). He was intubated
and a non-contrast computed tomography demonstrated a 1cm acute left frontotem-
poroparietal subdural hemorrhage (left) with associated diffuse sulcal and left lateral
ventricle effacement, and approximately 1cm midline shift to the left with associated
left uncal herniation (right). The patient underwent an emergency craniectomy with
evacuation of the subdural hemorrhage. His hospital course was protracted by sustained
elevation of intracranial pressure that was managed with hyperosmolar therapy. Following
resolution of the elevated intracranial pressure, he was discharged to a traumatic
brain injury rehabilitation center on hospital day #18 with residual hemiparesis, and
cognitive and memory difficulties. Ten months later, the patient underwent an autologous
cranioplasty and a year later, had recovered with no neurological deficits, except for
occasional left-sided headaches.
Boxing-Related Head Injuries
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ment of second-impact syndrome, especially in the absence
of intracranial hemorrhage, is generally nonsurgical and sup-
portive in nature.
Delayed Brain Injuries in Boxing
e 2 most common delayed brain injuries seen in boxers are
postconcussion syndrome and chronic traumatic encephal-
opathy (CTE).
Postconcussion Syndrome
Postconcussion syndrome is the second late effect of a
concussion. It consists of headache (particularly with exertion),
dizziness, fatigue, irritability, and impaired memory and
concentration. Its true incidence is unknown, but it correlates
directly with the duration of postconcussive amnesia. Return to
play must be deferred until all diagnostic and clinical ndings
are normal.
Chronic Traumac Encephalopathy
Chronic traumatic encephalopathy or punch drunk syndrome
represents the chronic eects of repeated head trauma that
lead to anatomical patterns of brain injury with correlating
clinical features. It is estimated that between 15% and 40%
of boxers demonstrate symptoms of chronic brain injury.68
Punch drunk syndrome was rst described by Martland69
in 1928 as being characteristic of boxers who had sustained
frequent, repetitive head trauma of concussive or subcon-
cussive force. In this article, Martland69 described the early
symptoms of punch drunk syndrome as “mental confusion,
slowness of muscle movements, speech hesitancy, and trem-
ors of the hands.” Occasionally, these symptoms progressed
and a more chronic state resulted, which manifested with
marked truncal ataxia, gross mental deterioration, and a
syndrome similar to Parkinsonism.
Over the next half century, multiple retrospective studies
(eg, Roberts70) were conducted, which supported Martland’s
observations. In 1973, pathological evidence was oered by
Corsellis etal,71 who conducted postmortem studies on the
brains of 15 boxers. Corsellis’s team documented 4 types of
changes in the brain tissue. e most common was rupture of
the septum pellucidum (leading to cavum septum pellucidum),
which they correlated with the emotional lability and rage
reactions of the boxers. e second was scarring of the under-
surface of the cerebellum, which was thought to occur because
of the cerebellum being repeatedly forced through the foramen
magnum. is cerebellar injury was associated with slurred
speech, slowing of motor movements, and a broad-based gait.
In some, there was progression of pathological changes, which
was characterized by a decrease of pigment in the substantia
nigra. is is also seen in Parkinson’s syndrome, and 4 of the
boxers who had tremors and rigidity of the limbs were actually
hospitalized with Parkinson’s syndrome. e fourth change
was neurofibrillary tangles, which represents tau protein
deposition in nerve cells. ese neurotoxic tau protein deposits
were especially prevalent in the medial temporal lobes. is
was seen in . 90% of the boxers. e study by Corsellis etal71
also demonstrated that the most successful boxers had the
most brain damage. ey reasoned that this was because the
boxers had the longest careers, fought the most ghts and, as
a consequence, had received the most head trauma.
