Pediatr Clin N Am 49 (2002) 723 – 741

Central nervous system trauma

Management of concussions in athletes
Gregory L. Landry, MD
Department of Pediatrics, University of Wisconsin – Madison, 2870 University Avenue,
Suite 200, Madison, WI 53705, USA

No injury creates more anxiety in the team physician than a concussion. The
young athlete often wants to know how soon he can resume play, whereas the
physician worries about whether the athlete is being truthful about his symptoms.
There may also be a question of whether the athlete and the athlete’s parents are
being truthful about a history of concussions. There are numerous reviews and
opinions on concussion, but they are based on little scientific evidence. Most
studies are done on inpatients who have moderate to severe brain injuries. There
is a gap between the knowledge about brain injuries and their treatment in the
office and on the athletic field [1]. The physician’s discomfort is a result of the
high stakes. Virtually any concussion can result in permanent brain injury.
Fortunately, the new interest in the sports medicine community has begun to
provide some information about the management of concussions.

Definition
There is no universal agreement on the standard definition or nature of
concussion. Traditionally, concussion has been associated with a loss of con-
sciousness; however researchers in the field recognize that significant brain
injuries can occur without a loss of consciousness. In an attempt to resolve the
confusion, the Committee on Head Injury Nomenclature of the Congress of
Neurologic Surgeons, proposed a consensus definition of concussion in 1966 [2].
Later endorsed by the American Medical Association and International Neuro-
traumatology Association, the Congress of Neurologic Surgeons definition states
that concussion is ‘‘a clinical syndrome characterized by the immediate and
transient post traumatic impairment of neurological functions such as alteration of
consciousness, disturbance of vision or equilibrium, etc., due to brain stem in-

E-mail address: gllandry@facstaff.wisc.edu (G.L. Landry).

0031-3955/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved.
PII: S 0 0 3 1 - 3 9 5 5 ( 0 2 ) 0 0 0 2 4 - X
724 G.L. Landry / Pediatr Clin N Am 49 (2002) 723–741

volvement.’’ This is not an adequate definition for concussions in sports; athletes

can exhibit a wide range of symptoms, and most concussions are not associated
with a loss of consciousness. Concussions are sometimes described as mild
traumatic brain injuries (MTBI), which is a phrase that does not serve athletes
well. In the past, MTBI was used to define an injury that occurred in motor
vehicle accidents with an initial Glascow coma scale of 13 to 15 [3]. The
American Congress of Rehabilitation Medicine has proposed that MTBI is ‘‘a
traumatically induced physiologic disruption of brain function’’ with at least one
of the following: (1) any period of documented loss of consciousness, (2) any
memory loss for events just before or just after the injury event, (3) any alteration
of mental state at the time of the injury event, and (4) focal neurologic deficits
that may or may not be transient [4]. This newer definition is closer to the one
that should be used for athletes and could be used synonymously with concus-
sion. It is not accurate to describe brain injuries as head injuries, because a variety
of injuries involving the head do not injure the brain. There are several common
features of concussions that help define the nature of the concussive head injury.
The features of concussion as listed by Johnston et al include: (1) caused either
by a direct blow to the head or elsewhere on the body with an ‘‘impulsive’’ force
transmitted to the head; (2) results in an immediate and short-lived impairment of
neurologic function; (3) may result in neuropathologic changes, although the
acute clinical symptoms largely reflect a functional disturbance rather than
structural injury; and (4) may result in a graded set of clinical syndromes that
may or may not involve loss of consciousness [5]. The resolution of the clinical
and cognitive symptoms typically follows a sequential course.

Epidemiology
Despite problems with the definition of concussion, researchers have attemp-
ted to estimate the frequency of this injury. At least 300,000 sports-related brain
injuries occur each year in the United States; 250,000 are related to high school
football [6]. Athletic trainers at the high school and collegiate level have collected
the best current data. In the 1995 – 97 National Athletic Trainers Association
(NATA) Injury Surveillance Program, 5.5% of all injuries in high school sports
were thought to be due to a concussion [7]. Football is responsible for 7.3% of all
injuries (0.59/1,000 AE = athletic exposures), followed by wrestling at 4.4%
(0.25/1,000 AE), girls’ soccer at 4.3% (0.23/1,000 AE) and boys’ soccer at 3.9%
(0.18/1,000 AE). Girls’ basketball accounted for 3.6% (0.16/1,000 AE), and
boys’ basketball for 2.6% (0.11/1,000 AE). The National Collegiate Athletic
Association (NCAA) Injury Surveillance System reported a concussion rate in
football of 4.2/1,000 athletic exposures which represented 7.5% of all injuries [8].
Concussion accounted for about 7% of all game injuries in men’s soccer, but 11%
of game injuries in women’s soccer. Concussion rates in men’s ice hockey were
1.9/1,000 athletic exposures, or one concussion every 35 games per team.
Wrestling concussions occur one time in every 38 matches per team. Concussion
 G.L. Landry / Pediatr Clin N Am 49 (2002) 723–741 725

