Mild head injury is of growing interest because of its underdiagnosed prevalence and underestimated clinical importance. Half of the patients in emergency departments report sport-related head injuries or concussions. Knowledge of symptoms and appropriate management can be improved and is a matter of practical interest for healthcare providers as well as coaches, parents and athletes in order to improve patient care and prevent future injuries. An acute concussion presents with a combination of physical, cognitive, and emotional symptoms, which are usually self-limited and resolve within a week. However, significant sequelae from even mild impacts, such as headaches, prolonged cognitive impairment, or even death, are known. A second impact before full recovery from the first may have deleterious consequences and should be avoided by observing strict rules for «return to play.» Recent research suggests that repetitive minor hits my cause delayed brain damage (dementia pugilistica or the «punch-drunk syndrome»). A link to neurodegenerative diseases such as dementia, Alzheimer’s disease (AD) and parkinsonism (tauopathies) is described by amyloidβ plaques in those brains. A genetic predisposition (apolipoprotein) is discussed.
14
Abstract
Mild head injury is of growing interest be-
cause of its underdiagnosed prevalence
and underestimated clinical importance.
Half of the patients in emergency depart –
ments report sport-related head injuries or
concussions. Knowledge of symptoms and
appropriate management can be improved
and is a matter of practical interest for
healthcare providers as well as coaches,
parents and athletes in order to improve
patient care and prevent future injuries. An
acute concussion presents with a combina –
tion of physical, cognitive, and emotional
symptoms, which are usually self-limited
and resolve within a week. However, signi –
ficant sequelae from even mild impacts,
such as headaches, prolonged cognitive
impairment, or even death, are known. A
second impact before full recovery from
the first may have deleterious consequen –
ces and should be avoided by obser ving
strict rules for «return to play.» Recent re –
search suggests that repetitive minor hits
my cause delayed brain damage (dementia
pugilistica or the «punch-drunk syndro –
me»). A link to neurodegenerative diseases
such as dementia, Alzheimer’s disease (AD)
and parkinsonism (tauopathies) is descri –
bed by amyloidβ plaques in those brains. A
genetic predisposition (apolipoprotein) is
discussed. This review will focus on the impact of mild
head injuries in young athletes and present
the current «return to play» rules to avoid
the second-impact syndrome. We describe
in detail standardized guidelines for appro
–
priate diagnosis and treatment and discuss
the association between repetitive minor
injuries and chronic traumatic encephalo –
pathy and neurodegenerative diseases.
Introduction
Mild head injuries in general are a serious
healthcare problem contributing to 0.5% of
all visits to emergency departments and re –
sulting in 10% of all pediatric admissions. In
adolescents mild head injuries are often re –
lated to sport. Recent studies
1), 2) have shown
that 20–50% of the minor head injuries trea –
ted in an emergency department are sport-
related. Public knowledge about mild head
injuries is astonishingly poor: only less than
10% of the population believe that a head
injury could cause a brain injury, more than
25% think it is harmless and never causes
long-term problems and up to 40% believe a
second blow to the head may help someone
remember things they forgot after a first in –
jury
3). Also, many professional healthcare
providers think a concussion, even in sports,
is necessarily accompanied by a period of
unconsciousness, which stands in contrast
to the opinion of most experts
4), 5), 6) . The lack of a consensus on the definition
and terminology of mild head injury, trau
–
matic brain injury (TBI) and concussion
contributes to the misunderstanding and
underestimation of this disease entity. For
this reason, mild head injuries or concus –
sions are often misjudged as minor and not
recognized by the children who sustain
them, their parents, coaches, or by physi –
cians. Often only concussions with loss of
consciousness are regarded as signifi –
cant
7). To prevent athletes from incurring
subsequent injuries, initial symptoms ( Ta –
b l e 1) should be recognized and athletes as
well as trainers encouraged to report sym –
ptoms.
It follows that patients who are not investi –
gated according to standardized protocols
are not protected from a second injury by
adhering to instructions for the follow-up
4).
The team sports with the highest risk are
ice hockey and football, where 1.0 concus –
sions occur per 1000 exposures (games or
training sessions), followed by soccer (0.3
per 1000 exposures), basketball and base –
ball
2), 5), 8) . In other words, 10% of all football
players will sustain at least one minor head
injury per season
9) and one in 15 players
with a concussion may suffer an additional
concussion during the same playing
season
9), 10) .
