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Home , Head injury, Sports injury

Br3JSports Med 1996;30:289-296 289

REVIEW

Head in

Robert C Cantu

Historical perspective because there presently is no equipment capa- If we define a direct fatality as one occurring ble of preventing this .9 20 directly from participation in the skills of a sport, as opposed to an indirect fatality which Injury recognition is one caused by systemic failure as a result of Recognition of a is easy if the ath- exertion while participating in a sport, head lete has loss of consciousness. It is the far more injury is the most frequent direct cause of frequent head injuries in which there is no loss in sport.' Furthermore, injury to the of consciousness but rather only a transient head takes on a singular importance when we loss of alertness that are much more difficult to realise the is neither capable of regenera- recognise. More than 90% of all cerebral con- tion nor, unlike many other body parts and cussions fall into this most mild category where organs, oftransplantation. Every effort must be there has not been a loss of consciousness but made to protect the athlete's head as injury can rather only a brief period of post-traumatic lead to dementia, epilepsy, , and or loss of mental alertness.'9 Because death. the dreaded second impact syndrome can Starting with President Theodore Roose- occur after a grade I , just as it can velt's threat to ban American football in 1904, after more serious. head injuries, it becomes injuries from this sport have received more very important to recognise all grades of media attention and reports in the medical lit- concussion.202' erature than any other organised sport because none has contributed more fatalities.2 Starting Mechansm of injury with the 19 athletes killed or paralysed in 1904 There are three distinct types of stress that can from American football injuries which led to be generated by an acceleration force to the the formation of the National Collegiate head. The first is compressive; the second is Athletic Association (NCAA)' as a governing tensile, the opposite of compressive and some- body to establish rules for safer athletic times called negative pressure; and the third is competition, fatalities in American football shearing-a force applied parallel to a surface. peaked in 1964 at 30.4 Between the years 1931 Uniform compressive and tensile forces are and 1986 at least 819 were directly relatively well tolerated by neural tissue but attributed to American football, most from shearing forces are extremely poorly tolerated. head injury followed by cervical spinal cord The (CSF) that sur- injury.5 Fatalities in American football from rounds the brain acts as a protective shock 1973 to 1983 exceeded the deaths in all other absorber converting focally applied external competitive combined.2 stress to compressive stress because the fluid Yet, per 100 000 participants American follows the contours of the sulci and gyri of the football is not as likely to result in a fatal head brain and distributes the force in a uniform injury as horseback riding,67 sky diving,89 or fashion. The CSF, however, does not totally car or motorcycle racing. It has about the same prevent shearing forces from being transmitted of a fatal head injury as gymnastics'0 and to the brain, especially when rotational forces ice hockey."' Other sports historically shown to are being applied to the head. These shearing have a high rate of head injury includes forces are maximal where rotational gliding is boxing,'2-4 the martial arts,'5 and rugby hindered within the brain such as at the dura Service, football,'6 though a fatal head injury in rugby is matter-brain attachments-the rough, irregu- Emerson Hospital, 18 Concord, rare."7 lar surface contacts between the brain and the Massachusetts 01742, Over the last 20 years there has been a especially prominent in the floor of the USA dramatic decrease in the most serious head frontal and middle fossa. R C Cantu injuries - especially the incidence of subdural In understanding how acceleration forces haematoma-due to multiple factors including are applied to the brain, it is important to keep Correspondence to: Dr Robert C Cantu, Chief of rule changes such as outlawing spear tackling in mind Newton's law: force = mass x Neurosurgery Service and and butt blocking in American football, equip- acceleration, or stated another way, force Director, Service of Sports ment standards, better conditioning of the divided by mass equals acceleration. There- Medicine. neck, and improved on-field medical care. The fore, an athlete's head can sustain far greater Accepted for publication reduction of the most serious neck injuries, forces without injury if the neck muscles are 1O June 1996 quadriplegia, has been less impressive likely tensed, as when the athlete sees the collision 290 Robert C Cantu

