Br3JSports Med 1996;30:289-296
`
`REVIEW
`
`Head injuries in sport
`
`Robert C Cantu
`
`Historical perspective
`If we define a direct fatality as one occurring
`directly from participation in the skills of a
`sport, as opposed to an indirect fatality which
`is one caused by systemic failure as a result of
`exertion while participating in a sport, head
`injury is the most frequent direct cause of
`death in sport.' Furthermore, injury to the
`head takes on a singular importance when we
`realise the brain is neither capable of regenera-
`tion nor, unlike many other body parts and
`organs, oftransplantation. Every effort must be
`made to protect the athlete's head as injury can
`paralysis, and
`lead to dementia, epilepsy,
`death.
`Starting with President Theodore Roose-
`velt's threat to ban American football in 1904,
`injuries from this sport have received more
`media attention and reports in the medical lit-
`erature than any other organised sport because
`none has contributed more fatalities.2 Starting
`with the 19 athletes killed or paralysed in 1904
`from American football injuries which led to
`the formation of the National Collegiate
`Athletic Association (NCAA)' as a governing
`for
`safer
`body to
`establish
`rules
`athletic
`competition, fatalities in American football
`peaked in 1964 at 30.4 Between the years 1931
`and 1986 at least 819 deaths were directly
`attributed to American football, most from
`head injury followed by cervical spinal cord
`injury.5 Fatalities in American football from
`1973 to 1983 exceeded the deaths in all other
`competitive sports combined.2
`Yet, per 100 000 participants American
`football is not as likely to result in a fatal head
`injury as horseback riding,67 sky diving,89 or
`car or motorcycle racing. It has about the same
`risk of a fatal head injury as gymnastics'0 and
`ice hockey."' Other sports historically shown to
`have a high rate of head injury includes
`boxing,'2-4
`arts,'5 and rugby
`the
`martial
`football,'6 though a fatal head injury in rugby is
`rare."7 18
`Over the last 20 years there has been a
`dramatic decrease in the most serious head
`injuries - especially the incidence of subdural
`haematoma-due to multiple factors including
`rule changes such as outlawing spear tackling
`and butt blocking in American football, equip-
`ment standards, better conditioning of the
`neck, and improved on-field medical care. The
`reduction of the most serious neck injuries,
`quadriplegia, has been less impressive likely
`
`because there presently is no equipment capa-
`ble of preventing this injury.9 20
`Injury recognition
`Recognition of a head injury is easy if the ath-
`lete has loss of consciousness. It is the far more
`frequent head injuries in which there is no loss
`of consciousness but rather only a transient
`loss of alertness that are much more difficult to
`recognise. More than 90% of all cerebral con-
`cussions fall into this most mild category where
`there has not been a loss of consciousness but
`rather only a brief period of post-traumatic
`amnesia or loss of mental alertness.'9 Because
`the dreaded second impact syndrome can
`occur after a grade I concussion, just as it can
`after more serious. head injuries, it becomes
`very important to recognise all grades of
`concussion.202'
`Mechansm ofinjury
`There are three distinct types of stress that can
`be generated by an acceleration force to the
`head. The first is compressive; the second is
`tensile, the opposite of compressive and some-
`times called negative pressure; and the third is
`shearing-a force applied parallel to a surface.
`Uniform compressive and tensile forces are
`relatively well tolerated by neural tissue but
`shearing forces are extremely poorly tolerated.
`The cerebrospinal fluid (CSF) that sur-
`rounds the brain acts as a protective shock
`absorber converting focally applied external
`stress to compressive stress because the fluid
`follows the contours ofthe sulci and gyri of the
`brain and distributes the force in a uniform
`fashion. The CSF, however, does not totally
`prevent shearing forces from being transmitted
`to the brain, especially when rotational forces
`are being applied to the head. These shearing
`forces are maximal where rotational gliding is
`hindered within the brain such as at the dura
`matter-brain attachments-the rough, irregu-
`lar surface contacts between the brain and the
`skull especially prominent in the floor of the
`frontal and middle fossa.
