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
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 (tauopa –
thies) is described by amyloidβ plaques in
those brains. A genetic predisposition (apo –
lipoprotein) 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 rela –
ted to sport. Recent studies
1), 2) have shown
that 20–50% of the minor head injuries
treated 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 injury
3). Also, many professional heal –
thcare providers think a concussion, even in
sports, is necessarily accompanied by a pe –
riod 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 symp –
toms.
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 sea –
son
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).
Physical Cognitive 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 No. 1 2013
Formation continue
15
Investigations
On the field, athletes should be managed
according to standard emergency prin-
ciples (ABC rule), giving particular atten –
tion to the cervical spine. On the sideline,
a neuropsychological assessment must
follow either briefly using the Maddocks
questions
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 in –
cludes symptom evaluation, calculation of
the Glasgow Coma Scale score, sideline
assessment (Maddocks questions) and –
importantly – a cognitive, balance and
coordination assessment. However, the
SCAT2 has never been evaluated in a pros –
pective study. Consequently, no normative
data or «cut-offs» are available for it. Ne –
vertheless, it is a useful, practicable and
standardized tool for estimating the risk for
athletes following a head injury. Other
neuropsychological tests are web-based
(imPACT
®, HeadMinder ®, Cog State ®)5) and
developed specifically for athletes’ inju –
ries. 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 al –
lowed 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 sustaining a hit
to the head in order to not miss any dete –
rioration, 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 –
cal/mental and cognitive rest. This means
Recently, another proteinopathy was des
–
cribed in former athletes
16) that is associa –
ted with the loss of the first motor neuron
and corticospinal tract degeneration:
amyotrophic 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 wit –
hin 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
symptoms 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 neuroima –
ging is normal 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-
concussion syndrome
18), a mix of physical,
emotional, and behavioral problems simi –
lar to depression, anxiety and attention
deficit disorder
5), 18), 19) . The post- concus –
sion syndrome is seen in more than half
(58%) of concussion patients after one
month, in more than 10% after three
months, and still in 2.3% of patients (e. g.
headache) 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 defi
–
ned as a «… complex process affecting the
brain, induced by traumatic biochemical
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 cy –
toskeletal 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 da –
maged axons. This may mitigate the nega –
tive 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 Alzhei –
mer’s (AD) and Parkinson’s disease («pugi –
listic 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 No. 1 2013
Formation continue
16
AD is 33). Striking arguments for this hy-
pothesis 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 syn –
drome
7), 40), 41) . The proposed pathophysio –
logical 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 de –
gree of second head injury
7). For this
reason, all recent guidelines strongly
advocate adherence to the return to play
rule as outlined above
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) . Already in
the 1920ies, in boxers (prize fighters) with
recurrent head injuries a syndrome called
the «punch-drunk syndrome» or «dementia
pugilistica» was described. It is characte –
rized by dysarthria, pyramidal and cognitive
signs as well as other neuropsychiatric
symptoms like long-term cognitive impair-
ment
8), anxiety or depression 24). This disor-
der, currently defined as chronic traumatic
encephalopathy (CTE)
30), is a rare event, gi –
ven the high number of concussions occur-
ring each year. Case studies demonstrate
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) polymor –
phism
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
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 symp –
toms must be discontinued before training
starts. There is no cure for a concussion,
but treatment can help. For prolonged
symptoms 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 re –
sources (neuropsychological assessment,
neuroimaging) at his disposal
29). This ap –
proach 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
coaches, athletics trainers and even players
to undergo safety training such as in cardio –
pulmonary resuscitation. The Zackery
Lystedt Law (May 2009) urged the develop –
ment of guidelines and educational mate –
rials for athletes, parents and coaches. All
athletes suspected of having a concussion
must be removed from play and may not
return before they have been cleared by a
licensed healthcare professional. In Swit –
zerland guidelines for athletes, coaches and
parents are published by the Swiss Ice
Hockey League
43), but no obligatory/man –
datory 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 No. 1 2013
Formation continue
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) .
Lastly, written information must be provi –
ded for the athletes and their parents simi –
lar 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.
References
1) Callahan JM. Pediatric Concussions in United
States Emergency Depar tments: The Tip of the
Iceberg. J. Pediatr 2010; 157: 873–5.
2) Bakhos LL, Lockhar t GR, Myers R, Linakis JG. Emer –
gency depar tment visits for concussion in young
child athletes. Pediatrics 2010; 126: e550–6.
3) Guilmette TJ, Paglia MF. The public’s misconception
about traumatic brain injury: a follow-up survey.
Arch Clin Neuropsychol 2004; 19: 183–9.
4) Meehan WP. Mannix R. Pediatric concussions in
United States emergency depar tments in the years
2002 to 2006. J Pediatr 2010; 157: 889–93.
