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Sports related brain injuries represent approximately 20% of the 1.5 million
brain injuries estimated annually in the United States. Concussion, a term
synonymous with “Mild Traumatic Brain Injury” (MTBI), is an alteration
in mental status due to biomechanical forces affecting the brain which may
or may not cause loss of consciousness. This article will provide an
overview of the challenging problems facing clinicians responsible for the
health of athletes in recognizing and appropriately managing concussion.
Definition and Neurobiology. “Mild” traumatic brain injury (MTBI) or
concussion is becoming an increasingly recognized injury resulting from both
contact and in some circumstances, non-contact sports.1, 2 The most widely
accepted definition of concussion was originally proposed by the Congress of
Neurological Surgeons in 1964. This stated “concussion is a clinical
syndrome characterized by the immediate and transient post-traumatic
impairment of neural function.” Therefore, trauma which leads to mental
status alteration without a clear-cut loss of consciousness was considered a
form of concussion.3 The distinction between these “milder” forms of
brain injury and more serious injury is based on the absence or presence of
disturbed consciousness including post-traumatic amnesia and other
post-traumatic historical and physical findings. While MTBI can occur with
direct trauma to the head during contact sports, it can also occur as a
result of collisions or falls from all forms of athletic activity.4 This
even includes events whereby sufficient force is applied in a so-called “whiplash
mechanism.”5 In 1974, Gennarelli and Ommaya created an animal model of TBI.
In this model, 3 of the 6 grades of concussion did not involve loss of
consciousness. They demonstrated that brain injury can occur from angular or
linear forces applied to the brain. Frequently, in human experiences both
forces act together with a rotational component and are more likely to cause
diffuse axonal injury associated with shearing forces affecting brain
tissue. Most recently, it has been noted that axonal swelling and metabolic
changes occur following
these forces.
Following concussion, frequently there may be no objective neuroanatomic or
physiologic measure which can be used to determine injury severity. Studies
are under way to further define the pathophysiologic basis for why a
seemingly mild insult may lead to an “injury – induced vulnerability and
clinical symptomatology.” Experimental studies have demonstrated that for
up to 3 days following a concussion or more severe cerebral insult, there is
a reduction in cerebral blood flow which would normally be well-tolerated,
but renders the brain susceptible to physiologic and anatomical neuronal
cell loss.8
Although not entirely understood in terms of its underlying cellular
mechanisms, experimental studies have identified following acute injury, a
period of enhanced metabolic vulnerability.8 This consists of an increase in
glucose metabolism and the relative reduction in cerebral blood flow
rendering the brain in a state of metabolic induced cellular vulnerability.
In experimental MTBI, this metabolic dysregulation may play a role in
prognostication. Therefore, the “mis-match” between glucose demand and
fuel availability is the key to future research correlating those cellular
changes with clinical manifestations the athlete may be experiencing.
Medical Management of Concussion. There are a number of health concerns
which need to be addressed at the time of a suspected concussion.9, 10 These
include:
- Appropriate management of the injured athlete at the time of the injury
to identify potential neurosurgical emergencies, ie, subdural, epidural, and
intracerebral hemorrhages.
- Prevention of catastrophic outcomes related to a loss of central vascular
auto-regulation from repeated concussion occurring over a short span of time
– Second Impact Syndrome.
- Avoidance of cumulative cognitive deficits and chronic post-concussive
somatic, behavioral and emotional symptomatology.
- Clinical decisions regarding return to play.
- Treatment considerations
Recognition and Acute Management. The early signs and symptoms of concussion
(seconds to minutes) may include a brief disturbance of consciousness or a
lack of awareness of surroundings, nausea, vomiting, headache, dizziness, or
vertigo. Athletes on the field or sideline may display impaired attention
manifested as a vacant stare, delays in response time, or the inability to
focus. Additional deficits may include slurred or incoherent speech,
uncoordination, disorientation, memory impairments, or emotional reactions
out of proportion to the situation. Any observable or documented loss of
consciousness should also be noted and may represent a more serious injury.
Later signs of concussion (hours to days) may include persistent headache,
dizziness/vertigo, diminished attention, concentration and memory, nausea or
vomiting, fatigue, irritability, intolerance
of loud noises or bright lights, anxiety and/or depression, and sleep
disturbance. The “post-concussive syndrome” is when somatic, cognitive,
and/or emotional deficits persist for weeks or months following injury.