Table 1 Glasgow scale = E + M + V Table 2 Sports with helmets

Eye opening (E) Ice hockey 0.27 Spontaneous (4) Football 0.25 To speech (3) Men's lacrosse 0.19 To pain (2) Women's softball 0.11 No response (1) Rate of per 1000 athlete-exposures.25 Motor response (M) Obeys commands (6) Localised pain (5) syndrome, intracranial haemorrhage, and post- Withdraws from pain (4) concussion syndrome. Decorticate posturing (3) Decerebrate posturing (2) No response (1) CONCUSSION Verbal responses Concussion is derived from the Latin concussus Oriented which means "to shake violently". Initially it Confused conversation Inappropriate words was thought to produce only a temporary Incomprehensible words disturbance of brain function due to neuronal, No response chemical, or neuroelectrical changes without gross structural damage. We now know that coming. In this state, the mass of the head is structural damage with loss of brain cells does essentially the mass of the body. In a relaxed occur with some concussions. The most state, however, the mass of the head is common athletic head injury is concussion, essentially only its own weight and therefore with one in five high school American football the same degree of force can impart far greater players one annually.22 Furthermore, acceleration. the risk of sustaining a concussion in football is four22 to six2' times greater for the player who Injury assessment techniques has sustained a previous concussion. It can In assessing a brain injury, if the athlete is occur with direct head trauma in collisions or it must be assumed that there falls, or may occur without a direct blow to the has been a neck fracture and the neck must be head when sufficient force is applied to the immobilised. In assessing an athlete with a brain, as in a whiplash injury.24 head injury who is conscious, the level of con- The rates of concussion in some popular sciousness or alertness is the most sensitive cri- sports are listed in tables 2 and 3.25 Earlier esti- terion for both establishing the nature of the mates of concussion in American football at all head injury and for subsequent follow up. Ori- levels put the number at 250 000 per year in entation to person, place, and time should be this country alone.26 This number was based ascertained. The presence or absence of on a single survey that found that 20% of high post-traumatic amnesia, and the ability to school American football players had sustained retain new information such as the ability to some form of concussion22 and 10% of the col- repeat the names of four objects two minutes lege football players sustained concussion in after having been given them, or the ability to another study.27 Current estimates of the repeat one s assignments with certain plays of incidence of concussion in football at all levels the contest should be determined. It is also suggest that about 100 000 per year may be important to ascertain the presence, absence, more accurate (personal communication, Pow- and severity of the neurological symptoms ell J, Medical Sports Systems, Iowa City, Iowa, such as , lightheadedness, difficulty conducting ongoing surveillance of concussion with balance, coordination, and sensory or incidence in NCAA football). No matter motor function. Whereas a complete but brief whose estimates are used, the dimension ofthis involving cranial problem warrants more attention than it has , motor, sensory, and reflex testing is received thus far. appropriate, it is the mental examination and It must be realised that universal agreement especially the level of consciousness that on the definition and grading of concussion should be stressed. does not exist.2&SO This renders the evaluation of epidemiological data extremely difficult. As a neurosurgeon and team physician, I have When time permits the use of the Glasgow evaluated many football players who suffered coma scale (table 1), can be very useful in not concussion. Most of these injuries were mild only predicting the chances for recovery but and were associated with retrograde amnesia, also in assessing whether the injured athlete is which is helpful in making the diagnosis, espe- improving or deteriorating from a given head cially in mild cases. I have developed a practical injury. An initial score of greater than 11 is scheme for grading the severity of a concussion associated with more than a 90% chance of an based on the duration of unconsciousness essentially complete recovery, whereas an and/or posttraumatic amnesia (table 4)." initial score under 5 is associated with more The most mild concussion (grade I) occurs than an 80% chance of death or survival in a without loss of consciousness and the only vegetative state. neurological deficit is a brief period of or post-traumatic amnesia, by defi- Differential diagnosis nition lasting less than 30 minutes. The differential diagnosis with a head injury With the moderate (grade II) concussion includes a cerebral concussion, the second there is usually a brief period of unconscious- impact syndrome or malignant brain oedema ness, by definition not exceeding five minutes. Head injuries in sport 291