accounts for 11% of all injuries in men’s and women’s lacrosse and 8% of all
game injuries in women’s basketball.
One of the problems inherent in the NATA and NCAA surveillance systems is
the dependence on the athlete reporting the injury. Usually the concussion is
counted only if there is time lost from practice or a game. This skews the data
toward more severe concussions and they may not include many of the injuries.
Of 3063 high school athletes, in 103 Minnesota secondary schools, who
completed questionnaires, 19% reported loss of consciousness or loss of aware-
ness during the preceding season [9]. These data were not based on time lost from
practice or games and were dependent on self-report, which may have resulted in
an over-reporting of insignificant injuries. This study is more than 20 years old
and may not reflect what is presently occurring in football.
Thankfully, concussions are rare in organized youth sports. In youth football,
where collisions are frequent, only four concussions were reported in 436 9- to
14-year-old players players, in one season [10]. Concussions become more
frequent after puberty when players generate more force.

Is there a cumulative effect of multiple concussions?

A single concussion can result in permanent brain injury and repeated mild
concussions can have the same result. This was first documented in boxers and has
several names such as ‘‘punch drunk’’ syndrome, dementia pugilistica, and
chronic traumatic brain injury (CTBI) [11]. This permanent brain injury represents
the cumulative, long-term neurological consequences of repetitive concussive and
sub-concussive blows to the brain. It has been estimated that about 17% of retired
professional boxers suffer from this syndrome [12]. Although not studied in
amateur boxing, it is thought to occur much less frequently because of different
rules. It is unclear how long it takes for symptoms of CTBI to appear. Older boxers
are more likely to exhibit symptoms. Motor impairment can include ataxia,
spasticity, impaired coordination and Parkinsonism [11]. Cognitive impairment
in CTBI is most likely to affect attention, memory, and frontal function [13].
CTBI has been described in soccer but the prevalence is unknown. Con-
cussions occur frequently in high school and college soccer. Collisions predict-
ably occur and some will produce significant acceleration forces to the head. One
of the highest risk situations is when two players try to head a soccer ball
simultaneously [14]. CTBI in soccer appears to be a cognitive disorder without
motor signs or symptoms and does not appear to be as severe as in boxing. In one
study, cognitive impairment was found to be cumulative [15] and neuropsycho-
logical testing results were inversely related to the number of concussions
incurred [16]. Despite wide media attention to the potential risk of brain injury
from heading soccer balls, there are virtually no published studies that dem-
onstrate that the simple act of heading is injurious [17]. In one study of 100
college soccer players, no changes in neuropsychological testing could be
demonstrated after practice sessions [18].
726 G.L. Landry / Pediatr Clin N Am 49 (2002) 723–741

In the sport of football, documentation of CTBI is scant. A case report

discuses the history of a professional linebacker who, after 13 years in the
National Football League and at least 15 concussions, had persistent difficulties
with memory and concentration [19]. In a survey of 1090 retired professional
football players, numerous neurologic symptoms were reported and correlated
with the self-reported history of concussion [20]. Other case reports have
appeared in the media, but not in the medical literature.
The risk of CTBI in other sports in unknown but is likely to occur in any of the
sports that have a significant incidence of concussion, including ice hockey,
martial arts, and motor sports.