However, progressive tauopathy has been increasingly
identied in athletes with CTE.72 Pathological evidence has
demonstrated that there are high levels of abnormal TDP-43
inclusion bodies in patients with frontotemporal lobar degen-
eration, Alzheimer’s disease, and amyotrophic lateral sclero-
sis.73–76 Similar evidence was also demonstrated by King etal77
in boxers with CTE. ese aspects were further evaluated, and
a recent study by McKee etal78 on athletes (including boxers)
sustaining repetitive head trauma suggests a link between
TDP-43, the development of CTE, and possibly even motor
neuron disease. Table1summarizes the main components of
brain injury in CTE and their associated clinical symptoms and
Table 1. Four Main Components of Chronic Brain Damage in Chronic Traumatic Encephalopathy
Area Damaged Clinical Symptoms and Signs
Septum pellucidum, adjacent periventricular grey matter, frontal
and temporal lobes
Altered affect (euphoria, emotionally lability) and memory
Degeneration of substantia nigra Parkinson’s syndrome (bradykinesia, rigidity, gait instability and tremor)
Cerebellar scarring and nerve loss Slurred speech, loss of balance and coordination
Diffuse neuronal loss Loss of intellect, Alzheimer’s syndrome
Adapted with permission from Cantu.18
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signs.18 e diagnosis of CTE is based primarily on symptoms,
physical examination, and neuropsychological tests, although
CT scan and MRI are benecial as well. In 1 report using the
CT scan, it was demonstrated that even boxers with a moder-
ate number of bouts may suer cerebral atrophy.79 Further-
more, the authors found that the extent of atrophy correlated
with the number of bouts the boxer in which the boxer had
participated. Other articles have since conrmed or indicated
similar ndings.80,81 Treatment of CTE is supportive, being
directed specically to the clinical presentation of the boxer.
Injury Prevenon in Boxing
Because boxing is a sport that involves frequent, high-intensity
impact to the head, it is inevitable that head injuries will
occur. To reduce the incidence of head injuries, including
concussions, the following are general recommendations for
all sports by the 3rd International Symposia on Concussion
in Sport19 and the National Center for Catastrophic Injury
Research (NCCSI):20,82
1. All athletes should be required to undergo a preparticipa-
tion physical examination.
2. All teams should have a qualied trainer, accessible written
emergency procedures, and safe facilities and equipment.
3. It is important, whenever possible, for a qualied physi-
cian to be on the eld of play during game and practice.
When this is not possible, arrangements must be made in
advance to obtain a physician’s immediate services when
emergencies occur. Each institution should have a team
trainer who is a regular member of the institution’s sta
and who is qualied in the emergency care for both treat-
ing and preventing injuries.
4. Coaches should be well trained in physical conditioning,
the skills of their sport, and the risks of injury. Coaches
should also be able to eectively teach these skills to
athletes.
5. Game ocials must enforce rules strictly, and coaches
sh ould suppo rt of fic ial s’ efforts to conduct saf e
competitions.
6. Fair play and respect should be supported as key elements
of sport, with violence and aggression being discouraged.
In addition, the following have already been or should be
considered for improvement of safety in boxing, especially
professional boxing:83
1. Establish a national registry for all professional boxers.
2. Authorize the ringside physician to terminate bouts.
3. Hold frequent medical training seminars for all ring
personnel, improve coaching, and certify trainers and
managers.
4. Provide adequate ringside life-support systems, emer-
gency evacuation plans and personnel, and hold boxing
matches only when proper neurosurgical facilities are
available nearby.
5. Establish mandator y safety standards for ringside
equipment.
6. Upgrade and enforce the medical evaluation of boxers by
boxing commissions.
7. Eliminate all “Tough Man” contests.
8. Do not allow the round-ending bell to save a boxer from
a knockout count.
9. Suspend boxers rendered unconscious or in bouts
terminated due to head blows, and prevent them from
participating in sparring and competitions. e following
are implemented or should be considered:
o 30-day suspension if the contest is stopped because
of excessive head blows or excessive standing 8
counts.
o 45 to 60days suspension if contest is stopped because
of technical knockout.
o 90 days suspension if contest is stopped because
of a knockout, or boxer is unresponsive for up to
2 minutes, or if the boxer has received multiple
30- or 45-day suspensions within 1 year.
o 180days suspension if the boxer has been unrespon-
sive for . 2minutes.