Table 3 Sports without helmets Table S Dementia pugilistica: areas ofbrain damage and resultant deficit Men's soccer 0.25 Women's soccer 0.24 Deficit Area Field hockey 0.20 Wrestling 0.20 1. Abnormalities of the septum Altered affect and memory pellucidum and the adjacent Rate of concussions per 1000 athlete-exposures.25 periventricular grey matter 2. Cerebellar scarring and nerve Slurred speech, loss of cell loss balance and coordination 3. Degeneration of the substantia Tremor Table 4 Severity ofconcussion nigra 4. The regional occurrence of Loss of intellect Grade Feature Duration offeature neurofibrillary tangles Grade 1 (mild) PTA < 30 minutes LOC None Grade 2 (moderate) PTA > 30 minutes, < 24 hours LOC < 5 minutes dementia with emotional lability, the victim Grade 3 (severe) PTA > 24 hours LOC > 5 minutes displaying little insight into his deterioration. Speech and thought become progressively PTA, post-traumatic amnesia; LOC, loss of consciousness. slower. Memory deteriorates considerably. There may be mood swings, intense irritability, and sometimes truculence leading to uninhib- Less commonly, there is no loss of conscious- ited violent behaviour. Simple fatuous cheer- ness but only a protracted period of post- fulness is, however, the most common prevail- traumatic amnesia lasting over 30 minutes but ing mood, though sometimes there is less than 24 hours. with paranoia. From the clinical Severe (grade III) concussion occurs with a standpoint, the neurologist may encounter more protracted period of unconsciousness almost any combination ofpyramidal, extrapy- lasting over five minutes. Rarely, it may occur ramidal, and cerebellar signs. Tremor and dys- with a shorter period of unconsciousness, but arthria are two of the most common findings. with a very protracted period ofpost-traumatic Corsellis et a?" described the necropsy find- amnesia lasting over 24 hours. ings in the ofmen who had been boxers. In 1991 Kelly et aP? proposed another They described a characteristic pattern of cer- guideline regarding the severity of concussion ebral change that appeared not only to be the in which the most mild concussion (grade I) result of boxing but also to underlie many fea- had no loss of consciousness and no post- tures of the punch drunk syndrome. They traumatic amnesia, but rather just a brief documented changes in the middle of the period of disorientation or confusion. A grade brain, which may shear into two layers or even II or moderate concussion was one in which be shredded by the distortions that follow there was no loss of consciousness but blows to the head. They found destruction of post-traumatic amnesia was present. In their the limbic system, a portion of the brain that guideline all athletes rendered unconscious- governs emotion and has a role in memory and ness were placed in the grade III, or severe, learning. There was a characteristic loss ofcells category. While it can be debated that post- from the cerebellum, a part of the brain that traumatic amnesia of over 24 hours may reflect governs balance and coordination. Finally, a more severe brain insult than 30 seconds of there was an unusual microscopic change unconsciousness, both guidelines will prevent widespread throughout the brain resembling the second impact syndrome, as no athlete still changes that occur with Alzheimer disease, symptomatic from a prior head injury is which causes progressive loss of intelligence, allowed to return to competition. but sufficiently different (neurofibrillary tan- Today it is recognised that after concussion gles only and no senile plaques) to be regarded the ability to process information may be as a distinct entity, unique to subjects suffering reduced,32 and the functional impairment may from blows to the head. be greater with repeated concussions.'233 Fur- thermore, these studies suggest that the damaging effects of concussion are cumulative. POSTCONCUSSION SYMPTOMS In proportion to the degree to which the A second late effect of concussion is the motion of the head is accelerated and to which postconcussion syndrome. This syndrome - these forces are imparted to the brain, concus- consisting of (especially with exer- sion may produce a shearing injury to nerve tion), dizziness, , irritability, and espe- fibres and neurones. cially impaired memory and concentration- The late effects of repeated head trauma of has