Second impact syndrome

Case reports of deaths thought to have been caused by a second concussion
that occurred before full recovery from the first have been reported in the
literature. The term second impact was first coined by Saunders and Harbaugh in
1984 when they reported a tragic case of a 19-year-old football player who
received a blow to the head during a fistfight, which resulted in a brief loss of
consciousness (LOC) [21]. The player reported a mild headache on the third day
following the injury and was cleared to play. On the fourth day following the
injury, he blocked on a running play, walked from the field, collapsed, and was
unresponsive. An autopsy revealed a frontal lobe cerebral contusion with massive
areas of anoxia, necrosis, and hemorrhage [21]. Second impact syndrome (SIS)
has been defined as occurring when ‘‘an athlete who has sustained an initial head
injury, most often a concussion, sustains a second injury before symptoms
associated with the first, have fully cleared’’ [22]. It has been postulated that
the second impact causes cerebral vascular congestion, which results in cerebral
swelling. Death usually follows rapidly because of transient brainstem herniation.
Despite widespread concern about this phenomenon, only 17 cases have been
reported in the literature [22]. McCrory and Berkovic recently published a critical
review of the reported cases of this phenomenon [23]. They felt that the clinical
evidence was insufficient to attribute any of these cases to SIS. They classified
five cases to ‘‘probable SIS’’ and the remaining 12 cases were ‘‘non SIS’’. Brain
edema can occur with virtually any brain injury. It remains unclear how important
this relatively rare event is in the management of concussions. It is more
important to realize that diffuse cerebral swelling can occur from a single brain
impact; physicians should be prepared to manage a severe brain injury when
attending any event where concussions may occur [24].

Etiology of concussions
Obviously, many injuries to the brain occur from a direct blow to the head. In
sports, however, an injury often is the result of the acceleration– deceleration
forces acting on the moving brain within the skull [25]. Shearing forces act on the
 G.L. Landry / Pediatr Clin N Am 49 (2002) 723–741 727

neurons and vascular tissue and cause diffuse injury to the axons and neurons [26].
When the head is immobilized, considerably more force is needed to produce a
brain injury. This explains why concussions are still common in American football
despite well-designed headgear. Often a blow to the moving head does not result
in much injury to the brain at the site of impact, but causes damage on the opposite
side. This phenomenon is called a contrecoup injury. Before the use of protective
helmets, more severe injuries to the brain occurred from direct blows to the head
(coup injury). This included depressed skull fractures. The majority of the injuries
that occur in athletes in sports where helmets are used are a result of the
acceleration/deceleration of the skull and brain. Unfortunately, because the
helmets are so well-made; athletes are using their head and helmet as a weapon.
This increases the risk of concussion and cervical spine injuries.
There has been concern about whether the type of helmet used and the risk of
concussion varies with the brand of the helmet. Zemper et al examined 8312
college player seasons and 618,596 athlete exposures and compared the brand of
American football helmet used with the rate of concussion per 1000 athlete
exposures [27]. They found that the two most frequently used brands of older
helmets had concussions rates of 0.53 and 0.62, whereas the Riddell brand helmet
had a concussion rate of 0.17. Soon after the data were published, most schools
purchased Riddell football helmets or other brands associated with the lower
concussion rates.

Genetics of concussion
There is limited evidence to show that there may be a genetic predisposition to
concussions. Pathologically, CTBI has characteristics similar to Alzheimer dis-
ease. Alzheimer disease has been shown to have a significant association with the
apolipoprotein E epsilon-4 gene (APOE). This has led to limited studies of athletes
with multiple concussions. Jordan et al surveyed 30 active and retired boxers and
examined their neurologic disability. The boxers who were more impaired were
more likely to have the APOE gene [28]. Kutner et al studied active professional
football players and found that the older players who possessed the APOE allele
had poorer scores on cognitive tests [29]. These two studies suggest that the brain
may have a genetic susceptibility to the effects of trauma [11]. Other athletic
populations at risk for CTBI have not been examined for the APOE gene.

Classifications and symptoms of concussions

Because of the anxiety and uncertainty in managing concussions, classifica-
tion systems have been developed to grade concussions based on a limited
number of symptoms. There are over 25 different classifications in the literature
and it is beyond the scope of this article to review all of them. One of the best
known was published by Cantu in 1986 [30]. In this classification system, a grade
I concussion does not induce a loss of consciousness and post-traumatic amnesia
728 G.L. Landry / Pediatr Clin N Am 49 (2002) 723–741

lasts for less than 30 minutes. A grade II concussion is characterized by a loss of

consciousness of less than 5 minutes’ duration or the presence of post-traumatic
amnesia of more than 30 minutes’ duration. A grade III concussion causes a loss
of consciousness for more than 5 minutes or posttraumatic amnesia that lasts for
more than 24 hours.
The Colorado Medical Society published another well-known classification
system in 1990 that was revised in 1991 [31,32]. In the Colorado guidelines, a
grade I concussion induces no loss of consciousness or amnesia, but transient
confusion is present. A grade II concussion produces no loss of consciousness
but does cause confusion and amnesia. A grade III concussion produces a loss of
consciousness. The most recent, widely used concussion guidelines were
formulated by the American Academy of Neurology (AAN) and were published
as a practice parameter [33]. In the AAN practice parameter, a grade I concussion
does not induce a loss of consciousness, and symptoms resolve in less than
15 minutes. A grade II concussion is associated with no loss of consciousness,
but symptoms persist for more than 15 minutes. A grade III concussion produces
a loss of consciousness. A summary of these three classifications and the
associated return-to-play recommendations appear in Table 1. Interestingly,