10. Mandatory neuroimaging and hospital evaluation for all
boxers who were unresponsive for . 1minute, and/or
sustained a knockout or technical knockout.
11. Improve and certify boxing equipment and make
protective equipment mandatory.
ere is no good clinical evidence that mouth guards
prevent head injury, although they have a definite role
in preventing dental and orofacial injury. Studies have
demonstrated that while the use of head gear and helmets
reduces the impact forces sustained by the head, it has not been
shown to reduce the incidence of concussions. Nonetheless, it
likely does have a role in reducing serious injuries to the head
and should therefore be considered.
The concept of “rule change” has been frequent ly
considered in boxing. Indeed, there have been articles calling
for the abolition of boxing based on moral, ethical, and medical
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grounds.84,85 One such rule change involved the reduction of
championship bouts from 15 to 12 following the death of
Duk Koo Kim in 1982 during the 14th round. At the time, the
World Boxing Council claimed that a study by their medical
advisors had determined that most severe boxing injuries
occurred during rounds 13 to 15. Additionally, an increase
in the number of ring ropes and preght medical checkups
were also made. A recent study by Baird etal86 evaluated the
relationship of boxing-related fatalities between 1950 and 2007
to knockouts, technical knockouts, number of rounds fought,
weight class, and location of preterminal event. Of the 339
deaths, 64% were associated with a knockout, 15% were associ-
ated with a technical knockout, and 61% were associated with
preterminal events occurring in the ring itself. Importantly,
they found no signicant variables to support that decreased
mortality was due to a reduction of rounds to 12, but rather
found that the highest number of fatalities occurred in the 10th
round. Whether a further reduction in bouts will reduce the
number of fatalities remains to be determined.
Conclusion
A professional boxer’s career, starting at the beginning of the
modern boxing era, generally lasts between 10 and 20years.
Additionally, many of these boxers had long amateur careers in
which they were not necessarily matched by skill or weight and
had minimal or no medical supervision. e dramatic reduction
of overall exposure to head trauma in a boxer’s career as well as
improvements in safety, ringside medical facilities, and medical
supervision have made it a safer sport. e observed decline in
boxing-related deaths aer 1983 is reective of these methods,
but is also likely due in part to the reduction in a boxers career
from 19 to 5years and in career bouts, from 336 to 13 matches.68
In this regard, stringent enforcement of boxing rules and
regulations, certication of trainers and managers, and manda-
tory hospital assessment with neuroimaging for boxers who
are unresponsive for > 1 minute as well as those who sustain a
knockout or technical knockout could lead to timely diagnosis
and intervention. Further, it is likely that with close certied
medical supervision and greater match control to the ringside
physician, there will be a further reduction in the incidence of
concussions and serious head injury.
Conict of Interest Statement
Mayur Jayarao, MD, MSc, Lawrence S. Chin, MD, FACS, and
Robert C. Cantu, MD, MA, FACS, FACSM disclose . . .
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... 30 Os golpes na cabeça podem ocasionar lesão neuronal direta, focal ou difusa, ou morte, consoante o grau de aceleração rotacional. 6 Os efeitos da aceleração na cabeça poderão ser minimizados através do fortalecimento da musculatura do pescoço, ocasionando maior capacidade de absorção do impacto e redução da força aplicada ao cérebro. 6 Para que ocorra uma concussão num adulto é necessária uma aceleração rotacional de 4500 rad/s2, sendo que para lesão axonal difusa ligeira e moderada são necessários valores de aceleração de 12 500 rad/s2 e 15 500 rad/s2, respetivamente. ...
... 6 Os efeitos da aceleração na cabeça poderão ser minimizados através do fortalecimento da musculatura do pescoço, ocasionando maior capacidade de absorção do impacto e redução da força aplicada ao cérebro. 6 Para que ocorra uma concussão num adulto é necessária uma aceleração rotacional de 4500 rad/s2, sendo que para lesão axonal difusa ligeira e moderada são necessários valores de aceleração de 12 500 rad/s2 e 15 500 rad/s2, respetivamente. 31 Valores de 18 000 rad/s2 poderão ocasionar lesão axonal difusa severa. ...