`In understanding how acceleration forces
`are applied to the brain, it is important to keep
`in mind Newton's law:
`force = mass x
`acceleration, or stated another way, force
`divided by mass equals acceleration. There-
`fore, an athlete's head can sustain far greater
`forces without injury if the neck muscles are
`tensed, as when the athlete sees the collision
`
`Neurosurgery Service,
`Emerson Hospital,
`Concord,
`Massachusetts 01742,
`USA
`R C Cantu
`Correspondence to:
`Dr Robert C Cantu, Chief of
`Neurosurgery Service and
`Director, Service of Sports
`Medicine.
`Accepted for publication
`1O June 1996
`
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`Table 1
`Glasgow coma scale = E + M + V
`Eye opening
`Spontaneous
`To speech
`To pain
`No response
`Motor response
`Obeys commands
`Localised pain
`Withdraws from pain
`Decorticate posturing
`Decerebrate posturing
`No response
`Verbal responses
`Oriented
`Confused conversation
`Inappropriate words
`Incomprehensible words
`No response
`
`(E)
`(4)
`(3)(2)
`(1)
`(M)
`(6)
`(5)
`(4)
`(3)(2)(1)
`
`coming. In this state, the mass of the head is
`essentially the mass of the body. In a relaxed
`state, however, the mass of the head is
`essentially only its own weight and therefore
`the same degree of force can impart far greater
`acceleration.
`Injury assessment techniques
`In assessing a brain injury, if the athlete is
`unconsciousness it must be assumed that there
`has been a neck fracture and the neck must be
`immobilised. In assessing an athlete with a
`head injury who is conscious, the level of con-
`sciousness or alertness is the most sensitive cri-
`terion for both establishing the nature of the
`head injury and for subsequent follow up. Ori-
`entation to person, place, and time should be
`or absence of
`ascertained. The presence
`post-traumatic amnesia, and the ability to
`retain new information such as the ability to
`repeat the names of four objects two minutes
`after having been given them, or the ability to
`repeat one s assignments with certain plays of
`the contest should be determined. It is also
`important to ascertain the presence, absence,
`and severity of the neurological symptoms
`such as headaches, lightheadedness, difficulty
`with balance, coordination, and sensory or
`motor function. Whereas a complete but brief
`neurological
`examination involving
`cranial
`nerve, motor, sensory, and reflex testing is
`appropriate, it is the mental examination and
`especially the level of consciousness that
`should be stressed.
`Glasgow coma scale
`When time permits the use of the Glasgow
`coma scale (table 1), can be very useful in not
`only predicting the chances for recovery but
`also in assessing whether the injured athlete is
`improving or deteriorating from a given head
`injury. An initial score of greater than 11 is
`associated with more than a 90% chance of an
`essentially complete recovery, whereas an
`initial score under 5 is associated with more
`than an 80% chance of death or survival in a
`vegetative state.
`Differential diagnosis
`The differential diagnosis with a head injury
`includes a cerebral concussion, the second
`impact syndrome or malignant brain oedema
`
`Sports with helmets
`Table 2
`Ice hockey
`Football
`Men's lacrosse
`Women's softball
`Rate of concussions per 1000 athlete-exposures.25
`syndrome, intracranial haemorrhage, and post-
`concussion syndrome.