It is recommended that all athletes suspected of having a concussion undergo
an objective and quantifiable initial assessment which includes a mental
status exam and neurological screen including exertional provocative
measures.10 The Standardized Assessment of Concussion (SAC) (Table 1) was
developed to establish a quantitative valid standardized systematic sideline
evaluation for the immediate assessment of concussion in athletes.11 The
Sideline Concussion Checklist (SCC-B) is a checklist that “provides a
systematic and structured format for evaluating physiological, neurological,
and cognitive effects associated with concussion.” It includes evaluation
of pupil size, orientation, fine motor dexterity, coordination, symptoms,
vision, gait, attention, concentration, memory, and exertional symptoms. It
takes about 3 minutes to administer. The SCC-B is a checklist, not a scale,
and has not been empirically validated. Close observation and serial
reliable assessments of the injured athlete are critical to the prevention
of serious or catastrophic complications and for the avoidance of
cumulative, cognitive, emotional, or behavioral impairments.
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Table 1. Sideline Evaluation |
Mental Status Testing
Orientation:
Time, place, person, and situation (circumstances of injury)
Concentration:
Digits backward (ie, 3-1-7, 4-6-8-2, 5-3-0-7-4). Months of
the year in reverse order.
Memory:
Names of teams in prior contest.
Recall of 3 words and 3 objects at 0 and 5 minutes.
Recent newsworthy events.
Details of contest (plays, moves, strategies, etc.)
Exertional Provocative Tests:
40 yard sprint, 5 sit-ups, 5 knee-bends
Neurological Tests:
Strength
Coordination and agility
Sensation
Any appearance of associated symptoms is abnormal, eg, headaches, dizziness,
nausea, unsteadiness, photophobia, blurred or double vision, emotional
liability, or mental status changes. |
The purpose of “concussion” grading systems are that one can reliably
assess depth and duration of disturbed consciousness including
post-traumatic amnesia in order to differentiate mild, moderate, and severe
injuries. There have been more than 15 concussion grading systems utilized
to assess the severity of an injury.3, 4, 10, 13, 14 It is the variability
of presenting symptoms which complicates any grading system. Most grading
systems are based on clinical observations. These grading systems have led
to numerous anecdotal guidelines assessing injury severity and subsequent
recommendations regarding return and/or exclusion from the sport. These
recommendations should be seen as guidelines only rather than scientific
fact. Despite concern regarding scientific validation of
any specific classification system, the majority of clinicians are familiar
with the Cantu Classification System,14 Colorado Guidelines or the
Classification System endorsed by
the American Academy of Neurology. (Table 2)14, 10 It is hoped that further research and validation of these
guidelines will lead
to more specific management and return to play recommendations.
Table 2. Concussion severity classifications. |
Grade
|
Cantu Guidelines
|
Colorado Guidelines
|
AAN Guidelines
|
Grade 1
(mild)
|
No LOC
PTA < 30 min
|
Confusion without amnesia
No LOC
|
Transient confusion, No LOC
Concussive symptoms
resolve < 15 min |
Grade 2
(moderate)
|
LOC < 5 min
PTA> 30 min
|
Confusion with amnesia
No LOC
|
Transient confusion, No LOC
Concussive symptoms last > 15 min
|
Grade 3
(severe) |
LOC > 5 min
PTA > 24 hours
|
LOC
|
Any LOC either brief (seconds) or prolonged (minutes)
|
|
Table 2. Adapted from Cantu, RC. Guidelines for return to contact sports after
cerebral concussion. Phys Sportsmed. 14:75-83, 1986; Colorado Medical
Society. Report of the Sports Medicine Committee: Guidelines for the
Management of Concusussions in Sport. (revised). Denver: Colorado Medical
Society, 1991; Report of the quality standards subcommittee. Practice
Parameter: The management of concussion in sports (summary statement).
Neurology, 1997: 48:581- |
Prevention of Complications. The differential diagnosis and pathophysiology
of concussion requires prompt recognition. It is important to rule out more severe
neurosurgical injuries such as skull
fracture, subdural or epidural hematoma
or intracerebral hemorrhage.
The neuronal insult from concussion causes an acute increased demand for
intracellular glucose and subsequently this is believed to alter the
regulation of cerebral blood flow. These changes, resulting in a heightened
metabolic vulnerability and must be recognized in avoidance of a
catastrophic “second impact syndrome.”12 The Second Impact Syndrome
(SIS) is felt to be caused by a loss of autoregulation of the vascular
components of the brain. This “SIS” occurs when an athlete sustains a
second brain or neuronal insult before recovering from the initial insult.