... 32 A lesão axonal difusa representa uma ampla percentagem das lesões traumáticas do cérebro em pugilistas, na qual se integram também as hemorragias intracerebrais, associadas a contusão intraparenquimal e hemorragias extracerebrais, epidurais e subdurais. 6 As lesões cerebrais causadas por um golpe direto na cabeça, podem ocorrer no local do impacto ou no ponto oposto ao local de impacto. 6 O ponto de impacto direto e a anatomia do crânio imediatamente interior poderão ditar a gravidade destas lesões. ...
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Although the injury risks of boxing is well known, this sport continuous to attract athletes and an increase of introduction to boxing is observed in the last decade. In terms of injury locations, head and face are reported as most common sports. Present study aimed to examine the hearing differences of elite amateur boxers as a result of punch strokes in boxing. Subjects are interested in active boxing for 5-14 years (mean 6.67) and between the age of 18-32 (mean 21.71). Screened group consisted of 21 male boxers. Auditory brainstem responses, pure tone and high frequency audiogram tests were conducted for boxers and unscreened groups in the standard acoustically controlled rooms using Interacoustics Clinical Computer Audiometer. Mean ± standard deviations are reported. Groups were compared by Student's t test p<0.05. Auditory brainstem responses and pure tone values were determined in range of I-V inter-pick latency (ms).There were no statistically significant differences in the hearing level of elite amateur boxers in contrast to non-boxers. It is seen to be important that amateur boxers wear protective materials as a helmet and mouth guard to minimize the risk of injury. The use of protective equipment must be encouraged for boxer's health.
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Although the injury risks of boxing is well known, this sport continuous to attract athletes and an increase of introduction to boxing is observed in the last decade. In terms of injury locations, head and face are reported as most common sports. Present study aimed to examine the hearing differences of elite amateur boxers as a result of punch strokes in boxing. Subjects are interested in active boxing for 5-14 years (mean 6.67) and between the age of 18-32 (mean 21.71). Screened group consisted of 21 male boxers. Auditory brainstem responses, pure tone and high frequency audiogram tests were conducted for boxers and unscreened groups in the standard acoustically controlled rooms using Interacoustics Clinical Computer Audiometer. Mean ± standard deviations are reported. Groups were compared by Student's t test p<0.05. Auditory brainstem responses and pure tone values were determined in range of I-V inter-pick latency (ms). There were no statistically significant differences in the hearing level of elite amateur boxers in contrast to non-boxers. It is seen to be important that amateur boxers wear protective materials as a helmet and mouth guard to minimize the risk of injury. The use of protective equipment must be encouraged for boxer's health.
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CATASTROPHIC brain injury following minor impact has been known to occur in contact sports, particularly football.1 This peculiar susceptibility remains unexplained. However, the common resumption of contact play soon after concussion suggests that sequential minor impacts may occasionally lead to major cerebral pathological conditions. If these injuries have a compounding effect rather than representing isolated events, then additional impact to an already compliance-compromised brain might precipitate a catastrophic increase in intracranial pressure, perhaps through loss of vasomotor tone. We report a case documenting a preexisting cerebral contusion and the lethal effect of a second minor impact. This case suggests that clinical examination alone may sometimes be inadequate in evaluating persisting symptoms after minor head injury. In the athlete who has had a cerebral concussion, computed tomographic (CT) scanning may be required before medical clearance to resume play is justified.Report of a Case A 19-year-old, right-handed, college football player
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The Concussion Resolution Index (CRI) is an online assessment tool designed to track resolution of symptoms following sports-related concussion. The CRI is composed of six subtests measuring reaction time, visual recognition, and speed of information processing. Three factors are derived from the subtests: Simple Reaction Time (SRT), Complex Reaction Time (CRT), and Processing Speed (PS). Multiple alternate forms within subtests afford simple, reliable, assessment of change, relative to a baseline test completed by an athlete. The test also assesses self-reported neurophysiological symptoms at the time of injury and tracks resolution of these symptoms. The data demonstrate the CRI is a valid and reliable measure of cognitive performance in a relatively heterogeneous group of athletes aged 13–35. Two methods of statistical analysis for assessing change from baseline were compared to establish a psychometric basis for return-to-play decision-making: the Reliable Change Index (RCI) and multiple regression. Multiple regression was more accurate than the RCI in determining a decline in performance relative to the baseline.
