Head Injuries and Sport

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Chapte

r 5

- Injuries

- Head

Introduction

Mechanisms of brain injury

Forces producing brain injury

Pathophysiology of primary brain injury

Pathophysiology of secondary brain injury

Intracranial complications

Extracranial complications

Non-traumatic sports related brain injury

Cerebral air embolism

High altitude cerebral oedema

Clinical features of brain injury

Concussion

On site assessment and management of head injury

Assessment and management of the unconscious athlete

Assessment and management of the head injured conscious athlete

Gradings of concussion and return to competition

Post concussion monitoring if not hospitalised

On going management of mild head injury

Clinical assessment of recovery

Post concussion symptoms

Cumulative effects of concussion

Chronic traumatic encephalopathy

Psychometric indices of impairment and recovery

Prevention of sporting head injuries

Devices reducing the severity of the initial injury

Mouthguards


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Helmets

Selection and conditioning of individual athletes

Rules regulating play and individual participation

Education of athletes and officials - structured interview Introduction

Head injury is one of the most common forms of acquired neurological damage, particularly in

young males. Head injuries are especially prevalent in contact sports that produce collisions, in

sports where participants move or fall at high velocity and in sports that involve the use of force

imparting implements (1). The incidence is highest in combat sports, such as boxing, where the

head is a legitimate target. However, head injury is also common in contact sports such as the

various codes of football, especially gridiron, where the annual incidence may be as high as 10 -

20% of participants, and rugby, which has up to twice the risk of other (non gridiron) football

codes (2, 3). Other non-contact sports with a higher risk of head injury include motor racing,

equestrian and gymnastic events, snow, board and blade sports, and cycling. Sports where

head injury is rare but potentially severe include golf, shooting, cricket, baseball, and field

hockey.

The focus in this chapter is on brain injury. However, head injuries often involve significant

damage to scalp, skull, meninges and blood vessels as well as the face, jaws, eyes, ears and

neck. While the initial assessment and management of head injury described in this chapter

includes injuries to these other tissues and sites, the subsequent management of extra-cranial

head injuries is dealt with in Chapters 6 and 7.

The most common form of head injury in sport is an episode of concussion (Latin: concutere, to

shake violently), from which a full recovery is usual. However, any head injury can have

immediate or delayed life threatening consequences and serious long-term sequelae. As such,

all head injuries require thorough systematic assessment by the sports physician (a) to

recognise and manage the acute consequences, including the prevention of secondary brain

damage (b) to arrange the safe transfer of the injured athlete to an appropriate treatment facility

when necessary or (c) to ensure that the athlete is closely monitored for at least 24 hours and

returns to participation only when fully recovered. Finally, (d) prevention also needs to be

addressed by the sports physician.

This chapter has five main sections:

Mechanisms of brain injury, which provides a summary of the anatomical,

physiological, and pathological issues that influence management and prevention.

Clinical features of brain injury, including symptoms and signs of concussion.

On site assessment and management of head injuries.

Post acute assessment and management of concussion, which includes clinical and


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psychometric assessment of recovery and guidelines for the return to participation in

sport.

Prevention measures including athlete preparation, protective devices and rule

modifications.

Mechanisms of brain injury

Head injuries in sport usually result from direct impact of the head but can occur when the head

is subjected to forces translated from elsewhere on the body. Brain injury may be primary, due to

the direct application of physical forces damaging brain and associated vascular tissue, or

secondary, arising from intracranial and extracranial complications of injuries to the head and

other parts of the body (4, 5, 6).

Forces producing brain injury

Forces acting on the brain produce three types of tissue stress: compressive, tensile,

and shearing. Compressor forces tend to produce focal contusions and if relieved

promptly produce the least long-term consequences. Tensile (stretching) forces act

mainly on long fibre pathways and damage tends to be more diffuse (diffuse axonal

injury). Shearing forces operate parallel to surfaces and can produce serious

consequences by tearing brain and vascular tissue.

Most forces are dynamic and result in propulsion and rotation of the brain within the

cranium following impacts to either the head or body. Cerebro spinal fluid (CSF)

dissipates focally applied forces and permits gliding of the hemispheres within the

cranium.

A forceful blow to the head usually produces maximal brain injury at the site of impact

(coup injury) particularly if the head is stationary before impact. A moving head striking

a non-moveable surface, as in falls or collisions, may also produce brain injury at the

opposite pole of the cranium (contra coup injury). This is because the brain lags behind

in the moving cranium, thereby squeezing protective CSF away from the trailing pole

(Fig 1).

The magnitude of any force is the product of mass and acceleration (Newtons Law). If

the neck muscles are tensed at impact, the mass of the head approximates that of the

whole body and acceleration (or deceleration) of the head is greatly reduced for any

given force. Conversely, when the head is not braced, as in unanticipated blows or

further blows in an already stunned state, a given force produces much greater

acceleration of the head.