Definitions
The degree of head injury is defined accor-
ding to the Glasgow Coma Scale (GCS) as
mild (GCS 13–15), moderate (GCS 9–12) or
severe (GCS ≤ 8) TBI. By contrast, the word
«concussion» describes the pathophysio –
Mild Head Injury in Young Athletes
Burkhard Simma, Daniela Jonas, Jürg Lütschg, Feldkirch, Austria
Ta b l e 1: One or more symptoms may suggest a concussion. This may or may not include loss of consciousness (LOC).
PhysicalCognitive Emotional Sleep
Headache Feeling mentally «foggy» IrritabilityDrowsiness
Nausea Feeling slowed down SadnessSleeps more than usual
Vomiting Difficulty concentrating More emotionalSleeps less than usual
Balance problems Difficulty remembering NervousnessDifficulty falling asleep
Visual problems Forgetful of recent information
Fatigue Confused about recent events
Sensitivity to light Answers questions slowly
Sensitivity to noise Repeats questions
Dazed
Stunned
Vol. 24 Nr. 1 2013
Fortbildung
15
Investigations
On the field, athletes should be managed
according to standard emergency princip-
les (ABC rule), giving particular attention to
the cer vical spine. On the sideline, a neu –
ropsychological assessment must follow
either briefly using the Maddocks ques –
tions
26) or in more detail with the Sport
Concussion Assessment (SCAT2) 5), 6) or
other tests 43). The Maddocks questions
(Table 2) pertain only to orientation (time,
place, person) and are not a substitute for
a proper and more detailed examination in
the locker room or the coach’s office. The
SCAT2
5), 6) is a standardized tool that inclu –
des symptom evaluation, calculation of the
Glasgow Coma Scale score, sideline asses –
sment (Maddocks questions) and – impor –
tantly – a cognitive, balance and coordina –
tion assessment. However, the SCAT2 has
never been evaluated in a prospective
study. Consequently, no normative data or
«cut-offs» are available for it. Nevertheless,
it is a useful, practicable and standardized
tool for estimating the risk for athletes
following a head injury. Other neuropsy –
chological tests are web-based (imPACT
®,
HeadMinder ®, Cog State ®)5) and developed
specifically for athletes’ injuries. For all
these tests a pre-injury test should ideally
be obtained at the beginning of the season
to assist in interpreting any post-injury
result
27).
Return to Play Rule
The main message is that any player with a
diagnosed concussion should never be
allowed to return to play on the same day,
no matter how brief the symptoms are or
how well the player looks («when in doubt,
sit them out»). They should never be left
alone in the hours subsequent to sustai –
ning a hit to the head in order to not miss
any deterioration, and they are not allowed
to drive a vehicle until medically cleared
5),
6), 43)
.
The return to play protocol
5), 6) is a six step
process ( Ta b l e 3), where each step takes 24
hours. If any symptoms recur, the athlete is
put back to the previous level until he/she
is finally symptom-free. This protocol is to
be applied in all athletes, regardless of
whether the concussion is simple or com –
plex, or the athletes are professionals or
amateurs. The concept is based on physi –
Recently, another proteinopathy was de
–
scribed in former athletes
16) that is associ –
ated with the loss of the first motor neuron
and corticospinal tract degeneration: amy –
otrophic lateral sclerosis (ALS) has been
repeatedly obser ved and confirms reports
that (Italian) soccer players with previous
repetitive head injuries have a higher risk
for ALS
17 ).
Symptoms
Symptoms of mild head injury or concus –
sion are physical, cognitive, emotional,
or related to balance, coordination and
sleep disturbance (Table 1) . Symptoms
may or may not involve loss of conscious –
ness
5), 6), 18), 19), 20) . They subside by half wi –
thin 24–48 hrs and usually reach the pre-
injury level by day 7. Metabolic and neuro –
transmitter abnormalities
21) as well as
subtle neuropsychological, cognitive sym –
ptoms and balance disturbances may last
up to 30–45 days. Brain electrical activity
is abnormal at the time of injury and still
at day 8, despite the fact that symptoms
had already disappeared by that time
22).
Standard structural neuroimaging is nor –
mal
5), 6) .
The subsequent course is unpredictable.