been reported in football players, but its concussive or even subconcussive force leads to true incidence is not known. In my experience anatomical patterns of chronic brain injury it is uncommon. The persistence of these with correlating . Mar- symptoms reflect altered neurotransmitter tland34 first introduced the term "punch function and usually correlate with the dura- drunk" (dementia pugilistica) in 1928. Al- tion of post-traumatic amnesia.36 When these though first described in boxers, this traumatic symptoms persist, the athlete should be evalu- encephalopathy may occur in anyone subjected ated with a computed tomography (CT) scan to repeated blows to the head from any cause. and neuropsychiatric tests. Return to competi- The characteristic symptoms and signs of tion should be deferred until all symptoms the punch drunk state (table 5) include the have abated and the diagnostic studies are gradual appearance of a fatuous or euphoric normal. 292 Robert C Cantu

INTRACRANIAL HAEMORRHAGE An intracerebral haematoma is the third type The leading cause of death from athletic head of intracranial haemorrhage seen after head injury is intracranial haemorrhage. There are trauma. In this instance, the is into four types of haemorrhage, to which the exam- the brain substance itself, usually from a torn ining trainer or physician must be alert in every artery. It may also result from the rupture of a instance of head injury. Because all four types congenital vascular lesion such as an of intracranial haemorrhage may be fatal, a or arteriovenous malformation. Intracerebral rapid and accurate initial assessment, as well as haematomas are not usually associated with a appropriate follow up, is mandatory after an and may be rapidly progressive. athletic head injury. Death occasionally occurs before the injured An epidural or extradural haematoma is athlete can be moved to a hospital. Because of usually the most rapidly progressing intracra- the intense reaction such a tragic event precipi- nial haematoma. It is frequently associated tates among fellow athletes, family, students, with a fracture ofthe temporal bone and results and even the community at large, and because from a tear in one of the arteries supplying the of the inevitable rumours that follow, it is covering (dura) of the brain. The haematoma imperative to obtain a complete necropsy in accumulates inside the skull but outside the such an even to clarify the causative factors covering of the brain. Arising from a torn fully. Often the necropsy will reveal a congeni- artery, it may progress quite rapidly and reach tal lesion that may indicate that the cause of a fatal size in 30 to 60 minutes. Although this death was other than presumed and was does not always occur, the athlete may have a ultimately unavoidable. Only by such full, fac- lucid interval, that is, initially the athlete may tual elucidation will inappropriate feelings of regain consciousness after the head trauma and guilt in fellow athletes, friends, and family be before starting to experience increasing head- assuaged. ache and progressive deterioration in the level A fourth type of intracranial haemorrhage is of consciousness as the clot accumulates and subarachnoid, confined to the surface of the the increases. This lesion, brain. Following head trauma, such bleeding is if present, will almost always declare itself the result of disruption ofthe tiny surface brain within an hour or two from the time of injury. vessels and is analogous to a . As with the Usually the brain substance is free from direct intracerebral haematoma, there is often brain injury; thus, if the clot is promptly removed swelling, and such a haemorrhage can also surgically, full recovery is to be expected. result from a ruptured cerebral aneurysm or Because this lesion is rapidly and universally arteriovenous malformation. Because bleeding fatal if missed, all athletes receiving a head is superficial, surgery is not usually required injury must be closely and frequently observed unless a congenital vascular anomaly is during the ensuing several hours, preferably present. the next 24 hours. This observation should be done at a facility where full neurosurgical serv- Post-traumatic ices are immediately available. If a seizure occurs in an athlete with a head A subdural haematoma, the second type of injury, it is important to log-roll the patient intracranial haemorrhage, occurs between the onto his side. By this manoeuvre, any blood or brain surface and the dura. The acute subdural saliva will roll out of the mouth or nose, and is the leading direct cause of death in athletes.37 the tongue cannot fall back and obstruct the It is thus located under the dura and directly airway. If one has a padded tongue depressor or on the brain. It often results from a