Pathophysiology of primary brain injury

Gliding of the brain within the cranium is impeded at three main sites (a) dura mater -


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brain attachments e.g. midline falx cerebri and tentorium cerebelli (b) irregular and

protuberant surfaces of the frontal and middle fossa of the base of the skull (c)

wherever CSF is dissipated by acceleration, especially at the poles of the frontal and

temporal lobes.

Focal contusions occur mainly at or opposite sites of impact and comprise local

petechial haemorrhages and necrotic damage, which are often accompanied by

surrounding oedema and subarachnoid haemorrhage.

Propulsion and rotation of the hemispheres on the relatively fixed brainstem may cause

damage to ascending brain stem pathways, ranging from stretching with transient

impairment of consciousness to tearing of subcortical fibre tracts with immediate

unconsciousness and coma.

General cerebral oedema due to a combination of local metabolic derangement,

breakdown of the blood-brain barrier and obstructions to venous outflow, leads to a rise

in intracranial pressure (see below).

Pathophysiology of secondary brain injury

Head injuries may result in complications that are life threatening and can have serious long-

term consequences. Because they are often remediable in their early stages, they require

immediate attention.

Intracranial complications

Intracranial complications include skull fracture, intracranial haemorrhage, raised intracranial

pressure, cerebral hypoxia, and infection.

Skull fractures may result in direct brain compression, intracranial bleeding, CSF leaks

and infection. Brain injury may occur without a skull fracture; however the presence of

a skull fracture greatly increases the risk of intracranial bleeding and infection. The site

of a fracture is also critical in anticipating complications e.g., temporo-parietal damage

to meningeal vessels, frontal damage to sinuses. Fractures may be either of the vault

or the base of the skull.

Vault fractures, which may be linear or depressed, are usually associated with scalp

haematomas or a localised area of swelling and tenderness.

Basal fractures are harder to detect and usually involve intracranial bleeding.

Periorbital haematomas, subconjunctival haemorrhage and CSF rhinorrhoea are signs

of an anterior fossa fracture; CSF otorrhoea, haemotympanum and retromastoid

bruising (Battles sign) are signs of a petrous bone fracture.

Close observation and radiological investigation are required for all suspected skull

fractures. Opinions differ on the value of routine CT scan for all mild head injuries.

Early CT scan and early discharge of patients with normal radiological and neurological


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findings has been advocated as being as safe and more cost effective than

hospitalization for observation with CT scan performed only after clinical deterioration

(7).

Intracranial haemorrhage may result in local compression, raised intracranial pressure,

and ischaemia to the area of supply of the damaged vessel. All intracranialhaematomas constitute a priority in the management of head injury because of their

immediate threat to life and eventual recovery of function and because they may be

surgically remediable. Haematomas may develop immediately or some time after the

initial injury preceded by a lucid interval. Delay in recognising and treating intracranial

bleeding is the most common cause of avoidable mortality and morbidity due to head

injury. Vigilance needs to be maintained for at least 24 hours. The four types of

intracranial haemorrhage are:

(a) Extradural haematomas result from shearing forces or skull fractures that tear blood

vessels supplying the dura and skull. Haematomas may form rapidly (high pressure bleeding

between dura and skull) and compress the brain leading to early loss of consciousness and

localising neurological signs or they may occur up to several hours following the initial injury.

(b) Subdural haematomas are the most common form of sports related intracranial bleeding.

Shearing and direct impact forces tear small veins resulting in low pressure bleeding between

the brain and dura matter. Signs and symptoms may be subtle and develop insidiously over

days or even weeks.

(c) Subarachnoid haemorrhage may result from any head injury, however mild. Severe

headache and localising signs usually develop rapidly.

(d) Intracerebral haemorrhage occurs with major brain injury. Intraventricular haemorrhage

may lead to subsequent blockade of CSF outflow. Brainstem haematomas are life threatening.

Raised intracranial pressure is a serious consequence of brain injury that may result

from several causes including depressed fractures, hypoxia, hypercapnia,

hyperperfusion, hypoperfusion, intracranial haemorrhage, and intracranial infection.

Raised intracranial pressure leads to cerebral compression, which may be followed by

herniation around the brainstem with venous obstruction and infarction. Signs include

fluctuations in consciousness, fits and focal neurological deficits.

Two rare conditions are associated with life threatening rises in intracranial pressure

after even minor head injuries (4).

Malignant brain oedema syndrome occurs in children and adolescents as diffuse brain

swelling with extreme hyperaemia. It may be due to loss of autoregulation but the

mechanism is unknown. After even relatively minor head injury, there is a deterioration

of consciousness resembling, in its rapidity, extradural bleeds in adults. Prompt


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intubation and measures to reduce intracranial pressure such as hyperventilation and

osmotic diuretics are required. The mortality rate is high.