In general, children need a longer period
for resolution of symptoms than do adults,
and most children will recover unremar-
kably. Risk factors for a slower recovery
are loss of consciousness > 1 min, prior
injuries, attention deficit hyperactivity
syndrome (ADHS), psychiatric disease,
depression, and anxiety
6). In some patients
recovery is complicated by the post-con –
cussion syndrome
18), a mix of physical,
emotional, and behavioral problems simi –
lar to depression, anxiety and attention
deficit disorder
5), 18), 19) . The post-concussi –
on syndrome is seen in more than half
(58%) of concussion patients after one
month, in more than 10% after three mon –
ths, and still in 2.3% of patients (e. g. hea-
dache) after one year. Symptoms are more
likely to persist in children older than 6
years, in those with preexisting injuries,
ADHS, or psychiatric disease
6), 24) . Recent
studies report that after a mild head injury,
75% of the young patients will show endo –
crinological dysfunction after six months
and almost 30% will suffer from thyroid
hypofunction, growth hormone deficiency
or premature puberty after one year
4), 25) .
logical und functional rather than the
structural aspects of the injury and is de
–
fined as a «… complex process affecting
the brain, induced by traumatic biochemi –
cal forces… »
5), 6) , or as a brain injury with
«… transient, traumatic disruption of brain
activity …»
11 ). A concussion is described as
a direct blow to the head, face or neck,
which results in short-lived impairment of
the neurological function of the brain.
Pathophysiology
Pathological studies have demonstrated
that head injuries – predominantly inflicted
by diffuse rotational and, to a lesser extent,
linear forces – destroy the axonal and cyto –
skeletal structures, which causes axonal
swelling and bulb formation. Failed axonal
transport in the injured axons causes an
accumulation of several proteins such as
amyloid precursor protein (APP), preseni –
lin-1 (PS-1), and β -APP cleaving enzyme
(BACE). Condensation of APP, PS-1 and
BACE causes amyloid β (A β) formation and
accumulation. The damaged neuronal cells
then release the accumulated A β. The en –
zyme neprilysin (NEP), that clears A β, is
also increased and released by the dama –
ged axons. This may mitigate the negative
effect of increased A β deposition in the
brain parenychma, which sometimes per –
sists for years and results in neurodegene –
ration and brain atrophy seen many years
after brain injury
12), 13) .
Additionally, the destruction of the cytos –
keletal structure increases the amount of
tau proteins in the brain. These features, A β
plaques and abnormal tau accumulation,
share many characteristics with Alzheimer’s
(AD) and Parkinson’s disease («pugilistic
parkinsonism»)
14). Elevation of tau proteins
in the CSF is also an ominous sign in severe
head injury patients
15).
Which field are we on?
Which team are we playing today?
Which quarter (period) is it?
Which side scored the last goal?
Which team did we play last week?
Did we win last week?
Table 2: Sideline evaluation:
Maddocks questions
Vol. 24 Nr. 1 2013
Fortbildung
16
AD is 33). Striking arguments for this hypo-
thesis are found in autopsies of former
athletes, who sustained multiple minor
head injuries
12), 30), 35) . A β plaques are found
even in children who died following a TBI 12).
These plaques are similar to those found in
the early stages of AD; they occur rapidly
within a few hours and appear not only in
the white, but also in the grey matter of the
brain parenchyma.
It is unclear and the subject of discussion
whether all athletes with recurrent injuries
have the same risk for developing CTE, or
only those with a genetic predisposition.
Susceptibility depends on (epi)genetic
factors, such as age, sex and ApoE4 and
other unknown genetic factors. In the non-
sporting population, ApoE4 polymorphism
is a risk factor for AD
33) and is associated
with a significantly poorer outcome for all
degrees of head injury
34), 36), 37) , especially
in children aged less than 15 years 38).
ApoE4 is also associated with earlier onset
of Aß deposition
33), 39) and a decreased
volume of the entorhinal cortex and hippo –
campus as compared to those without
ApoE4
33). Consequently, an ApoE4 poly –
morphism is a highly suspicious risk factor
for the development of CTE in athletes
with repetitive mild head injuries.
Second-Impact Syndrome (SIS)
Sustaining a second head trauma before
full recovery from the previous one
may bring on the second-impact syndro –
me
7), 40), 41) . The proposed pathophysiologi –
cal pathway is not known exactly 41 ). It is a
rare condition seen only in young athletes
(boxers, football, baseball but also soccer
players) under the age of 21 years
21). It is
often fatal (1–2 deaths per year in the US)
and may occur within up to two weeks
after taking the first hit, and can even be
triggered by the mildest degree of second
head injury
7). For this reason, all recent
guidelines strongly advocate adherence
to the return to play rule as outlined abo –
ve
7).
Prevention
In order to reduce and minimize the risk for
mild head injury in athletes, an attempt
must be made to improve several aspects:
firstly, injuries should be prevented by
changing the athletes’ attitude: respect the
Repetitive Mild Head Injury –
Chronic Traumatic Encephalo –
pathy, CTE
Recently, concerns about repetitive minor
traumatic head injuries came to public at –
tention in the media. National Geographic
(February 2011 issue) reported the history
of a 21–year-old football defensive back,
who took 537 (!) hits to the head in games
and practice during one season. Several
(> 20) had an impact equal to that sustained
when hitting a windshield in a car crash at
approx. 20 mph. After two hits he showed
symptoms of a concussion without loss of
consciousness.