This may result in massive cerebral edema over seconds to minutes resulting
in permanent damage and/or death. It has been most reported in boxers and
football players with the majority of cases reported in children and
adolescence.6 The Malignant Brain Edema Syndrome 3,12 is also
a poorly understood and rare condition that may occur in young children
following a single brain trauma. The pathophysiology of this condition
resembles SIS with the loss of vascular autoregulation and resultant diffuse
brain hyperemia. In these situations there
may be a rapid decline leading to coma and possibly death. Therefore, an
athlete that has sustained a concussion should not be allowed to return to
practice or competition while symptomatic or displaying ANY signs of
concussion.1-3, 9, 10,13, 14
Seizures or “concussive convulsions”
in collision sports are an uncommon but traumatic symptom following
concussion.12 These concussive convulsions occur within seconds of impact
and are not felt to be associated with structural brain injury. It is
speculated that the concussive impact itself creates a transient functional
decerebration akin to the cortico-medullary disassociation seen in
convulsive syncopy. These players frequently have a good outcome and do not
display any evidence of structural cerebral injury or long-term neuropsychological damage. Therefore, it is felt that these
events are relatively benign, late seizures
do not occur, and anti-epileptic therapy is not indicated. Also, there should not be necessarily a future prohibition
from participating in collision sports and the
overall management plan should center on the appropriate treatment of the concussion injury
itself.3
Assessment. Following the initial assessment of concussion, utilizing the
SAC
or SCC-B, a more detailed neuropsychological evaluation may be useful.6 Also
a detailed neurological examination may be necessary. Follow-up neuroimaging
studies may also be useful. Acutely, CT scans are more readily available and
can detect bleeding or swelling that may require neurosurgical intervention.
More sensitive MRI techniques may detect subtle anatomical and/or
physiologic injury which may correlate with longer lasting post- concussive
symptomatology and may help guide treatment.
Return to Play. Theoretically, acute return to play decisions should be
based on the assumption that there is neurovascular intracerebral stability
with re-establishment of normal chemical and ionic environments within the
brain. Therefore, medical consensus is that any athlete who is continuing to
experience signs or symptoms of concussion would preclude their ability to
return to practice or competition. Controversy exists within the medical
community regarding the theoretical or emperical guidelines and return to play
decisions.15 The American Academy of Neurology has published “Return to
Play Guidelines.”4,10 (Table 3) These guidelines should not be viewed as
fixed standards of care and return to play decisions should be made on an
individual basis.15
Table 3. Management of concussion in sports |
|
Grades of Concussion |
| Grade 1 |
Transient confusion (inattention, inability to maintain a
coherent stream of thought and carry out goal-directed movements)
No loss of consciousness
|
|
Grade 2 |
Transient confusion
No loss of consciousness
Concussion symptoms or mental status abnormalities (including amnesia) on
examination last more than 15 minutes
|
|
Grade 3 |
Any loss of consciousness
a) Brief (seconds)
b) Prolonged (minutes)
|
|
Management Recommendations |
Grade 1
|
Remove from contest
Examine immediately and at 5-minute intervals for the development of
mental status abnormalities or
post-concussive symptoms at rest and with exertion
|
|
Grade 2 |
Remove from contest and disallow return that day
Examine on-site frequently for signs of evolving intracranial pathology
A trained person should re-examine the athlete the following day
A physician should perform a neurologic examination to clear the athlete
for return
to play after one full asymptomatic week at rest and with exertion
|
| Grade 3 |
- Transport the athlete from the field to the nearest emergency
department by ambulance if still
unconscious or if worrisome signs are detected (with cervical spine
immobilization, if indicated)
- A thorough neurologic evaluation should be performed emergently,
including appropriate
neuroimaging procedures when indicated.
- Hospital admission is indicated if any signs of pathology are detected,
or if the mental
status of the athlete remains abnormal.
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Treatment Considerations. The natural history of post concussion
symptomatology is improvement over time.16 However, a small percentage of
injured athletes may continue
to complain of somatic, behavioral and/or emotional symptomatology lasting
one or more years post injury.15 Repeated concussions can cause cumulative
cognitive, emotional, and behavioral impairments.17
This may include impaired attention, concentration, memory, and slurred
speech. Even when concussive events are separated by months or years, there
may also be a stepwise decline in a person’s abilities. Symptoms may be
evident even when no abnormalities are detectable on further detailed
neurological exams. Also, an athlete with a history of concussion may also
be more likely to suffer subsequent concussions compared to an athlete who
has never had one, an area requiring further study.
Recent studies indicate that an
early preventative model is effective in the management of MTBI.18 Education
focused on the understanding and management of symptoms has been empirically
demonstrated to reduce the number and duration of symptoms.17, 19 Early
selective neuropsychological evaluation of attention, memory, information
processing, and executive functioning provides a framework in the management
of symptoms and structuring a gradual resumption of activities.6
It is also helpful to manage neuromedical and somatic symptoms of pain,
headaches, cervicogenic and vestibular dysfunction, irritability,
sleeplessness, and mood dysfunction. “Rational” pharmacotherapy and a
brief program of goal specific rehabilitation services frequently are useful
during the early recovery period.18 In our experience, pharmacologically
stabilizing sleep induction and maintenance patterns with low dose SSRI’s or sedating
tricyclic
antidepressants have an immediate positive effect on symptom presentation.