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SYNOPSIS The brains of 15 retired boxers have been studied and the lives of the men concerned have been investigated in retrospect. A characteristic pattern of cerebral change has been identified which appears not only to be a result of the boxing but also to underlie many features of the punch-drunk syndrome.
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For some time fight fans and promoters have recognized a peculiar condition occurring among prize fighters which, in ring parlance, they speak of as "punch drunk." Fighters in whom the early symptoms are well recognized are said by the fans to be "cuckoo," "goofy," "cutting paper dolls," or "slug nutty."Punch drunk most often affects fighters of the slugging type, who are usually poor boxers and who take considerable head punishment, seeking only to land a knockout blow. It is also common in second rate fighters used for training purposes, who may be knocked down several times a day. Frequently it takes a fighter from one to two hours to recover from a severe blow to the head or jaw. In some cases consciousness may be lost for a considerable period of time.The early symptoms of punch drunk usually appear in the extremities. There may be only an occasional
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OBJECTIVE: To conduct a topic review of studies related to cerebral concussion in athletes, as an aid to improving decision-making and outcomes. METHODS: We review the literature to provide an historical perspective on the incidence and definition of and the management guidelines for mild traumatic brain injury in sports. In addition, metabolic changes resulting from cerebral concussion and the second-impact syndrome are reviewed, to provide additional principles for decision-making. Neuropsychological testing, as it applies to athletes, is discussed in detail, to delineate baseline assessments, the characteristics of the neuropsychological evaluation, the neuropsychological tests used, and the methods for in-season identification of cerebral concussion. Future directions in the management of concussions are presented. RESULTS: The incidence of cerebral concussions has been reduced from approximately 19 per 100 participants in football per season to approximately 4 per 100, i.e., 40,000 to 50,000 concussions per year in football alone. The most commonly used definitions of concussion are those proposed by Cantu and the American Academy of Neurology. Each has associated management guidelines. Concussion or loss of consciousness occurs when the extracellular potassium concentration increases beyond the upper normal limit of approximately 4 to 5 mmol/L, to levels of 20 to 50 mmol/L, inhibiting the action potential and leading to loss of consciousness. This phenomenon helps to explain the delayed effects of symptoms after trauma. CONCLUSION: Neuropsychological testing seems to be an effective way to obtain useful data on the short-term and long-term effects of mild traumatic brain injury. Moreover, knowledge of the various definitions and management strategies, as well as the utility of neuropsychological testing, is essential for those involved in decision-making with athletes with mild traumatic brain injuries.
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The majority of boxing-related fatalities result from traumatic brain injury. Biomechanical forces in boxing result in rotational acceleration with resultant subdural hematoma and diffuse axonal injury. Given the inherent risk and the ongoing criticism boxing has received, we evaluated mortalities associated with professional boxing. We used the Velaquez Fatality Collection of boxing injuries and supplementary sources to analyze mortality from 1950 to 2007. Variables evaluated included age at time of death, association with knockout or other outcome of match, rounds fought, weight class, location of fight, and location of pretermial event. There were 339 mortalities between 1950 and 2007 (mean age, 24 ± 3.8 years); 64% were associated with knockout and 15% with technical knockout. A higher percentage occurred in the lower weight classes. The preterminal event occurred in the ring (61%), in the locker room (17%), and outside the arena (22%), We evaluated for significant changes after 1983 when championship bouts were reduced from 15 to 12 rounds. There was a significant decline in mortality after 1983. We found no significant variables to support that this decline is related to a reduction in rounds. Rather, we hypothesize the decline to be the result of a reduction in exposure to repetitive head trauma (shorter careers and fewer fights), along with increased medical oversight and stricter safety regulations. Increased efforts should be made to improve medical supervisions of boxers. Mandatory central nervous system imaging after a knockout could lead to a significant reduction in associated mortality.