`
`0.27
`0.25
`0.19
`0.11
`
`CONCUSSION
`Concussion is derived from the Latin concussus
`which means "to shake violently". Initially it
`was thought to produce only a temporary
`disturbance of brain function due to neuronal,
`chemical, or neuroelectrical changes without
`gross structural damage. We now know that
`structural damage with loss of brain cells does
`occur with some concussions. The most
`common athletic head injury is concussion,
`with one in five high school American football
`players suffering one annually.22 Furthermore,
`the risk ofsustaining a concussion in football is
`four22 to six2' times greater for the player who
`has sustained a previous concussion. It can
`occur with direct head trauma in collisions or
`falls, or may occur without a direct blow to the
`head when sufficient force is applied to the
`brain, as in a whiplash injury.24
`The rates of concussion in some popular
`sports are listed in tables 2 and 3.25 Earlier esti-
`mates of concussion in American football at all
`levels put the number at 250 000 per year in
`this country alone.26 This number was based
`on a single survey that found that 20% of high
`school American football players had sustained
`some form of concussion22 and 10% ofthe col-
`lege football players sustained concussion in
`another study.27 Current estimates of the
`incidence of concussion in football at all levels
`suggest that about 100 000 per year may be
`more accurate (personal communication, Pow-
`ell J, Medical Sports Systems, Iowa City, Iowa,
`conducting ongoing surveillance of concussion
`incidence in NCAA football). No matter
`whose estimates are used, the dimension ofthis
`problem warrants more attention than it has
`received thus far.
`It must be realised that universal agreement
`on the definition and grading of concussion
`does not exist.2&SO This renders the evaluation
`of epidemiological data extremely difficult. As
`a neurosurgeon and team physician, I have
`evaluated many football players who suffered
`concussion. Most of these injuries were mild
`and were associated with retrograde amnesia,
`which is helpful in making the diagnosis, espe-
`cially in mild cases. I have developed a practical
`scheme for grading the severity of a concussion
`based on the duration of unconsciousness
`and/or posttraumatic amnesia (table 4)."
`The most mild concussion (grade I) occurs
`without loss of consciousness and the only
`brief period
`of
`neurological
`deficit
`is
`a
`confusion or post-traumatic amnesia, by defi-
`nition lasting less than 30 minutes.
`With the moderate (grade II) concussion
`there is usually a brief period of unconscious-
`ness, by definition not exceeding five minutes.
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`Sports without helmets
`Table 3
`Men's soccer
`Women's soccer
`Field hockey
`Wrestling
`Rate of concussions per 1000 athlete-exposures.25
`
`0.25
`0.24
`0.20
`0.20
`
`Table 4
`Grade
`Grade 1 (mild)
`Grade 2 (moderate)
`Grade 3 (severe)
`
`Severity ofconcussion
`Duration offeature
`Feature
`< 30 minutes
`PTA
`LOC
`None
`> 30 minutes, < 24 hours
`PTA
`< 5 minutes
`LOC
`PTA
`> 24 hours
`LOC
`> 5 minutes
`PTA, post-traumatic amnesia; LOC, loss of consciousness.
`
`Less commonly, there is no loss of conscious-
`ness but only a protracted period of post-
`traumatic amnesia lasting over 30 minutes but
`less than 24 hours.
`Severe (grade III) concussion occurs with a
`more protracted period of unconsciousness
`lasting over five minutes. Rarely, it may occur
`with a shorter period of unconsciousness, but
`with a very protracted period ofpost-traumatic
`amnesia lasting over 24 hours.
`aP?
`In 1991 Kelly et
`proposed another
`guideline regarding the severity of concussion
`in which the most mild concussion (grade I)
`had no loss of consciousness and no post-
`traumatic amnesia, but rather just a brief
`period of disorientation or confusion. A grade
`II or moderate concussion was one in which
`there was no loss
`of consciousness but
`post-traumatic amnesia was present. In their
`guideline all athletes rendered unconscious-
`ness were placed in the grade III, or severe,
`category. While it can be debated that post-
`traumatic amnesia of over 24 hours may reflect
`a more severe brain insult than 30 seconds of
`unconsciousness, both guidelines will prevent
`the second impact syndrome, as no athlete still
`symptomatic from a prior head injury is
`allowed to return to competition.
`Today it is recognised that after concussion
`the ability to process information may be
`reduced,32 and the functional impairment may
`be greater with repeated concussions.'233 Fur-
`thermore,
`these
`that
`studies
`the
`suggest
`damaging effects of concussion are cumulative.