Table 1
Published grading scales for severity of concussion and guidelines for playability
Grade Cantu (1986) Colorado Medical Society (1991) Am Acad Neurology (1997)
1 No LOC No LOC No LOC
PTA lasts less than 30 min Confusion Transient confusion
No amnesia Symptoms and mental-
status abnormalities
resolve in less than 15 min
RTP OK if no symptoms RTP permitted if no symptoms RTP if abnormalities or
AROAE otherwise, no AROAE after at least 20 min symptoms AROAE
symptoms for 1 wk AROAE of observation resolve within 15 min
before RTP
2 LOC lasts less than 5 min No LOC Transient confusion
PTA lasts 30 min to 24 hr Confusion No LOC
Amnesia Symptoms and mental status
changes last longer than 15 min
RTP OK if no symptoms RTP OK if no symptoms RTP OK after 1 wk with
for 1 wk AROAE for 1 wk no symptoms AROAE
3 LOC lasts 5 min or more or Any LOC, brief (s) or
PTA lasts 24 hrs or more prolonged (min)
RTP not allowed for at least RTP not allowed for at least Brief: RTP OK after no
1 mo. OK to RTP 1 mo. OK if no symptoms for symptoms for 1 wk
RTP if no symptoms for at least 2 wks. AROAE Prolonged: RTP
1 wk AROAE OK after no symptoms
for 2 wks AROAE
Abbreviations: AROAE, at rest or after exertion; LOC, Loss of consciousness; PTA, post traumatic
amnesia; RTP, return to play.
Modified from Guskiewicz K. Sports related concussion: bridging the gap between research and
clinical practice. Athletic Training Today 2001;6(1):24.
 G.L. Landry / Pediatr Clin N Am 49 (2002) 723–741 729

virtually all of the classification systems use loss of consciousness and

its duration as a factor in determining the severity of concussion. The only
symptom that most of the concussion classification systems use is the loss
of memory.
The duration of the loss of consciousness has been shown to have some
correlation with the severity of the brain injury. Until recently, little data on less
severe injuries have been available. Lovell et al studied 383 hospitalized patients
who had sustained brain trauma and had Glascow Coma Scale scores of 14 or 15
(15 = normal) [34]. The patients were classified as positive, negative, or uncertain
for LOC. The majority of the patients who had a LOC were unconscious for less
than 1 minute. Neuropsychological tests were administered to all of the patients
and no statistical significance was noted between the three groups. The results
raise doubts about the importance of brief LOC as a predictor of outcome
following a mild concussion.
The list of common symptoms and signs of concussion are quite extensive and
can be found in Box 1. The symptom of headache in collision sports can be
problematic; as many as 20% of football players report getting headaches on a
regular basis when competing [35]. If an athlete says that he always gets a
headache then he may be telling the truth. It may be more appropriate to ask if the
headache is more intense than usual or has a different quality.
Few athletes exhibit all of the symptoms and signs of concussion. It is unclear
whether the presence of absence of these symptoms predicts a more severe brain
injury. It is interesting to note that almost all concussion classification systems are
based on only two or three signs or symptoms. Researchers in the field have long
been concerned that current classifications systems oversimplify a complex
clinical entity.

The immediate evaluation of the concussed athlete

When an athlete appears to be impaired because of a blow to the head, it is
very important to examine him for any signs of concussion and to ask about any
symptoms. The presence of any symptoms or signs of concussion precludes play.
Evaluation of facial expression is helpful because the athlete may appear dazed
and have a vacant expression. Most practitioners ask about orientation to time,
place, and person, although this is not a very sensitive test for memory. It is
helpful to ask the athlete what he remembers about the blow to the head. Loss of
memory at the time of the injury or of events following the injury signifies
antegrade amnesia. It is also helpful to determine whether there is loss of memory
of events prior to the injury. For example, if the athlete cannot remember a
pregame meal or how s/he got to the locker room, then retrograde amnesia, which
may signify a more severe injury, is indicated. It is important to evaluate gait; this
should include running if the athlete is able to do so. Any concussed athlete
should receive a good neurological evaluation. In addition, tests should be done
to evaluate memory and the ability to process because these are more likely to
730 G.L. Landry / Pediatr Clin N Am 49 (2002) 723–741