torn vein oral airway, it can be inserted between the running from the surface of the brain to the teeth. Under no circumstances should one dura. It may also result from a torn venous insert one s fingers into the mouth of an sinus or even a small artery on the surface of athlete who is having a seizure, as a traumatic the brain. With this injury, there is often asso- can easily result from such an ciated injury to the brain tissue. If a subdural unwise manoeuvre. Usually such a traumatic haematoma needs surgery in the first 24 hours, seizure will last only for a minute or two. The the mortality is high, not because of the clot athlete will then relax, and transportation to itself but because of the associated brain dam- the nearest medical facility can be effected. age. With a subdural haematoma that progresses rapidly, the athlete usually does not Malignant brain oedema syndrome regain consciousness and immediate neurosur- This condition is found in athletes in the gical evaluation is obviously required. Occa- paediatric age range and consists of rapid sionally, the brain itself will not be injured, and neurological deterioration from an alert con- a subdural haematoma may develop slowly scious state to coma and sometimes death, over a period of days to weeks. This chronic minutes to several hours after head trauma.3839 subdural haematoma, although often associ- Although this sequence in adults almost always ates with headache, may initially cause a variety is due to an intracranial clot, in children of very mild, almost imperceptible mental, pathology studies show diffuse brain swelling motor, or sensory signs and symptoms. Since with little or no brain injury.39 Rather than true its recognition and removal will lead to full cerebral , Langfitt and colleagues4041 recovery, it must always be suspected in an ath- have shown that the diffuse cerebral swelling is lete who has previously sustained a head injury the result of a true hyperaemia or vascular and who, days or weeks later, is not quite right. engorgement. Prompt recognition is extremely A computerised axial tomography scan of the important because there is little initial brain head will definitively show such a lesion. injury and the serious or fatal neurological Head injuries in sport 293

outcome is secondary to raised intracranial CT scan is usually adequate to show bleeding pressure with herniation. Prompt treatment or midline shifts of the brain requiring with intubation, hyperventilation, and osmotic neurosurgical intervention. This is important agents has helped to reduce the mortality.4243 because CT scanning is cheaper, more widely available, and more quickly performed than Second impact syndrome MRL. RECOGNISING THE SYNDROME What Saunders and Harbaugh called "the sec- ond impact syndrome of catastrophic head INCIDENCE injury" in 1984" was first described by Schnei- While the precise incidence per 100 000 der in 1973.45 The syndrome occurs when an participants is not known because the precise athlete who sustains a head injury-often a population at risk in unknown, nonetheless the concussion or worse injury, such as cerebral second impact syndrome is more common contusion-sustains a second head injury than previous reports have suggested. Between before symptoms associated with the first have 1980 and 1993, the National Center for Cata- cleared.202'1 46 strophic Research in Chapel Hill, Typically, the athlete suffers postconcus- North Carolina, USA, identified 35 probable sional symptoms after the first head injury. cases among American football players alone. These may include visual, motor, or sensory Necropsy or surgery and MRI findings con- changes and difficulty with thought and firmed 17 of these cases. An additional 18 memory processes. Before these symptoms cases, though not conclusively documented resolve-which may take days or weeks-the with necropsy findings, most probably are athlete returns to competition and receives a cases of second impact syndrome. Careful second blow to the head. scrutiny excluded this diagnosis in 22 of 57 The second blow may be remarkably minor, cases originally suspected.20 perhaps only involving a blow to the chest that Second impact syndrome is not confined to jerks the athlete's head and indirectly imparts American football players. Head injury reports accelerative forces to the brain. Affected of athletes in other sports almost certainly rep- athletes may appear stunned but usually do not resent the syndrome but do not label it as such. lose consciousness and often complete the Fekete, for example, described a 16 year old play. They usually remain on their feet for 15 high school hockey player who fell during a seconds to a minute or so but seem dazed, like game, striking the back of his head on the ice." someone suffering from a grade