`In proportion to the degree to which the
`motion of the head is accelerated and to which
`these forces are imparted to the brain, concus-
`sion may produce a shearing injury to nerve
`fibres and neurones.
`The late effects of repeated head trauma of
`concussive or even subconcussive force leads to
`anatomical patterns of chronic brain injury
`with correlating signs and symptoms. Mar-
`tland34
`first introduced the term "punch
`drunk" (dementia pugilistica) in 1928. Al-
`though first described in boxers, this traumatic
`encephalopathy may occur in anyone subjected
`to repeated blows to the head from any cause.
`The characteristic symptoms and signs of
`the punch drunk state (table 5) include the
`gradual appearance of a fatuous or euphoric
`
`Dementia pugilistica: areas ofbrain damage and
`Table S
`resultant deficit
`Deficit
`1. Abnormalities of the septum
`pellucidum and the adjacent
`periventricular grey matter
`2. Cerebellar scarring and nerve
`Slurred speech, loss of
`cell loss
`balance and coordination
`3. Degeneration of the substantia Tremor
`nigra
`4. The regional occurrence of
`Loss of intellect
`neurofibrillary tangles
`
`Area
`Altered affect and memory
`
`dementia with emotional lability, the victim
`displaying little insight into his deterioration.
`Speech and thought become progressively
`slower. Memory deteriorates
`considerably.
`There may be mood swings, intense irritability,
`and sometimes truculence leading to uninhib-
`ited violent behaviour. Simple fatuous cheer-
`fulness is, however, the most common prevail-
`mood,
`though
`ing
`sometimes
`there
`is
`depression with paranoia. From the clinical
`standpoint, the neurologist may encounter
`almost any combination ofpyramidal, extrapy-
`ramidal, and cerebellar signs. Tremor and dys-
`arthria are two of the most common findings.
`Corsellis et a?" described the necropsy find-
`ings in the brains ofmen who had been boxers.
`They described a characteristic pattern of cer-
`ebral change that appeared not only to be the
`result of boxing but also to underlie many fea-
`tures of the punch drunk syndrome. They
`documented changes in the middle of the
`brain, which may shear into two layers or even
`be shredded by the distortions that follow
`blows to the head. They found destruction of
`the limbic system, a portion of the brain that
`governs emotion and has a role in memory and
`learning. There was a characteristic loss ofcells
`from the cerebellum, a part of the brain that
`governs balance and coordination. Finally,
`there was an unusual microscopic change
`widespread throughout the brain resembling
`changes that occur with Alzheimer disease,
`which causes progressive loss of intelligence,
`but sufficiently different (neurofibrillary tan-
`gles only and no senile plaques) to be regarded
`as a distinct entity, unique to subjects suffering
`from blows to the head.
`
`POSTCONCUSSION SYMPTOMS
`A second late effect of concussion is the
`postconcussion syndrome. This syndrome -
`consisting of headache (especially with exer-
`tion), dizziness, fatigue, irritability, and espe-
`cially impaired memory and concentration-
`has been reported in football players, but its
`true incidence is not known. In my experience
`is uncommon. The persistence of these
`it
`symptoms reflect
`neurotransmitter
`altered
`function and usually correlate with the dura-
`tion of post-traumatic amnesia.36 When these
`symptoms persist, the athlete should be evalu-
`ated with a computed tomography (CT) scan
`and neuropsychiatric tests. Return to competi-
`tion should be deferred until all symptoms
`have abated and the diagnostic studies are
`normal.
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`INTRACRANIAL HAEMORRHAGE
`The leading cause of death from athletic head
`injury is intracranial haemorrhage. There are
`four types ofhaemorrhage, to which the exam-
`ining trainer or physician must be alert in every
`instance of head injury. Because all four types
`of intracranial haemorrhage may be fatal, a
`rapid and accurate initial assessment, as well as
`appropriate follow up, is mandatory after an
`athletic head injury.