Box 1. Signs and symptoms of concussion

Memory or orientation
Unaware of time, date or place
Unaware of period, opposition or score of game
General confusion

Symptoms
Headache
Dizziness
Feeling stunned or numb
Feeling dazed
Feeling slow
Seeing stars or flashing lights
Tinnitis
Sleepiness
Blurred vision
Loss of field of vision
Double vision
Nausea

Physical signs
Poor coordination
Poor balance
Glassy eyed/vacant stare
Vomiting
Slurred speech
Slow to answer questions
Slow to follow directions
Easily distracted/poor concentration
Unusual/inappropriate emotions (eg, laughing or crying)
Personality change
Inappropriate behavior on field of play (e.g. running the wrong
direction)
Significant playing ability compared to earlier in contest

Modified from Canadian Academy of Sport Medicine Concus-

sion Committee: guidelines for assessment and management of
sport-related concussion. Clin J Sport Med 2000;10:210; with
permission.
 G.L. Landry / Pediatr Clin N Am 49 (2002) 723–741 731

reveal a deficit in function. It is often helpful to have an athlete or coach quiz the
injured athlete regarding plays or strategies, especially if they are fairly sophis-
ticated. It is also helpful to ask the athlete to remember three or four nonsensical
objects and then determine if s/he can recall them 5 minutes later. Even if the
athlete provides the correct answers, the speed of processing should be observed.
If it is slow, it is likely a deficit from the concussion. Simple mathematics tests
have been used but many athletes cannot succesfully perform these even when
uninjured. Young et al evaluated the ability of 522 uninjured high school students
to perform serial sevens [‘‘what is 100 minus seven?’’ (answer: 93), ‘‘minus
seven again’’ (answer: 86), and so forth) [36]. Only 50% of the students could do
serial sevens without errors. In the same study, 89% of the students could
correctly recant the months of the year in reverse order (MOYR). Therefore
MOYR is probably a more reliable test for high school and college athletes. It is
best utilized when baseline data are available. Current research is being done to
determine more sensitive mental processing tools that can be used on the sideline
or in the office.
Previous classifications and return to play criteria are very conservative and are
probably appropriate for the inexperienced practitioner. Because the guidelines are
extremely conservative the majority of experienced team physicians deviate from
them. The consensus among experienced practitioners, however, is that any athlete
who has symptoms or signs of a concussion should not play [37]. The longer
symptoms persist, the longer the athlete will need to be held out of competition.
During a practice or competition, if the athlete’s symptoms do not clear within
approximately 15 minutes, s/he is usually unable to return to the same contest. The
classification systems do not work well in practice, because the symptoms and
signs are different in every case. Although he published one of the most well-
known classification systems in 1986, Cantu wrote ‘‘the final decision regarding
returning to competition after head injury is always a clinical judgment in every
case. Deviation from written text based on the clinical judgment of the treating
physician or trainer may be entirely appropriate’’ [30].
It is important to evaluate the athlete on a frequent basis if he or she has
sustained a concussion. The athlete should not go to the locker room or shower.
The athlete should be observed in the event that they require further medical
assistance. If the symptoms do not worsen, the athlete may continue to stay on the
field. If there is evidence that the symptoms are worsening, or there are additional
signs, the athlete must be transported to the nearest emergency facility. With
sports that require a helmet, it is best to keep possession of the athlete’s helmet so
that he or she cannot return to the event prematurely in the heat of the battle.
Many pediatricians attend athletic events to watch their son or daughter play
even if they are not the official team physician. If the pediatrician is the only
physician present at the event, s/he may be asked to evaluate an injured athlete.
One must consider that any unconscious athlete has a cervical spine injury until
proven otherwise. The helmet must not be removed until a cervical spine injury
has been ruled out. The facemask can usually be removed, without moving the
cervical spine, to access the airway.
732 G.L. Landry / Pediatr Clin N Am 49 (2002) 723–741

Indications for CT scanning for mild brain injuries are controversial [38 – 41].
Any LOC warrants an evaluation in an emergency facility and strong considera-
tion must be given to performing a head CT scan. A practice parameter on
management of minor closed head injury in children published by the American
Academy of Pediatrics discussed patient observation as an acceptable option in the
asymptomatic patient despite inadequate data to fully assess the risk-benefit ratio
[42]. Although the yield is exceedingly low, performing a CT scan when there is
any LOC has become standard practice for medical-legal reasons, especially in
emergency department settings. CT or MRI scans should be considered in an
athlete whose symptoms have not significantly cleared in 7 to 10 days.