I concussion The boy lost consciousness and afterward without loss of consciousness. Often affected complained of unsteadiness and headaches. athletes remain on the playing field or walk off While playing in the next game four days later, under their own power. he was checked forcibly and again fell striking What happens in the next 15 seconds to sev- his left temple on the ice. His pupils rapidly eral minutes sets this syndrome apart from a became fixed and dilated, and he died within concussion or even a subdural haematoma. two hours while in transit to a neurosurgical Usually within seconds to minutes of the facility. Necropsy revealed contusions of sev- second impact, the athlete-conscious yet eral days' duration, an oedematous brain with a stunned-quite precipitously collapses to the thin layer of subdural and subarachnoid haem- ground, semicomatose with rapidly dilating orrhage, and bilateral herniation ofthe cerebel- pupils, loss of eye movement, and evidence of lar tonsils into the foramen magnum. Though respiratory failure. Fekete did not use the label "second impact The pathophysiology of second impact syndrome", the clinical course and necropsy syndrome is thought to involve a loss of findings in this case are consistent with the autoregulation of the brain's blood supply. syndrome. This loss of autoregulation leads to vascular Other cases include an 18 year old male engorgement within the cranium, which in downhill skier described by McQuillen et al,46 turn markedly increases intracranial pressure who remains in a persistent vegetative state, and leads to herniation either of the medial and a 17 year old football player described by surface (uncus) of the or lobes Kelly et al who died.28 Such cases indicate that below the tentorium or of the cerebellar tonsils the brain is vulnerable to accelerative forces in through the foramen magnum. Animal re- a variety of contact and collision sports. There- search has shown that vascular engorgement of fore, physicians who cover athletic events, the brain after a mild head injury is difficult if especially those in which head trauma is likely, not impossible to control.4748 The usual time must understand the second impact syndrome from second impact to brainstem failure is and be prepared to initiate emergency treat- rapid, taking two to five minutes. Once brain ment. herniation and brainstem compromise occur, ocular involvement and respiratory failure pre- cipitously ensue. Demise occurs far more rap- PREVENTION IS PRIMARY idly than usually seen with an epidural For a catastrophic condition that has a haematoma. mortality rate approaching 50% and a morbid- Magnetic resonance imaging (MRI) and CT ity rate nearing 100%, prevention takes on the scan are the neuroimaging studies most likely utmost importance. An athlete who is sympto- to demonstrate the second impact syndrome. matic from a head injury must not participate in While MRI is the more sensitive to traumatic contact or collision sports until all cerebral brain injuries, especially true oedema,4950 the symptoms have subsided, and preferably not 294 Robert C Cantu

for at least one week after. Whether it takes Table 6 Guidelines for return to sports after concussion days, weeks, or months to reach the asympto- First Second Third matic state, the athlete must never be allowed concussion concussion concussion to practice or compete while still suffering Grade 1 May return to Return to Terminate postconcussion symptoms. (mild) play if play in 2 season; may Players and parents as well as the physician asymptomatic weeks if return to play and medical team must understand this. Files for 1 week asymptomatic next season if of the National Center for Catastrophic Sport at that time asymptomatic for 1 week Injury Research include cases ofyoung athletes Grade 2 Return to Minimum of Terminate who did not report their cerebral symptoms. (moderate) play after 1 month; may season; may Fearing they would not be allowed to compete asymptomatic return to play return to play for 1 week then if next season if and not knowing they were jeopardising their asymptomatic asymptomatic lives, they played with postconcussional symp- for 1 week; toms and tragically developed second impact consider terminating syndrome. season Grade 3 Minimum of Terminate (severe) 1 month; may season; may then return to return to play play if next season This condition results when severe shearing asymptomatic forces are imparted to the brain and axonal connections are literally severed, in the absence WHEN TO OPERATE of intracranial haematoma. The patient is usu- Closed head injuries such as concussion and ally deeply comatose with a low Glasgow coma diffuse axonal injury ofthe brain do not require scale and a negative head CT. Immediate surgery. However, significant intracranial