Second impact syndrome is a variant of malignant brain oedema syndrome that is seen

in adults following even minor head trauma when still suffering symptoms of a previous

head injury. Loss of autoregulation precipitated by an unknown mechanism leads to

massive and diffuse hyperaemia and oedema of the brain. Intracranial pressure rises

within minutes and may lead to herniation and coma. Prompt measures to maintain

respiration and reduce intracranial pressure as above are indicated. The mortality rate

approaches 50% and morbidity is near to 100%.

Hypoxia due to loss of CNS control of airway patency and breathing may occur

following either serious primary injury to the brain stem or may be secondary to raised

intracranial pressure with brain herniation. Brain hypoxia may also result from

extracranial complications (see below).

Infection (meningitis or brain abscess) may occur when the dura is penetrated. Direct

contamination of the intracranial cavity may occur in compound depressed fractures of

the vault, whereas contact with middle ear cavity and nasal sinuses may introduce

infection in basal fractures.

Concussive convulsions seen within seconds of insult are to be distinguished from later

epileptic seizures. Such concussive convulsions are rare, transient and do not

necessarily lead to the development of epilepsy (8).

Post-traumatic epilepsy may develop within days to months. It usually follows traumatic

brain injury with prolonged periods of unconsciousness, and occurs in about 23% of

hospital admissions of sports-related head injury (9).

Extracranial complications

Extracranial complications of head or associated injuries may interfere with brain

metabolism and perfusion. Given the immediate dependency of brain tissue on its

oxygen supply and the potential for remediation of many of the complications,

recognition and management of extracranial causes of secondary brain damage

constitutes a clinical priority. Causes include injuries interfering with ventilation, such as

chest, neck or facial injuries that obstruct airways and affect chest movement, and

injuries interfering with brain circulation by producing haemodynamic instability and

hypovolaemia.

Non-traumatic sports related brain injury

There are two main causes of non-traumatic sports related brain injury (10).

Cerebral air embolism

unique to underwater diving, second most common cause of death after drowning


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occurs in rapid ascents from > 10 metres

symptoms may occur within moments to hours of surfacing

signs include: seizure, hemiplegia, diplopia, tunnel vision, vertigo, or dysarthria

if diver surfaces unconscious, diagnosis is strong presumption

seek to recompress subject as soon as possible

High-altitude cerebral oedema

accounts for up to 5% of deaths above 4000 metres

symptoms develop within 72 hours and include ataxia, vertigo, confusion, and

hallucinations

immediate treatment is return to lower elevation and oxygenate

monitor for signs of raised intracranial pressure and treat accordingly

Clinical features of brain injury

The primary clinical features of brain injury are loss or alteration in consciousness,

orientation and responsiveness, followed by a period of post-traumatic amnesia. Other

clinical features will depend on the nature and severity of the injury and any

supervening complications (4, 5, 6, 11)

Head injuries may be open or closed. Open head injuries may arise from skull fractures

or as a result of a penetrating missile or implement, whereas closed head injuries

usually result from blunt impacts or translation of dynamic forces to the head. There are

no universally agreed clinical criteria for classifying the severity of closed head injury

(12, 13, 14). Gradings into mild, moderate and severe categories based on the duration

of loss of consciousness, the period of post traumatic amnesia and the initial Glasgow

Coma Scale score are shown in Table 1.

About 80% of head injuries are defined as mild as they result in post traumatic amnesia

of less than 24 hours duration (15). Approximately 2/3 of these mild head injuries occur

as the result of a sporting injury (16).

Concussion

The commonest consequence of a sports head injury in concussion.

Concussion is a trauma induced transient alteration in mental status that may or may

not involve loss of consciousness. Confusion and amnesia are the hallmarks of

concussion and may be immediate or delayed by several minutes. Other neurological

features may include temporary disturbances of balance and vision (17).

Depending on severity and recency of the trauma, athletes may display some or all of

the clinical features of concussion listed in Table 2 (18).


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Signs and symptoms may occur immediately or take several minutes to evolve.

Concussed athletes may be able to continue to play automatically with sensorimotor

functions intact.

On site assessment and management of head injury

The sports physician may be required to triage and respond on site to four main categories of

head injury:

Injuries requiring resuscitation of the unconscious athlete, stabilisation and transport to

an appropriate clinical facility.

Injuries requiring withdrawal from contest and transport to an appropriate clinical

facility.

Injuries requiring withdrawal from contest and monitoring on site and at home.

Injuries sufficiently minor to permit resumption but with monitoring.

The following description refers to injuries sustained in a team game and needs to be modified

for the circumstances prevailing in individual sports.

Assessment and management of the unconscious athlete

This is an emergency that supersedes all other event considerations.

Take charge of the situation and direct others in accordance with their training and the

situation.

Institute resuscitation (DR ABC) procedure (see Table 3). Airway protection and

maintenance takes precedence over possible spinal injury.