`An epidural or extradural haematoma is
`usually the most rapidly progressing intracra-
`nial haematoma. It is frequently associated
`with a fracture ofthe temporal bone and results
`from a tear in one of the arteries supplying the
`covering (dura) of the brain. The haematoma
`accumulates inside the skull but outside the
`covering of the brain. Arising from a torn
`artery, it may progress quite rapidly and reach
`a fatal size in 30 to 60 minutes. Although this
`does not always occur, the athlete may have a
`lucid interval, that is, initially the athlete may
`regain consciousness after the head trauma and
`before starting to experience increasing head-
`ache and progressive deterioration in the level
`of consciousness as the clot accumulates and
`the intracranial pressure increases. This lesion,
`if present, will almost always declare itself
`within an hour or two from the time of injury.
`Usually the brain substance is free from direct
`injury; thus, if the clot is promptly removed
`surgically, full recovery is to be expected.
`Because this lesion is rapidly and universally
`fatal if missed, all athletes receiving a head
`injury must be closely and frequently observed
`during the ensuing several hours, preferably
`the next 24 hours. This observation should be
`done at a facility where full neurosurgical serv-
`ices are immediately available.
`A subdural haematoma, the second type of
`intracranial haemorrhage, occurs between the
`brain surface and the dura. The acute subdural
`is the leading direct cause of death in athletes.37
`It is thus located under the dura and directly
`on the brain. It often results from a torn vein
`running from the surface of the brain to the
`dura. It may also result from a torn venous
`sinus or even a small artery on the surface of
`the brain. With this injury, there is often asso-
`ciated injury to the brain tissue. If a subdural
`haematoma needs surgery in the first 24 hours,
`the mortality is high, not because of the clot
`itself but because of the associated brain dam-
`With
`subdural haematoma that
`age.
`a
`progresses rapidly, the athlete usually does not
`regain consciousness and immediate neurosur-
`gical evaluation is obviously required. Occa-
`sionally, the brain itself will not be injured, and
`a subdural haematoma may develop slowly
`over a period of days to weeks. This chronic
`subdural haematoma, although often associ-
`ates with headache, may initially cause a variety
`of very mild, almost imperceptible mental,
`motor, or sensory signs and symptoms. Since
`its recognition and removal will lead to full
`recovery, it must always be suspected in an ath-
`lete who has previously sustained a head injury
`and who, days or weeks later, is not quite right.
`A computerised axial tomography scan of the
`head will definitively show such a lesion.
`
`An intracerebral haematoma is the third type
`of intracranial haemorrhage seen after head
`trauma. In this instance, the bleeding is into
`the brain substance itself, usually from a torn
`artery. It may also result from the rupture of a
`congenital vascular lesion such as an aneurysm
`or arteriovenous malformation. Intracerebral
`haematomas are not usually associated with a
`lucid interval and may be rapidly progressive.
`Death occasionally occurs before the injured
`athlete can be moved to a hospital. Because of
`the intense reaction such a tragic event precipi-
`tates among fellow athletes, family, students,
`and even the community at large, and because
`of the inevitable rumours that follow, it
`is
`imperative to obtain a complete necropsy in
`such an even to clarify the causative factors
`fully. Often the necropsy will reveal a congeni-
`tal lesion that may indicate that the cause of
`death was other than presumed and was
`ultimately unavoidable. Only by such full, fac-
`tual elucidation will inappropriate feelings of
`guilt in fellow athletes, friends, and family be
`assuaged.
`A fourth type of intracranial haemorrhage is
`subarachnoid, confined to the surface of the
`brain. Following head trauma, such bleeding is
`the result ofdisruption ofthe tiny surface brain
`vessels and is analogous to a bruise. As with the
`intracerebral haematoma, there is often brain
`swelling, and such a haemorrhage can also
`result from a ruptured cerebral aneurysm or
`arteriovenous malformation. Because bleeding
`is superficial, surgery is not usually required
`congenital
`unless
`vascular anomaly is
`a
`present.