neurological for treatment of increased blood accumulations, whether epidural, sub- intracranial pressure is indicated. dural, or intracerebral, may require prompt surgical evacuation. Congenital vascular anomalies such as an aneurysm or arterial Management guidelines venous malformation may require planned IMMEDIATE TREATMENT deliberate surgical intervention. With a head injury the ABCs of first aid must be followed. Before a neurological examination APPROPRIATE TIME COURSE FOR RESOLUTION is undertaken, the treating physician must Table 6 provides guidelines for return to com- determine if the airway is adequate, and that petition after a cerebral concussion whether circulation is being maintained. Thereafter grade I, grade II, or grade III, and whether this attention may be directed to the neurological was a first, second, or third concussion examination. sustained in a given season. I believe it is important to realise that other concussion DEFINITIVE TREATMENT guidelines exist."' While none are in precise Definitive treatment of grade II and grade III agreement as to the timing of return to sport concussions as well as of the second impact after the various degrees and numbers of con- syndrome and intracranial haematoma should cussions received in a given season, and thus all take place at a medical facility where neurosur- are truly only guidelines, all do agree on the gical and neuroradiological capabilities are most salient point-that is, that no athlete still present. In the case of the intracranial hae- symptomatic from a previous injury should be matoma, definitive surgical evacuation is indi- allowed to risk a second head injury, either by cated, and in cases of the closed head injuries practice or by event participation. Therefore, and more severe degrees of concussion, obser- while the grading and return dates may vary vation is appropriate, with careful neurological slightly, all the guidelines will prevent the monitoring. dreaded second impact syndrome. An athlete who has sustained a second impact syndrome who is in the small that survives WHAT TESTS TO ORDER AND WHEN and minority After a grade I concussion, observation alone without significant morbidity would not be may be all that is indicated. In instances of allowed to return to a contact or collision grade II and grade III concussion, however, a sport. So too an athlete who has undergone CT scan or MRI of the brain in recommended. surgery for an intracranial haemorrhage would It is recommended that these athletes be be ill advised to return to contact or collision removed from the contest and sent to a defini- sports, as both the surgery and the underlying tive neurological facility where such imaging haemorrhage have caused an alteration of CSF can take place upon arrival. In the case of the fluid dynamics and the ability of the CSF fluid second impact syndrome and intracranial to protect the brain from subsequent head haemorrhage, urgent scanning with either a injury. CT or MRI is also appropriate. A final comment on concussions WHEN TO REFER Following a concussion, a thorough review of All head injuries other than a grade I the circumstances resulting in the concussion concussion should be referred for neurological should occur. In my long experience as a team or neurosurgical evaluation following removal physician, those athletes subjected to repeated of the athlete from the contest. concussions were often using their head Head injuries in sport 295

Table 7 Conditions that contraindicate competition in the NOCSAE, whose research has led to contact sports improved and better fitting headgear and the 1. Persistent post concussion symptoms recognition of the need to discard or renovate 2. Permanent central neurological sequelae from head injury worn equipment, the risk of head injury has (eg, organic dementia, hemiplegia, homonymous been reduced. Finally, the risk of head injury hemianopsia) 3. has been lessened by improved medical super- 4. Spontaneous subarachnoid haemorrhage from any cause vision, especially in the areas of on-field recog- 5. Symptomatic neurological or pain-producing abnormalities nition and treatment ofhead injuries and guid- about the foramen magnum ance for return to competition after such injuries. unwisely, illegally, or both. If available, vide- otapes of the incident should be reviewed by Conclusion the team physician, trainer, coach, and player Although fatalities and catastrophic head to see if this was a factor. Equipment should injury will never be totally eliminated from also be checked to be certain that it fits athletics, their occurrence, especially in Ameri- precisely, that the athlete is wearing it properly, can football, is now low compared to previous and that it is being maintained, especially the decades. This reduction in