If airway is clear, strong rhythmical breathing is present and pulse is normal, then log

roll into coma position, manually controlling head and neck, and check for other

injuries using primary survey protocol (see Tables 4 and 5).

If the athlete has required resuscitation or has not recovered consciousness or has a

GCS


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mental status examination (see Table 8 and Appendix A). If neurological and mental

status examinations are clear and there are no apparent signs or symptoms, conduct

physical tests if return to participation is contemplated. Physical provocation tests

should include two 20 metre shuttle runs out of play, 10 sit-ups, 10 push-ups, and 10

squats. Then check for complaints and assess capability to perform sport specifictasks.

Gradings of concussion and return to competition

Gradings of concussion shown in Table 9 (not to be confused with gradings of severity

of closed head injury, Table 1) are used to facilitate clinical decisions about mild head

injuries, which constitute an overwhelming majority of sports head injuries.

After a Grade 1 concussion athletes may return to play, providing mental status is

normal and they are symptom and sign free, after physical exertion testing.

If symptoms persist longer than 15 minutes (Grade 2), or if there was a brief loss of

consciousness (Grade 3), or if a second Grade 1 concussion has been sustained,

return to participation should be prohibited that day.

Post concussion monitoring if not hospitalized

Athletes with Grade 2 or 3 concussions should have their mental status rechecked

every 15 minutes, until they respond to all items appropriately on three consecutive

occasions, indicating a continually lucid period of 30 minutes.

Record duration of post traumatic amnesia, which is defined as the period of time

following trauma when the athlete is disoriented, confused, and unable to lay down

new memories reliably.

If there is no further deterioration, and signs and symptoms are resolving, concussed

athletes may be allowed to return home in the company of a responsible adult. If

supervision is not available referral to hospital is advisable.

Provide written instructions for monitoring in the next 24 hours (see Table 10).

Any of the criteria listed in Table 11 are an indication for referral to hospital. Negative

changes in mental status (other than minor expansion of retrograde amnesia in the first

few hours) or any deterioration in physical condition necessitates immediate transport

to a hospital.

On going management of mild head injury

This is a contentious area because there are no agreed objective measures of individual

recovery from concussion. New guidelines for return to competitive sport (Table 12) that have

been designed to assist the decision about duration of absence from sport are based on the

severity of the presenting injury, recent history of other concussions and extent of recovery (17).

Clinical assessment of recovery


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Milder injuries commonly cause headaches, fatigue, dizziness, loss of concentration

and impaired higher mental function for up to several weeks before recovery.

More severe nonfatal injuries lead to long term changes in cognitive and emotional

function including loss of intellectual capacity, memory, motivation and personality as

well as more specific cognitive and behavioural deficits related to the location anddepth and of lesions. Physical sequelae may include localized neurological deficits and

post-traumatic epilepsy.

CT or MRI scans (even if obtained earlier) may be required if symptoms persist longer

than 1 week or worsen.

Post concussion symptoms

Symptoms may be classified as acute (minutes to hours), prolonged (days to weeks),

or chronic (months to years). Acute symptoms are presented in Table 2. Prolonged

symptoms include persistent low-grade headache, concentration and memory deficits,

sleep disturbance, reduced alcohol tolerance, irritability and lowered frustration

tolerance, sensitivity to light and noise, tinnitus, easily fatigued, anxiety and/or

depressed mood, specific cognitive dysfunction. Chronic symptoms include those listed

for prolonged symptoms, but are usually accompanied by changes to behaviour,

secondary changes in mood/affect, and family and/or social problems (18).

Acute and prolonged symptoms require monitoring to determine when an athlete may

return to participation. In the absence of any generally accepted clinical measures that

assess extent of recovery the protocol detailed in Table 13 is recommended.

Chronic post concussive sequelae may be minimized through counselling player,

coach, and parents of the likely course of recovery and likely negative effects of early

return to high-risk activities.

The unrealistic expectations of athlete, family, peers, or work colleagues have been

linked to the onset and persistence of post concussive complaints. Graded return to

work or school activity minimizes the effects of symptoms and maximizes opportunity

for recovery.

Cumulative effects of concussion

Successive episodes of concussion may have cumulative effects.

Post-concussive symptoms, such as poor co-ordination or balance, impaired

concentration, judgement and fatigue may predispose the player to further head or

other injuries. An athlete with a history of concussion is up to four times more likely to

receive a further concussion (or injuries) than an athlete with a clear history (3).

Appendix B provides a structured interview covering previous sports head injuries.

Psychometric tests indicate greater initial impairment and extended recovery of mental

functions in individuals with previous episodes of concussion (22).


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A second, even lesser, insult may have a disproportionately large effect. Repeated

concussion predisposes athletes to a catastrophic outcome (Second impact syndrome)

if the brain has not sufficiently recovered (23).