For life reintegration issues, such as school and/or work, a program
designed to gradually increase tolerance for cognitive demands and organized
problem-solving strategies can be helpful.19 Since chronic dysfunction
following MTBI is often accompanied by negative emotional sequelae, it is
important to address secondary factors by teaching athletes to cope with
symptoms, resume activities, and avoid over-dependence on the healthcare
system.19
Summary. It is important to identify and educate others about optimal
prevention of concussion in sports. Implementing sideline evaluations and
treatment recommendations will help to prevent further morbidity and fatal
injury including the second impact syndrome and persistent post-concussive
symptomatology. Preventative tools include rule changes, and the further
development of design changes in helmets and other protective equipment.
Ongoing research regarding education, risk factors, and the
early detection of concussion using reliable and valid assessment tools,
such as the SAC and SCC-B, are crucial to further guideline improvement.
In order to make sports safer and increase awareness about sports related
concussion, interdisciplinary efforts of medical personnel, trainers,
coaches, officials, parents, and participants are necessary. This will
ultimately allow young players to reach their fullest potential beyond
sports and in life.
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References
1. Wojtysem, Hovda D, Landry G, et al. Concussion in Sports. American
Journal of Sports Medicine. 1999;27(5):676-686.
2. Sturmi JE, Smith C, Lombardo JA. Mild brain trauma in sports medicine.
Sports Medicine. 1998; 25(6)351-358.
3 McCrory PR.Were you knocked out? A team physicians approach to initial
concussion management. Medicine and Science in Sports and Exercise.1997;S207-S212.
4. Clark KS. Epidemiology of athletic head injury. Neurologic Athletic Head
and Neck Injuries. 1998;17(1):1-11.
5. Yarnell P, Lynch S.
The ‘ding’ amnestic
state in football trauma. Neurology. 1973;23:196-197.
6. Erlang DM, Kutner KC, Barth JT, Barnes R. Neuropsychology of sports
related head injury: Dementia pugilistica to post concussion syndrome.
Clinical Neuropsychologist. 1999;13(2):193-209.
7. Dick RW. A summary of head and neck injuries in collegiate athletics
utilizing the NCAA surveillance system. In: Hoerner EF, ed. Head and Neck
Injuries in Sports. Philadelphia, PA; 1994.
8. Houda DA, Lehm, Lifshitz J, et al. Long-term changes in metabolic rates
for glucose following mild, moderate and severe concussive head injuries in
adult rats. J Neurosurg. 376A; 1995.
9. Kelly JP, Rosenberg JH. The development for the management of concussion
in sports. J Head Trauma Rehabil. 1998;13(2):53-65.
10. Report of the Quality Standards Subcommittee: Practice Parameter:
The Management of Concussion in Sports (Summary Statement). Neurology.
1997;48:581-585.
11. McCrea M, Kelly JP, Kluge J, Ackley B, Randolf C. Standardized
Assessment of Concussion in Football Players. Neurology. 1997; 45:586-588.
12. Cantu RC. Second-impact Syndrome. Neurologic Head and Neck Injuries.
1998;17:137-43.
13. Cantu RC. Return to play guidelines after a head injury. Clinic Sports
Medicine. 1998;17:45-60.
14. Cantu RC. Return to play guidelines after a head injury. Neurologic
Athletic Head and Neck Injuries. 1998;17:145-160.
15. McCrory P. The eighth wonder of the world: The mythology of concussion
management. British Journal Sports Medicine. 1999;33(2):136-137.
16. Levin HS, Mattis S, Ruff RM, et al. Neurobehavioral outcome following
minor head injury: A three center Study. J Neurosurg. 1987;66:234-243.
17. Gronwall D. Cumulative and persisting effects of concussion on attention
and cognition. In: Levin H, Eisenberg H, Benton A, eds. Mild Head Injury.
New York, NY: Oxford University. 1989.
18. Wrightson P. Management of disability and rehabilitation services after
mild head injury. In: Levin H, Eisenberg H, Benton A, eds. Mild Head Injury.
New York, NY: Oxford University. 1989.
19. Gerber D, Berry J, Schraa J. Mild traumatic brain injury: Acute
neurobehavioral treatment. CNI Review. 1997;8:23-27.
20. Kutner K, Barth J. Sport related head injury. The Bulletin of the
National Academy of Neuropsychology. 1998;14(1):19-23.
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