`Post-traumatic seizure
`If a seizure occurs in an athlete with a head
`injury, it is important to log-roll the patient
`onto his side. By this manoeuvre, any blood or
`saliva will roll out of the mouth or nose, and
`the tongue cannot fall back and obstruct the
`airway. Ifone has a padded tongue depressor or
`oral airway, it can be inserted between the
`teeth. Under no circumstances should one
`insert one s fingers into the mouth of an
`athlete who is having a seizure, as a traumatic
`amputation can easily result from such an
`unwise manoeuvre. Usually such a traumatic
`seizure will last only for a minute or two. The
`athlete will then relax, and transportation to
`the nearest medical facility can be effected.
`Malignant brain oedema syndrome
`This condition is found in athletes in the
`paediatric age range and consists of rapid
`neurological deterioration from an alert con-
`scious state to coma and sometimes death,
`minutes to several hours after head trauma.3839
`Although this sequence in adults almost always
`is due to an intracranial clot, in children
`pathology studies show diffuse brain swelling
`with little or no brain injury.39 Rather than true
`cerebral edema, Langfitt and colleagues4041
`have shown that the diffuse cerebral swelling is
`the result of a true hyperaemia or vascular
`engorgement. Prompt recognition is extremely
`important because there is little initial brain
`injury and the serious or fatal neurological
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`outcome is secondary to raised intracranial
`pressure with herniation. Prompt treatment
`with intubation, hyperventilation, and osmotic
`agents has helped to reduce the mortality.4243
`Second impact syndrome
`RECOGNISING THE SYNDROME
`What Saunders and Harbaugh called "the sec-
`ond impact syndrome of catastrophic head
`injury" in 1984" was first described by Schnei-
`der in 1973.45 The syndrome occurs when an
`athlete who sustains a head injury-often a
`concussion or worse injury, such as cerebral
`contusion-sustains a second head injury
`before symptoms associated with the first have
`cleared.202'1 46
`Typically, the athlete suffers postconcus-
`sional symptoms after the first head injury.
`These may include visual, motor, or sensory
`changes and difficulty with thought and
`memory processes. Before these symptoms
`resolve-which may take days or weeks-the
`athlete returns to competition and receives a
`second blow to the head.
`The second blow may be remarkably minor,
`perhaps only involving a blow to the chest that
`jerks the athlete's head and indirectly imparts
`forces
`the brain. Affected
`accelerative
`to
`athletes may appear stunned but usually do not
`lose consciousness and often complete the
`play. They usually remain on their feet for 15
`seconds to a minute or so but seem dazed, like
`someone suffering from a grade I concussion
`without loss of consciousness. Often affected
`athletes remain on the playing field or walk off
`under their own power.
`What happens in the next 15 seconds to sev-
`eral minutes sets this syndrome apart from a
`concussion or even a subdural haematoma.
`Usually within seconds to minutes of the
`second impact, the athlete-conscious yet
`stunned-quite precipitously collapses to the
`ground, semicomatose with rapidly dilating
`pupils, loss of eye movement, and evidence of
`respiratory failure.
`The pathophysiology
`of second impact
`syndrome is thought to involve a loss of
`autoregulation of the brain's blood supply.
`This loss of autoregulation leads to vascular
`engorgement within the cranium, which in
`turn markedly increases intracranial pressure
`and leads to herniation either of the medial
`surface (uncus) of the temporal lobe or lobes
`below the tentorium or of the cerebellar tonsils
`through the foramen magnum. Animal re-
`search has shown that vascular engorgement of
`the brain after a mild head injury is difficult if
`not impossible to control.4748 The usual time
`from second impact to brainstem failure is
`rapid, taking two to five minutes. Once brain
`herniation and brainstem compromise occur,
`ocular involvement and respiratory failure pre-
`cipitously ensue. Demise occurs far more rap-
`idly than usually seen with an epidural
`haematoma.