Chronic traumatic encephalopathy

Repeated concussion, which is most common in professional boxers, may lead to the

permanent structural changes of chronic traumatic encephalopathy (estimates vary from 17-

55%) (24).

MRI and/or CT scans providing evidence of atrophy or structural abnormality are an

indication for cessation of all high-risk sports or activities.

Signs and symptoms range from mild neurologic dysfunction to dementia, and evolve

slowly but may emerge more rapidly following a significant incident.

The full Dementia Pugilistica syndrome occurs over several years in a minority of

boxers and is more closely related to the number of bouts rather than knockouts.

Psychometric indices of impairment & recovery of function

Delayed onset of retrograde amnesia may occur within 10-15 minutes, and

the amnesia may initially extend to a period of several hours before reducing

(25).

Various post traumatic amnesia scales are available to measure the severity

of head injury but they were designed for hospital rather than on site testing

(26, 27, 28, 29), and for amnesia lasting longer than 24 hours. Since the

duration of post traumatic amnesia is rarely more than a few hours in most

sports head injuries, a more suitable instrument for measuring severity ofsports concussion is repeated administrations of the mental status

examination (see Table 8 and Appendix A) (20, 25).

Psychometric measures of attention, psychomotor speed, judgement and

decision making, and memory have been extensively studied as a means of

providing objective measures of subsequent recovery of function after the

period of post traumatic amnesia resolves. Currently the most widely used are

the Digit Symbol test (30) and the Paced Auditory Serial Addition Task (31).

However, the Digit Symbol test has proved relatively insensitive compared to

a more recent test, which involves judging whether sentences are true or false

(32). It is recommended that the following three psychometric tests are used

to monitor recovery of mentation from concussion: Digit Symbol subtest of the

WAIS-R (30), Symbol Digit Modalities Test (33), and the Speed of

Comprehension subtest of the Speed and Capacity of Language Processing

Test (32) at weekly intervals until performance returns to normal levels.

Performance levels of elite athletes on most tests of speed of information

processing are often better than comparable population norms. Since


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reference to regular norms could thus result in premature return to

participation, it is desirable for professional athletes in high risk sports to have

at least two baseline preseason measures on alternate forms of the three

tests (34).

Detailed psychometric testings (35, 36, 37), brain electrophysiological

measures (38) and computerized dynamic posturography (39) have

demonstrated recovery of cerebral function from concussion usually resolves

within 1 week to 3 months. However reliable correlations between measures

of severity of concussion and rate of recovery have yet to be established. Until

then, the exclusion guidelines listed in Table 13 should be considered in

conjunction with the results of individual based testing.

Prevention of sporting head injuries

Given the potentially irreversible effects of head injury, even after apparently minor trauma, the

sports physician has particular obligations to institute and advocate preventative measures

aimed reducing the severity of head trauma, minimizing secondary brain damage arising from

the initial incident and lowering the incidence of recurrent head injures (40).

Devices reducing the severity of initial injury

The use of protective devices such as mouthguards and helmets can reduce the degree of brain

injury sustained for a given force and also afford protection against associated injuries of the

skull, face, scalp and jaws(see chapter 24).

Mouthguards

Mouthguards protect teeth, facial bones and mandibles. Further, they open the

temporomandibular joint (double type more so than single) and thereby decrease the

force transmitted to the base of the skull by a mandibular blow.

Fitted mouthguards moulded by taking a cast are superior to the heat and mould

variety.

Fitted single upper are recommended for contact sport, whereas fitted double (upper

and lower) are necessary for combat sports.

Non fitted mouthguards are probably better than nothing

Helmets

There are two basic types, soft and rigid (often with soft inner). Soft helmets have been shown

to reduce scalp and eyebrow injuries, but their efficacy in preventing brain injury is unproven.

There are many types of rigid helmets can provide substantial protection to the head and face.

As a general principle, the use of rigid helmets is recommended (and in some sports mandatory)

unless there are compelling reasons for their avoidance, such as injuries to other athletes.

While helmets provide protection against direct blows, they have at least three disadvantages:


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Helmets increase size of the head, thereby permitting a blow which would otherwise

have missed to connect. The increase in diameter of the head can also increase the

rotational component of a blow.

Helmets can obstruct vision (especially if not correctly fitted) thereby hindering

avoidance manoeuvres.

Helmets may give a false sense of security, encouraging the athlete to perform more

recklessly.

Selection and conditioning of individual athletes

Selection and conditioning of athletes for particular sports and for roles within them is

best directed at selecting appropriate physiques for particular sports and roles within

them and at improving general physical fitness.

It is not possible to condition the brain to resist external force; on the contrary, damage

from repeated trauma, however minor, tends to be cumulative.

In certain sports and roles within them that have a higher risk of head injury, neck

strengthening exercises may have a protective effect by reducing acceleration of the

head following blows to the head or body and by protecting against cervical spine

injury.