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Epidemiological evidence suggests that the incidence of amyotrophic lateral sclerosis is increased in association with head injury. Repetitive head injury is also associated with the development of chronic traumatic encephalopathy (CTE), a tauopathy characterized by neurofibrillary tangles throughout the brain in the relative absence of β-amyloid deposits. We examined 12 cases of CTE and, in 10, found a widespread TAR DNA-binding protein of approximately 43kd (TDP-43) proteinopathy affecting the frontal and temporal cortices, medial temporal lobe, basal ganglia, diencephalon, and brainstem. Three athletes with CTE also developed a progressive motor neuron disease with profound weakness, atrophy, spasticity, and fasciculations several years before death. In these 3 cases, there were abundant TDP-43-positive inclusions and neurites in the spinal cord in addition to tau neurofibrillary changes, motor neuron loss, and corticospinal tract degeneration. The TDP-43 proteinopathy associated with CTE is similar to that found in frontotemporal lobar degeneration with TDP-43 inclusions, in that widespread regions of the brain are affected. Akin to frontotemporal lobar degeneration with TDP-43 inclusions, in some individuals with CTE, the TDP-43 proteinopathy extends to involve the spinal cord and is associated with motor neuron disease. This is the first pathological evidence that repetitive head trauma experienced in collision sports might be associated with the development of a motor neuron disease.
Article
The majority of boxing-related fatalities result from traumatic brain injury. Biomechanical forces in boxing result in rotational acceleration with resultant subdural hematoma and diffuse axonal injury. Given the inherent risk and the ongoing criticism boxing has received, we evaluated mortalities associated with professional boxing. We used the Velazquez Fatality Collection of boxing injuries and supplementary sources to analyze mortality from 1950 to 2007. Variables evaluated included age at time of death, association with knockout or other outcome of match, rounds fought, weight class, location of fight, and location of preterminal event. There were 339 mortalities between 1950 and 2007 (mean age, 24 +/- 3.8 years); 64% were associated with knockout and 15% with technical knockout. A higher percentage occurred in the lower weight classes. The preterminal event occurred in the ring (61%), in the locker room (17%), and outside the arena (22%). We evaluated for significant changes after 1983 when championship bouts were reduced from 15 to 12 rounds. There was a significant decline in mortality after 1983. We found no significant variables to support that this decline is related to a reduction in rounds. Rather, we hypothesize the decline to be the result of a reduction in exposure to repetitive head trauma (shorter careers and fewer fights), along with increased medical oversight and stricter safety regulations. Increased efforts should be made to improve medical supervision of boxers. Mandatory central nervous system imaging after a knockout could lead to a significant reduction in associated mortality.
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There have been a handful of previously published cases of athletes who were still symptomatic from a prior head injury, and then suffered a second injury in which a thin, acute subdural hematoma (SDH) with unilateral hemisphere vascular engorgement was demonstrated on CT scan. In those cases, the cause of the brain swelling/dysautoregulation was ascribed to the presence of the acute SDH rather than to the acceleration/deceleration forces that caused the SDH. We believe that the brain swelling is due to "second-impact dysautoregulation," rather than due to the effect of the SDH on the underlying hemisphere. To support our hypothesis, we present 10 additional cases of acute hemispheric swelling in association with small SDHs in athletes who received a second head injury while still symptomatic from a previous head injury. The clinical history and the unique neuroimaging features of this entity on CT are described and illustrated in detail. The CT findings included an engorged cerebral hemisphere with initial preservation of grey-white matter differentiation, and abnormal mass effect and midline shift that appeared disproportionately greater than the size of the SDH. In addition, the imaging similarities between our patients and those with non-accidental head trauma (shaken-baby syndrome) will be discussed.