When can the athlete play again?

When the athletic contest is over, the athlete needs to be re-evaluated. If there
has been no LOC and there is an improvement in symptoms, the athlete can go
home. A responsible adult must observe him during the first 24 hours following
the injury. The athlete should have telephone contact with a medical professional
or a clinic visit the following day. The athlete should be advised not to exercise
until he or she is totally asymptomatic. If a headache is present, there should be no
workout. The athlete must be informed about the importance of reporting
symptoms to assist the practitioner in determining playability. It may help to
discuss the chronic symptoms that some professional athletes have experienced by
playing too soon and not reporting symptoms. The athlete should be asked about
how well he can perform school and leisure activities. The inability to concentrate
or pay attention in class should be considered a significant symptom. If the athlete
is developing headaches when reading or studying, he is not ready to exercise or
participate in sports. If the athlete is asymptomatic for one day, s/he may start
biking or jogging. If the exercise produces a headache or causes any of the
concussion symptoms to recur, the athlete must stop and wait until the following
day to attempt further exercise. Activities, such as sit-ups or weight-lifting, may be
more likely than simple exercise, to produce headache or concussion symptoms.
Gradual increasing the intensity of exercise before allowing the athlete to go back
to full competition is often helpful. These criteria for return-to-play deviate
significantly from most of the published guidelines in the United States.
The functional regimen discussed previously is based on symptoms similar to
recent guidelines published by the Canadian Academy of Sport Medicine [43]. A
summary of the steps is listed in Box 2. It involves utilizing common sense and a
rapport with the athlete [44]. Unfortunately, it is not based on scientific evidence.
There is only anecdotal evidence that functional regimens work. During one
college football season in the Big Ten Conference, 11 universities reported sixty
concussions. All team physicians used functional return to play regimens. Of the
six athletes who sustained more than one concussion in the same season, none of
the individuals sustained their second concussion less than three weeks after the
first (J. Powell, personal communication, 1998) Apparently if athletes were
 G.L. Landry / Pediatr Clin N Am 49 (2002) 723–741 733

being returned to play too early, second concussions would have appeared in
successive weeks.

Box 2. Steps to return to play following a concussion from the

Canadian Academy of Sport Medicine

1. No activity, complete rest. Once asymptomatic, proceed to

level 2. Continue to proceed to the next level if asympto-
matic. If symptoms occur, drop back to a level where there
are no symptoms, and try to progress again.
2. Light exercise such as walking or stationery cycling.
3. Sport-specific activity (eg, skating in ice hockey)
4. On-field practice without body contact
5. On-field practice with body contact, once cleared to do so
by a medical doctor. The time required to progress from
noncontact to contact exercise varies with the severity of
the concussion.
6. Game play.

From Canadian Academy of Sport Medicine Concussion Commit-

tee: guidelines for assessment and management of sport-related
concussion. Clin J Sport Med 2000;10:210; with permission.

For the inexperienced practitioner there is nothing wrong with using one of
the published classification systems and the associated return-to-play criteria.
The classification systems are not based on scientific evidence. Even experi-
enced practitioners are more conservative when treating middle school and
high school athletes, or athletes whom they do not know very well. There are
no scientific data to compare how children and adult brains recover from mild
concussions or what role gender plays in rate of recovery. The risk of being
too conservative, however, is that the athletes will be less forthright about
reporting symptoms so they will not be held out of competition for prolonged
periods of time.

Two studies provide evidence that recovery from mild concussions occurs
promptly in young adults
In a study of 2300 collegiate football players, 183 concussed athletes were
matched with controls and underwent a neuropsychological battery within
24 hours of the injury, at 5 days after the injury, and at 10 days after the injury
[45]. Most players were back to normal at 5 days and all were back to normal at
the 10-day mark. Improvements in neuropsychological test performance par-
alleled the improvement in symptoms. The authors concluded that most football
734 G.L. Landry / Pediatr Clin N Am 49 (2002) 723–741

players with mild concussions recover quickly without apparent residual neuro-
cognitive impairment or symptoms. Delany et al studied symptoms in Canadian
professional football players during one season [46]. In studying 66 concussions,
they found that 95.5% of players were asymptomatic in 3 days. Two players were
asymptomatic after a week and one player’s symptoms lasted for two weeks.
Similar studies need to be performed on younger athletes.