Rules regulating play and individual participation

It is one of the sports physicians roles to advocate for rule changes that reduce the chance of

head injury. Such rules can be designed to reduce initial injury and prevent recurrence, by

regulating both the contest and individual athlete participation.

Hard objects in the arena of play should be padded wherever possible.

Rules requiring the use of protective devices are desirable.

Rules that require the presence of trained personnel with first aid qualifications are

highly desirable in high risk sports.

Rules that permit immediate assistance to injured athletes are essential.

Rules that prevent head injured athletes from resuming immediately without

appropriate screening are essential.

Rules that provide for mandatory exclusion periods following documented head injuries

are desirable.

Rules making the head an illegitimate target in contact sports are highly desirable.

Combat sports that encourage blows to the head such as boxing and martial arts,

provide a moral dilemma. Do sports physicians that attend such sports in order to

assess and manage head trauma, nevertheless lend sanction to them?

Education of athletes and officials

The sports physician not only has a clinical and an advocacy role as described above but also


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has a responsibility to educate those involved with the sport about its risks, the recognition of

head injury and its consequences, and the procedures for its assessment and management.

Bibliography

1. Lehman, L. B. and Ravich, S. J. (1990). Closed head injury in athletes. Clinics in SportsMedicine, 9, 247-261.

2. Seward, H., Orchard, J., Hazard, H., and Collinson, D. (1993). Football injuries in Australia at

the elite level. The Medical Journal of Australia, 159, 298-301.

3. Gerberich, S. G., Priest, J.D., Boen, J. R., Staub, C. P., and Maxwell, R. E. (1983).

Concussion incidences and severity in secondary school and varsity football players. American

Journal of Public Health, 73, 1370-1375.

4. Cantu, R. C. (1992). Cerebral concussion in sport: Management and prevention . Sports

Medicine, 14, 64-74.

5. Bruno, L. A., Gennarelli, T A., and Torg, J. S. (1987). Management guidelines for head injuries

in athletics. Clinics in Sports Medicine, 6, 17-29.

6. McLatchie, G. and Jennett, B. (1994). Head injury in sport. British Journal of Medicine, 308,

1620-1624.

7. Ingebrigtsen, T. and Romner, B. (1996). Routine early CT-scan is cost saving after minor

head injury. Acta Neurologica Scandanavica, 93, 207-210.

8. McCrory, P. R., Bladin, P. F., and Berkovic, S. F. (1997). Retrospective study of concussive

convulsions in elite Australian rules and rugby league footballers: phenomenology, aetiology,

and outcome. British Medical Journal, 314, 171-174.

9. Ryan, A. J. (1991). Protecting the sportsmans brain (concussion in sport). British Journal of

Sports Medicine, 25, 81-86.

10. Moriarty, J. M. and Simons, S. M. (1994). Sports Neurology. In Current Review of Sports

Medicine (eds. R. J. Johnson, and J. Lombardo), pp. 176-189. Current Medicine: Philadelphia.

11. Maroon, J. C., Bailes, J. E., Yates, A., and Norwig, J. (1992). Assessing closed head injuries.

The Physician and Sports Medicine, 20, 37-44.

12. Bigler, E. D. (1990). Neuropathology of traumatic brain injury. Traumatic Brain Injury (ed. E.

D. Bigler). Pro-ed: Austin, Texas

13. Jennet, B. and Teasdale, G. (1981). Management of head injury. F. A. Davis: Philadephia.

14. Rimel, R. W., Giordani, B., Barth, J. T., and Jane, J. A. (1982). Moderate head injury:

completing the clincial spectrum of brain trauma. Neurosurgery, 11, 344-351.

15. Levin, H. S., Eisenberg, H. M., and Benton, A. L. (1989). Mild Head Injury. Oxford University

Press: New York.

16. Wrightson, P. and Gronwall, D. (1980). Time off work and symptoms after minor head injury.

Injury, 12, 445-454.

17. Quality Standards Subcommittee, American Academy of Neurology. (1997). Practice

parameter: The management of concussion in sport. Neurology, 48, 581-585.

18. Kelly, J. P. and Rosenberg, J. H. (1997). Diagnosis and management of concussion in

sports. Neurology, 48, 575-580.


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1. IMMEDIATE MEMORY:

Say to the athlete I will say some words. Try to remember them.

Read the words aloud at one per second to the athlete. Then ask him/her to say all the words in

any order. Write the words as they are spoken. Read them again for Trial 2. Again ask for recall

including words they said before. Repeat for Trial 3.

TOTAL /15

LIST TRIAL 1 TRIAL 2 TRIAL 3

Baby

Monkey

Perfume

Sunset

Iron

No. of words

NOT tell the athlete that memory for the words will be tested later

2. PROCESSING SPEED: (no. sentences correctly judged in 2 min - see Table 9)

I am going to read you sentences which could be true or false. As I read each sentence please

say true if the sentence is sensible or false if it is silly.