incidence and air pressure in air helmets. Finally, neck severity of athletic head injury has been the strength and development should be assessed. result of changes and improvements instituted following constant study and research. Intracranial haemorrhage The initial management of intracranial haem- Summary orrhage, whether epidural, subdural, intracer- Injuries to the head and neck are the most fre- ebral, or subarachnoid, is the same as for a quent catastrophic sports injury, and head grade III concussion, that is, prompt triage injuries are the most common direct athletic with the neck immobilised to a hospital with cause of death. Although direct compressive neuroradiological and neurosurgery capability. forces may injure the brain, neural tissue is There the diagnosis is established by head CT particularly susceptible to injury from shearing or MRI scanning. The surgical treatment of stresses, which are most likely to occur when each of these conditions is beyond the scope of rotational forces are applied to the head. this review. The most common athletic head injury is Table 7 lists conditions that contraindicate concussion, which may vary widely in severity. returning to contact sports after a head injury. Intracranial haemorrhage is the leading cause These include spontaneous subarachnoid of head injury death in sports, making rapid haemorrhage or permanent neurological defi- initial assessment and appropriate follow up cit from a brain injury. This leaves the door mandatory after a head injury. Diffuse cerebral open for an athlete who makes a complete swelling is another serious condition that may neurological recovery following any of the four be found in the child or adolescent athlete, and types of traumatic intracranial haemorrhage to the second impact syndrome is a major return to contact sports at a distant point in concern in adult athletes. time (after at least one year). Extreme delibera- Many head injuries in athletes are the result tion should occur before affirming such a deci- of improper playing techniques and can be sion. reduced by teaching proper skills and enforc- ing promoting rules. Improved condi- tioning (particularly of the neck), protective Prevention headgear, and careful medical supervision of The brain cannot be preconditioned to accept athletes will also minimise this type of injury. trauma. The reverse may actually be true; that is, once injured, the brain is more easily 1 Mueller FO, Blyth CS. Survey of catastrophic football inju- susceptible to future injury.'2 There are five ries: 1977-1983. Ptys Sportsmed 1985;13:75. 2 Kraus JF, Conroy C. Mortality and morbidity from injuries areas that can affect a reduction in head in sports and recreation. Annu Rev Public 1984;5: injuries. The first two involve rules and coaching 163. 3 Albright JP McCauley E, Mortin RK. Head and neck inju- technique changes. American football is the ries in ; an eight year analysis. Am J Sports classic example. Once it was understood that Med 1985;13:147-52. 4 Schneider RC. Football head an neck injury. Surg Neurol the most serious head and neck injuries 1987;27:505-8. occurred when the head was used as a 5 Mueller FO, Schindler RD. Annual survey offootball injury ram in research 1931-1986. Chapel Hill, NC: American Football battering the neck flexed (spearing) Coaches Association, NCAA, and National Federation of position, this tactic was made illegal through State High School Associations, 1987. rule 6 Barclay WR. Equestrian sports. JAMA 1978;000: 1892. changes. Responsible coaches stopped 7 Barber HM. Horse-play: survey of accidents with horses. teaching it, and even warned against its use. BMJ 1973;iii:532. 8 Krel FW. Parachuting for sport-study of 100 deaths. The other three areas involve improvements JAMA 1965;194:264. in conditioning (especially of the neck), equip- 9 Petras AF, Hoffman EP. Roentgenographic skeletal injury patterns in parachute jumping. Am J Sports Med 1983;11: ment, and finally medical supervision. In 325. contrast to the brain, the neck can be strength- 10 Goldberg MJ. Gymnastic injuries. Orthop Clin North Am 1980;11:717. ened and the risk of injury reduced. 11 Fekete JF. Severe brain injury and death following rigid In addition to changes in rules and coaching hockey accidents. The effectiveness of the "safety helmets" techniques reflecting an understanding of the of amateur hockey players. Can Med.AssocJf 1968-99:1234. 12 Hillman H. Boxing. 1980-8:21 1. mechanisms of head injuries, athletic head 13 Van Allen MW. The deadly, degrading sport. JAMA injuries can also be prevented by 1983;249:250. improvement 14 Lundberg GD. Boxing should be banned in civilized coun- in protective headgear. Under the guidance of tries. JAMA 1983;249:250. 296 Robert C Cantu

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