When is it time to disqulaify the athlete with mulitple concussions?

After a young athlete has sustained three concussions, it is appropriate to sit
down with the athlete and his/her parents to discuss the potential risk of permanent
brain injury. It may be entirely appropriate to disqualify an athlete who has
sustained one or two severe concussions. There is no absolute number that must
preclude play. Mild concussions that result in symptoms of brief duration are not
as significant as concussions that cause symptoms of longer duration [47]. If the
athlete is cleared to continue to play, an informed consent statement should be
written to document the discussion with the athlete and the parents.
A permanent disqualification from a collision sport must be considered when
the following occur: (1) each subsequent concussion results in more severe or
longer lasting symptoms; (2) it appears to take less of a blow to the head to cause
a concussion (ie, an increasing susceptibility to a concussion); (3) the athlete’s
style of play makes more concussions likely (ie, the athlete is exceptionally
aggressive); (4) the athlete has a learning disability or already struggles with
schoolwork; or (5) the athlete is not receiving, and is not likely to receive, any
financial gain from participating in the sport. Neuropsychological testing of 16
concussed college athletes showed that the athletes who had the most significant
deficits were those who had a learning disability (LD) and a concussion [48]. The
authors theorized that the two variables may be synergistic or that the athlete with
a LD may have less reserve than one without a LD.

Prevention
There are few studies available to assist the practitioner in teaching ways to
prevent concussions in sports. In sports that require helmets, a properly fitted
helmet probably helps prevent some of the injuries. The effect of helmet fit on
risk of concussion has not been studied in athletes; however, one small study
showed that children from 2 to 14 years of age with poorly fitting bicycle helmets
were 1.96 times more likely to sustain a significant brain injury than children who
wore properly fitting helmets [49]. Only 15% of 1671 high school football
players surveyed in Wisconsin had helmets that fit well [50]. Athletes prefer
comfort over protection; a good-fitting helmet feels tight and is slightly
uncomfortable. Foam padding compresses with time and becomes less protective
and more comfortable. Officials play a role in prevention by calling appropriate
penalties. In American football and ice hockey, athletes must avoid using the
 G.L. Landry / Pediatr Clin N Am 49 (2002) 723–741 735

head as battering ram (‘‘spearing’’) and officials must penalize athletes who hit
with their helmets. The use of a mouthpiece may prevent some of the head trauma
but this has never been studied scientifically. Neck muscle strength programs may
also help prevent movement of the head in space, especially when the athlete sees
a blow coming, or in soccer when heading a ball and a collision with another
player occurs [14].

Future directions
Because the standard neurological examination and neuroimaging studies
available lack sensitivity for most mild injuries in athletes, practitioners need
more sensitive tools to assess mild concussions. Although neuropsychological
testing is the most sensitive testing to assess brain function, it takes several hours
to administer and is expensive. Also, it is also not readily available to many
athletes. Furthermore, the results are difficult to assess if baseline testing has not
been performed. It has become clearer that more baseline testing is needed on
athletes in high-risk sports. The National Football League and National Hockey
League administer a neuropsychological battery to every player at the beginning
of his career. If any concussion occurs, the battery is administered within 24 hours
of the injury and again 5 days following the injury [47]. This battery consists of
the following eight neuropsychological measures with the associated cognitive
skill evaluated in parentheses: Controlled Oral Word Association Test (word
fluency), Hopkins Verbal Learning Test (verbal learning, immediate and delayed
memory) Brief Visuospatial Memory Test-Revised (visual memory), Trail Making
Test A and B (visual scanning, complex attention, mental flexibility, visual-motor
speed), Digits Span (attention span, concentration, freedom from distractibility),
Symbol Digit Modalities Test (psychomotor speed, visual short-term memory),
and Grooved Pegboard Test (motor coordination, psychomotor speed). The
athletes also receive a symptom questionnaire similar to the one in Fig. 1 and
undergo a clinical history interview. Preliminary analysis shows that following a
concussion, the Brief Visuospatial Memory Test-Revised and Hopkins Verbal
Learning Test seem to have the most changes. Anecdotally, the testing has not
significantly changed the treatment of concussion but has made players more
aware of the problem. There is no standard neuropsychological battery for athletes
and there is controversy about the tests that should be included. Other researchers
have utilized different tests for their neuropsychological battery for athletes.
Because this type of testing is not practical for younger athletes, researchers have
designed shorter neuropsychological batteries that can be done on a laptop
computer. This reduces the cost and does not require a neuropyschologist to be
present for every examination. A computer-based program has the advantage of
testing reaction time and speed of processing, an important parameter not
available with traditional pencil and paper tests. These computer programs need
to be tested on large numbers of younger athletes before they can be used on a
widespread basis.
736 G.L. Landry / Pediatr Clin N Am 49 (2002) 723–741

Fig. 1. A checklist for the symptoms of a concussion including severity of the symptoms.