We will have a practice at these three sentences at your own speed.

1. Rats have teeth.

2. Nuns are made in factories.

3. Ants are living creatures.

Are there any questions?

Read each sentence aloud in a clear voice.

Read sentences at a natural rate - between 1.5-2.5 seconds per sentence. Allow 2 seconds

after the sentence is read for the answer.

As soon as the person responds place a T or F on the line for each block of 10 sentences.

Immediately read the next sentence aloud.

We are going to work quickly. Let us see how many you can do in 2mins.

Are you ready? I will start now.Begin stopwatch recording.

Read sentences from the Speed of Comprehension subtest of the Speed and Capacity of

Language Processing Test.(32).

After exactly two minutes stop testing.

Record the number of correct judgements made within the 2 minutes

1 - 10


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11 - 20

21 - 30

31 - 40

41 - 50

Number correct in 2 mins = ________________

Scores below 38 indicate impaired comprehension

3. ORIENTATION: eg., time - What is the time? the day? the month?

/3

place - Where are we?

/1

situation - What happened to you?

/1

TOTAL /5

4. RETROGRADE AMNESIA:

Ask the athlete up to 5 questions concerning events occurring before the incident. Ensure that

responses required are readily verifiable, and avoid questions using a true/false response

format.

TOTAL

/5

5. DELAYED RECALL: (approx. 5 minutes after completing List Learning - 1 point each)

DO NOT READ WORDS.

Say Can you tell me any those words I asked you to remember earlier.

DELAYED RECALL

TOTAL /5

SUMMARY

1. IMMEDIATE MEMORY

/15

2. PROCESSING SPEED (>38) Y/N

3. ORIENTATION /5

4. RETROGRADE AMNESIA /5

5. DELAYED RECALL /5


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All items must be passed to be considered clear of mental status abnormalities

USE A DIFFERENT FORM ON RETESTING

Appendix B Previous sports head injuries - structured interview

Explain the nature of concussion

A concussion can result from a direct blow to the head or even from the heavy contact of bodies,

without actual head contact. You may have been concussed if you were knocked unconscious

or if you were unable to remember part of a game clearly (that is, you had a gap in your

memory). You may have just been confused or disoriented for a period of time. After a

concussion you may have experienced headaches, blurred vision, nausea, dizziness, tiredness,

irritability, loss of co-ordination, or difficulty concentrating or remembering things.

Over your sporting career have you ever been concussed during an evrent? If YES go to (1)If NO go to (14)

(1) How many times have you been concussed?

(2) How long ago was your most recent concussion (weeks, months, years)?

(3) Were you knocked unconscious? If YES How long?

(4) Was there a period of time where you were confused or disoriented or you could not

remember the incident or you had a gap in your memory? If YES how long?

(5) How many times have you been actually been knocked unconscious?

Ask (6) to (10) only if a player has had more than one concussion.

(6) When was the last time you were knocked unconscious?

(7) What was the longest period of time you have been knocked unconscious?

(8) How many times have you had a memory gap after a concussion?

(9) What was the longest gap in your memory after a concussion?

(10) In which years did each of your concussions occur?

Re-start here if only one concussion

(11) Have you missed any games due to concussion? If YES how many?


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(12) Have you ever been off work or other activities because of a concussion? If YES how

long?

(13) Do you believe you have changed in any of the following ways as a result of your head

injuries?

Rate each 0 no to 4 greatly.

mental - attention, memory, decision making, follow conversation, detailed instructions, fatigue

easily

physical - fatigue more easily, increased sleep,

emotional - depressed, anxious, irritable more easily

social - enjoy leisure activities, relationships, friends, family commitments

work - maintaining workload, increasing productivity

playing ability - fatigue, decision speed, reaction time, skills under pressure

Begin here if no previous sports-related concussion(14) Over your career how many non-head injuries have you had that required you to miss a

game

(15) How many games have you missed due to non-head injuries?

(16) Have you ever received a head injury outside of competitive contact sport?

If the subject says YES...record length of unconsciousness, post traumatic amnesia, and

other clinical symptoms.

Table 1 A classification of severity of head injury

Mild loss of consciousness 0-5 min

post traumatic amnesia 6 hours

post traumatic amnesia >24 hours

Glasgow coma score


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reduced vigilance;

heightened distractibility;

inability to think coherently;

inability to sequence goal directed moments;

disorientation for person, time or place;

dazed facial expression.

Amnesia, including:

anterograde amnesia for events after the injury;

retrograde amnesia for events before the injury;

inability to acquire new memories.

Other neurological features including:

blurred vision or diplopia;

slurred speech;

dizziness;

impaired balance or incoordination;nausea or vomiting;

emotional lability;

convulsions.

Table 3 DR ABC procedure for resuscitation of unconscious athlete

Danger

Remove athlete and self from dangerous environment.