Repeated concussions have a long-lasting
effect on cognitive and motor function,
even decades after the last injury
3 0 ) , 31) . Al –
ready in the 1920ies, in boxers (prize figh –
ters) with recurrent head injuries a syndro –
me called the «punch- drunk syndrome» or
«dementia pugilistica» was described. It is
characterized by dysarthria, pyramidal and
cognitive signs as well as other neuropsy –
chiatric symptoms like long-term cognitive
impairment
8), anxiety or depression 24). This
disorder, currently defined as chronic trau –
matic encephalopathy (CTE)
30), is a rare
event, given the high number of concussi –
ons occurring each year. Case studies de –
monstrate that a significant percentage
(15–20%) of former and retired athletes in
any contact sport will develop symptoms of
CTE
32), with a higher prevalence in those
with three or more concussions in their
history and those with an apolipoprotein E4
(ApoE4) polymorphism
33), 34) .
Recent research suggests that there is a
link between TBI and the development of
neurodegenerative diseases like AD, par-
kinsonism or dementia. The more severe
and the more often a TBI occurs, the grea –
ter the risk for and the earlier the onset of
cal/mental and cognitive rest. This means
no physical (work, sport) or cognitive
(school, noise, television, internet or text
messaging, bright light, sleep shortage)
activities should be undertaken. Light aero
–
bic (stationary biking, jogging to sprinting)
is followed by sport-specific exercise, then
non-contact, contact training and practice.
Any medication prescribed to reduce sym –
ptoms must be discontinued before training
starts. There is no cure for a concussion,
but treatment can help. For prolonged sym –
ptoms antidepressants or amantadine
(NMDA receptor antagonist)
28) may be an
option.
An exception from the rule «no return to
play the same day» can be made if a player
was consistently free of symptoms for 20
minutes following the concussion, had a
negative test and the team physician has
sufficient experience and adequate resour-
ces (neuropsychological assessment, neu –
roimaging) at his disposal
29). This approach
is adequate for adult athletes, but children
and adolescents should be treated more
conservatively
6), 23) .
These recommendations are reflected in
various laws enacted in recent years in the
United States. In 2007 Texas passed the
Will’s Bill, which requires high school coa –
ches, athletics trainers and even players to
undergo safety training such as in cardiopul –
monary resuscitation. The Zackery Lystedt
Law (May 2009) urged the development of
guidelines and educational materials for
athletes, parents and coaches. All athletes
suspected of having a concussion must be
removed from play and may not return be –
fore they have been cleared by a licensed
healthcare professional. In Switzerland gui –
delines for athletes, coaches and parents
are published by the Swiss Ice Hockey Le –
ague
43), but no obligatory/mandatory law
has passed the legislature.
Symptom-free at rest (daily progression to next step; if symptomatic, go back one step)
Advance to full cognitive activities
Stationary biking, jogging to sprinting (light aerobic exercise)
Non-contact, sport-specific exercise
Non-contact training
Full-contact practice
Return to play
Table 3: Return to Play Rule
Vol. 24 Nr. 1 2013
Fortbildung
17
bodies and heads of the players on your and
your opponent’s team. Wear an intact and
fixed helmet and a mouth guard and play
«heads-up»
20), 43) . Secondly, laws must be
passed to ensure mandatory facilities (re –
quire emergency and safety training for
sports officials in high schools, emergency-
trained physicians on the field) and proce –
dures (return to play rule). Thirdly, trainers
must be educated to recognize symptoms
and adhere to safety guidelines
5), 6), 26) . Last –
ly, written information must be provided for
the athletes and their parents similar to the
information supplied for non-sport related
mild head injuries
42), and the competence
of our profession as medical doctors must
also be improved.
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Correspondence
Burkhard Simma, MD
Department of Pediatrics
Academic Teaching Hospital
Landeskrankenhaus Feldkirch
Feldkirch 6800, Austria
burkhard.simma@lkhf.at
The authors certify that no financial sup –
port or other conflict of interest is related
to this article.
Vol. 24 Nr. 1 2013
Fortbildung
Weitere Informationen
Autoren/Autorinnen
Burkhard Simma , Department of Pediatrics Academic Teaching Hospital Landeskrankenhaus Feldkirch Daniela Jonas Prof. Dr. med. Jürg Lütschg , Universitäts-Kinderklinik beider Basel (UKBB) Andreas Nydegger