McCrea et al created an even briefer evaluation, which they called the Stand-
ardized Assessment of Concussion (SAC) [51]. The SAC is a brief 3-minute
evaluation that can be administered by a trainer or anyone on the sideline. A pilot
study showed a significant difference in scores between six concussed high school
athletes and 141 uninjured athletes [51]. An example of the SAC appears in Box 3.
Within the SAC are important questions that should be asked of any concussed
athlete. There are concerns regarding the sensitivity and brevity of the SAC. It may
be more useful if baseline scores are collected before using it on injured athletes
(ie, using the individual as his own control). More research is needed before it can
be utilized on a widespread basis.
Guskiewicz et al have been working on utilizing balance tests to assess
concussed athletes [52]. This too requires preinjury measurement on specialized
equipment. In their research, nine conditions of balance testing were utilized
with the athlete standing on a pressure plate with four electronic pressure trans-
ducers. The nine conditions consist of three visual and three support surface
conditions. The three visual conditions are: athlete’s eyes open, blindfolded and
wearing a visual conflict dome. The three support surface conditions are: a normal
stable platform, foam-padded platform and dorsiflexion dynamic platform (moving
up and down). Seventy subjects aged 15 to 25 had preseason balance testing
performed and ten of those subjects suffered a concussion. Concussed athletes had
significant postural sway for up to 3 days following the concussion. Although a
 G.L. Landry / Pediatr Clin N Am 49 (2002) 723–741 737

Box 3. Tasks that comprise the Standardized Assessment of

Concussion (SAC)

Orientation (one point each)

Month
Date
Day of the week
Year
Time (within 1 hour)

Orientation score: 5

Immediate memory (one point for each correct, total over

three trials)
Word 1
Word 2
Word 3
Word 4
Word 5

Immediate memory score: 15

Concentration
Reverse digits (go to next string length if correct on first trial,
stop if incorrect on both trials; one point for each string length)
2-8-3
3-9-7-2
5-1-8-6-9
6-9-7-3-1
3-8-2
2-7-9-3
9-6-8-1-5
1-3-7-9-6

Months of the year in reverse order (one point for entire

sequence correct)
Dec-Nov-Oct-Sep-Aug-Jul-Jun-May-Apr-Mar-Feb-Jan
Concentration score: 5
738 G.L. Landry / Pediatr Clin N Am 49 (2002) 723–741

Delayed recall (approximately 5 minutes after immediate memory;

one point each)
Word 1
Word 2
Word 3
Word 4
Word 5

Delayed recall score: 5

Summary of total scores

Orientation 5
Immediate memory 15
Concentration 5
Delayed recall 5
Total score 30

The following may be performed between immediate memory

and delayed recall portions of this assessment when appropriate.

Neurologic screening
Recollection of injury
Strength
Sensation
Coordination

Exertional maneuvers
One 40-yard sprint
Five sit-ups
Five push-ups
Five knee bends

From McCrea M, Kelly JP, Kluge J, et al. Standardized assess-

ment of concussion in football players. Neurology 1997;48:586 – 8;
with permission.

high percentage of athletes exhibit impaired balance as a sign of a concussion,

others do not. Balance tests alone cannot be used as a measurement of recovery
from concussion. The equipment used in this study is expensive and not practical
for use on a widespread basis. Researchers are investigating balance tests for use in
concussed athletes that require less equipment.
 G.L. Landry / Pediatr Clin N Am 49 (2002) 723–741 739

Summary
The care of athletes with concussions is challenging because each patient has
different symptoms. An athlete should never be returned to play until com-
pletely asymptomatic. Classification systems for concussions are not based on
scientific evidence and represent some practitioners’ best guess at what is safe
for young athletes. Many experienced team physicians believe they can allow
an athlete to play safely if there are no symptoms at rest and no symptoms with
increasing intensity of exercise. Abbreviated neuropsychological testing and
balance tests show promise for use in the field to increase the sensitivity of our
neurological evaluation on injured athletes. Any neuropsychological or balance
evaluation is more helpful if baseline data is collected on athletes before they
are injured.

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