`Magnetic resonance imaging (MRI) and CT
`scan are the neuroimaging studies most likely
`to demonstrate the second impact syndrome.
`While MRI is the more sensitive to traumatic
`brain injuries, especially true oedema,4950 the
`
`CT scan is usually adequate to show bleeding
`requiring
`or midline
`shifts
`of the
`brain
`neurosurgical intervention. This is important
`because CT scanning is cheaper, more widely
`available, and more quickly performed than
`MRL.
`
`INCIDENCE
`While the precise incidence per 100 000
`participants is not known because the precise
`population at risk in unknown, nonetheless the
`second impact syndrome is more common
`than previous reports have suggested. Between
`1980 and 1993, the National Center for Cata-
`strophic Sports Injury Research in Chapel Hill,
`North Carolina, USA, identified 35 probable
`cases among American football players alone.
`Necropsy or surgery and MRI findings con-
`firmed 17 of these cases. An additional 18
`cases, though not conclusively documented
`with necropsy findings, most probably are
`cases of second impact syndrome. Careful
`scrutiny excluded this diagnosis in 22 of 57
`cases originally suspected.20
`Second impact syndrome is not confined to
`American football players. Head injury reports
`of athletes in other sports almost certainly rep-
`resent the syndrome but do not label it as such.
`Fekete, for example, described a 16 year old
`high school hockey player who fell during a
`game, striking the back ofhis head on the ice."
`The boy lost consciousness and afterward
`complained of unsteadiness and headaches.
`While playing in the next game four days later,
`he was checked forcibly and again fell striking
`his left temple on the ice. His pupils rapidly
`became fixed and dilated, and he died within
`two hours while in transit to a neurosurgical
`facility. Necropsy revealed contusions of sev-
`eral days' duration, an oedematous brain with a
`thin layer of subdural and subarachnoid haem-
`orrhage, and bilateral herniation ofthe cerebel-
`lar tonsils into the foramen magnum. Though
`Fekete did not use the label "second impact
`syndrome", the clinical course and necropsy
`findings in this case are consistent with the
`syndrome.
`Other cases include an 18 year old male
`downhill skier described by McQuillen et al,46
`who remains in a persistent vegetative state,
`and a 17 year old football player described by
`Kelly et al who died.28 Such cases indicate that
`the brain is vulnerable to accelerative forces in
`a variety ofcontact and collision sports. There-
`fore, physicians who cover athletic events,
`especially those in which head trauma is likely,
`must understand the second impact syndrome
`and be prepared to initiate emergency treat-
`ment.
`
`PREVENTION IS PRIMARY
`catastrophic
`For a
`condition that has a
`mortality rate approaching 50% and a morbid-
`ity rate nearing 100%, prevention takes on the
`utmost importance. An athlete who is sympto-
`matic from a head injury must not participate in
`contact or collision sports until all cerebral
`symptoms have subsided, and preferably not
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`for at least one week after. Whether it takes
`days, weeks, or months to reach the asympto-
`matic state, the athlete must never be allowed
`to practice or compete while still suffering
`postconcussion symptoms.
`Players and parents as well as the physician
`and medical team must understand this. Files
`of the National Center for Catastrophic Sport
`Injury Research include cases ofyoung athletes
`who did not report their cerebral symptoms.
`Fearing they would not be allowed to compete
`and not knowing they were jeopardising their
`lives, they played with postconcussional symp-
`toms and tragically developed second impact
`syndrome.
`
`Diffuse axonal injury
`This condition results when severe shearing
`forces are imparted to the brain and axonal
`connections are literally severed, in the absence
`of intracranial haematoma. The patient is usu-
`ally deeply comatose with a low Glasgow coma
`scale and a negative head CT. Immediate
`neurological triage for treatment of increased
`intracranial pressure is indicated.