Response

Loudly say Hello, can I help you? If athlete responds verbally then airway must be patent

and some cognition is present.

Airway

to clear - insert gloved finger into oral cavity and remove mouthguard, loose teeth, vomit etc.

to open - place athlete on back then move mandible anteriorly (jaw thrust).

if airway obstructed (full or partial) then slight cervical extension may help.

if available oropharangeal airway (Gaddell), supplemental oxygen and oral suctioning may

be necessary.

Breathing

check colour

listen to breathing rate and character

check chest for movement and air entry

if not breathing start expired air resuscitation

Circulation

Check carotid pulse (if palpable systolic BP is > 60 mmHg)

If absent commence cardiopulmonary resuscitation.

Check for torrential arterial bleeding and treat.


22/24

Table 4 Primary Survey

When resuscitated and in coma position:

Inspect and palpate scalp (for wounds or skull fractures)

Inspect and palpate face and anterior neck

Check cervical spine alignment (run fingers along supraspinatus processes)

Glasgow coma score (see Table 5)

Pupillary size, symmetry and reaction to light

Check nose and ears for bleeding or CSF leak

Inspect and palpate abdomen, pelvis and limbs

Table 5 Glasgow Coma Scale (19)

Eye Opening

Spontaneous 4To speech 3

To pain 2

None 1

Best verbal response

Oriented 5

Confused 4

Inappropriate words 3

Incomprehensible sounds 2

Nil 1

Best motor response

Obeys commands 6

Localizes to pain 5

Withdraws from pain 4

Abnormal flexion 3

Extension 2

Nil 1

Total Score 3-15

Table 6 Transport of head injured athlete to hospital

complete resuscitation and primary survey;

protect airway and cervical spine with sandbags or neck brace;

treat and stabilize other injuries;

arrange others to carry the injured athlete;

travel with patient if paramedics unavailable.

Table 7 Neurological screening examination

eyes: visual acuity and fields, pupil size and reflexes, nystagmus


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ears: haemotympanum

nose: rhinorrhea

power: all limbs

coordination: finger-nose touching, heel-toe walking, balance on one leg with eyes

closed

Table 8 Mental status examination for concussion (test form in Appendix A)

Immediate memory:

Five words read to athlete and recalled on three successive trials, scored out of 15.

Processing speed:

Sentences read aloud for two minutes, number correctly identified as true or false.

Scores less than 38 indicate impairment.

Orientation:

Query orientation for time, place, situation, scored out of 5.

Retrograde amnesia:

Query event recall prior to trauma (may vary with time post trauma), scored out of 5.Delayed recall

Free recall of five items presented at immediate recall, scored out of 5.

Table 9 Grading concussion

Grade 1

transient confusion

no loss of consciousness

concussive symptoms and/or mental status abnormalities fully resolve within 15 minutes.

Grade 2

as for Grade 1 except symptoms and abnormalities persist for longer than 15 minutes

Grade 3

any loss of consciousness whether it be brief (seconds, Grade 3a) or prolonged (minutes,

Grade 3b)

Table 10 Sports Head Injury Card

Name:

Time of concussion: Date:

Watch closely for the next 24 hours.

Take to hospital immediately if

they vomit

severe headache develops or increases

they become restless or irritable

they become dizzy, drowsy, or can not be aroused

they have a fit (convulsion)

anything else unusual occurs

For 24 hours after injury they should:

rest quietly


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not drive a vehicle or operate machinery

not consume alcohol or non prescribed drugs

Medical advice should be sought before returning to sport

Table 11 Criteria for referral to hospital

Loss of consciousness greater than 3 minutes

Post traumatic convulsion

Focal neurological signs

Symptoms of marked cerebral irritation persisting longer than 1 hour

Any deterioration of mental status, particularly the development of drowsiness following a

lucid period

More than one episode of concussion in any one playing session

Non-availability of responsible adult to monitor for next 24 hours.

Table 12 Guidelines for return to competitive sport

Grade of Concussion Number of concussions (within a calender

year)

Initial concussion Repeat concussions

Grade 1 same day if

asymptomatic within

15 mins

1 week or longer*

Grade 2 1 week asymptomatic 2 weeks or longer*

Grade 3a 1 week asymptomatic 1 month or longer*

3b 2 weeks

asymptomatic

1 month or longer*

* Period may be prolonged depending on frequency and severity of previous concussions.

Table 13 Recommendations for progressive return to activity

Training should not commence when symptomatic at rest

Training should cease upon development or recurrence of symptoms (requires systematic

questioning).

First day asymptomatic, allow brisk walk for at least 20 minutes. If still asymptomatic, allow

light exercise (20 minutes), then check for symptoms.

Second to seventh days, continue to monitor graded increases in training.

No full exertion until asymptomatic for at least one week with progressive loading

If symptoms persist or develop, a full medical examination is required

Documents

Head Injuries and Sport