`
`Management guidelines
`IMMEDIATE TREATMENT
`With a head injury the ABCs of first aid must
`be followed. Before a neurological examination
`is undertaken, the treating physician must
`determine if the airway is adequate, and that
`circulation is being maintained. Thereafter
`attention may be directed to the neurological
`examination.
`DEFINITIVE TREATMENT
`Definitive treatment of grade II and grade III
`concussions as well as of the second impact
`syndrome and intracranial haematoma should
`take place at a medical facility where neurosur-
`gical and neuroradiological capabilities are
`present. In the case of the intracranial hae-
`matoma, definitive surgical evacuation is indi-
`cated, and in cases of the closed head injuries
`and more severe degrees of concussion, obser-
`vation is appropriate, with careful neurological
`monitoring.
`WHAT TESTS TO ORDER AND WHEN
`After a grade I concussion, observation alone
`may be all that is indicated. In instances of
`grade II and grade III concussion, however, a
`CT scan or MRI ofthe brain in recommended.
`is recommended that these athletes be
`It
`removed from the contest and sent to a defini-
`tive neurological facility where such imaging
`can take place upon arrival. In the case of the
`second impact syndrome and intracranial
`haemorrhage, urgent scanning with either a
`CT or MRI is also appropriate.
`WHEN TO REFER
`other than a grade I
`All head injuries
`concussion should be referred for neurological
`or neurosurgical evaluation following removal
`of the athlete from the contest.
`
`Table 6
`
`Grade 1
`(mild)
`
`Grade 2
`(moderate)
`
`Guidelines for return to sports after concussion
`Second
`Third
`First
`concussion
`concussion
`concussion
`Terminate
`Return to
`May return to
`season; may
`play if
`play in 2
`return to play
`weeks if
`asymptomatic
`for 1 week
`asymptomatic
`next season if
`at that time
`asymptomatic
`for 1 week
`Minimum of
`Terminate
`1 month; may season; may
`return to play
`return to play
`then if
`next season if
`asymptomatic
`asymptomatic
`for 1 week;
`consider
`terminating
`season
`Minimum of
`Terminate
`1 month; may season; may
`then return to
`return to play
`play if
`next season
`asymptomatic
`
`Return to
`play after
`asymptomatic
`for 1 week
`
`Grade 3
`(severe)
`
`WHEN TO OPERATE
`Closed head injuries such as concussion and
`diffuse axonal injury ofthe brain do not require
`However,
`significant
`intracranial
`surgery.
`blood accumulations, whether epidural, sub-
`dural, or intracerebral, may require prompt
`surgical
`evacuation.
`Congenital
`vascular
`anomalies such as an aneurysm or arterial
`venous malformation may require planned
`deliberate surgical intervention.
`APPROPRIATE TIME COURSE FOR RESOLUTION
`Table 6 provides guidelines for return to com-
`petition after a cerebral concussion whether
`grade I, grade II, or grade III, and whether this
`first, second, or third concussion
`was a
`sustained in a given season. I believe it
`is
`important to realise that other concussion
`guidelines exist."' While none are in precise
`agreement as to the timing of return to sport
`after the various degrees and numbers of con-
`cussions received in a given season, and thus all
`are truly only guidelines, all do agree on the
`most salient point-that is, that no athlete still
`symptomatic from a previous injury should be
`allowed to risk a second head injury, either by
`practice or by event participation. Therefore,
`while the grading and return dates may vary
`all the guidelines will prevent the
`slightly,
`dreaded second impact syndrome. An athlete
`who has sustained a second impact syndrome
`and who is in the small minority that survives
`without significant morbidity would not be
`allowed to return to a contact or collision
`sport. So too an athlete who has undergone
`surgery for an intracranial haemorrhage would
`be ill advised to return to contact or collision
`sports, as both the surgery and the underlying
`haemorrhage have caused an alteration of CSF
`fluid dynamics and the ability of the CSF fluid
`to protect the brain from subsequent head
`injury.
`A final comment on concussions
`Following a concussion, a thorough review of
`the circumstances resulting in the conc