5) Halsted ME, Walter KD. Council on Sports Medicine
and Fitness. American Academy of Pediatrics. Cli –
nical report: Sport-related concussion in children
and adolescents. Pediatrics 2010; 126: 597–615.
6) McCror y P, Meeuwisse W, Johnston K, et al.
Consensus statement on concussion in spor t: The
3
rd International Conference on Concussion in
Spor t held in Zurich, November 2008. Br J Spor ts
Med 2009; 43 (Suppl I): i76–i90.
7) Smith BW. Head injuries. In SJ Anderson, SS Harris,
eds., Care of the Young Athlete, 2
nd. ed., pp. 185–
191. Elk Grove Village, IL: American Academy of
Pediatrics.
8) Guskiewicz KM, Weaver NL, Padua DA, et al. Epide –
miology of concussion in collegiate and high school
football players. Am J Spor ts Med 2000; 28: 643–
50.
9) Guskiewicz KM, McCrea M, Marshall SW, et al.
Cumulative effects associated with recurrent
concussion in collegiate football players. The NCA A
Concussion Study. JAMA 2003; 290: 2549–55.
10) Collins MW, Lovell MR, Iverson GL, et al. Cumulative
ef fects of concussion in high school athletes. Neu –
rosurger y 2002; 51: 1175–81.
11) Piatt JH. Traumatic brain injury In: Clinical Pediatric
Neurosciences. First Edition. Legido A, Piatt JH
(Eds), Elk Grove Village, American Academy of Ped –
iatrics, 2009; 171–215.
12) Johnson VE, Stewar t W, Smith DH. Traumatic brain
injur y and amyloid-ß pathology: a link to Alzhei –
mer’s disease? Nat Rev Neurosci 2010; 11: 361.
13) Miller G. A Late Hit for Pro Football Players. Science
2009; 325: 670–2.
14) DeKosky ST, Ikonomovic MD, Gandy S. Traumatic
Brain Injur y- Football, War fare, and Long-Term Ef –
fects. N Eng J Med 2010; 363: 1293–6.
15) Liliang PC, Liang CL, Weng HC,et al. Tau proteins in
serum predict outcome after severe traumatic
brain injur y. J Surg Res. 2010; 160: 302–7.
16) McKee AC, Gavett BE, Stern RA, et al. TDP- 43
proteinopathy and motor neuron disease in chronic
traumatic encephalopathy. J Neuropathol Exp Neu –
rol 2010; 69: 918–29.
17) Chio A, Benzi G, Dossena M, et al. Severely in –
creased risk of amyotrophic lateral sclerosis
among Italian professional football players. Brain
2005; 138: 472–6.
18) Barlow KM, Craw ford S, Stevenson A et al. Epide –
miology of post- concussion syndrome in pediatric
mild traumatic brain injury. Pediatrics 2010; 126:
373 – 81.
19) McCrea M, Guskiewicz KM, Marshall SW, et al.
Acute ef fects and recover y time following concus –
sion in collegiate football players: the NCA A
Concussion Study. JAMA 2003; 290: 2556–63.
20) American Academy of Neurolog y. Practice parame –
ters: the management of concussion in sports:
Centers for Disease Control and Prevention.
http://www.cdc.gov/ncipe/pub-res/tbi_tollkit/
physician/concussions_sports.pdf (accessed Au-
gust 23
rd 2012).
21) Zanfonte R. Diagnosis and management of sports-
related concussion: a 15 -year- old athlete with a
concussion. JAMA. 2011; 306: 79–86.
22) Barr WB, Prichep LS, Chabot R, et al. Measuring
brain electrical activity to track recover y from sport-
related concussion. Brain Inj 2012; 26: 58–66.
23) Zuckerman SL, Odom M, Lee YM, et al. Spor t-rela –
ted concussion and age: number of days to neuro –
cognitive baseline. Neurosurger y 2012; 71: 558.
24) Guskiewicz KM, Marshall SW, Bailes J, et al. Recur –
rent concussion and risk of depression in retired
professional football players. Med Sci Sports Exerc
2007; 39: 903–9.
25) Kaulfers A, Backeljauw PF, Reifschneider K, et al.
Endocrine dysfunction following traumatic brain
injur y in children. J Pediatr 2010; 157: 894–9.
26) Maddocks DL, Dicker GD, Saling MM. The assess –
ment of orientation following concussion in ath –
letes. Clin J Spor ts Med 1995; 5: 32–5.
27) Jinguji TM, Bompadre V, Harmon KG, et al. Spor t
Concussion Assessment Tool 2: baseline values for
high school athletes. Br J Spor ts Med 2012; 46:
365 –70.
28) Giacino JT, Whyte J, Bagliella E. Placebo – controlled
trial of amantadine for severe traumatic brain inju –
r y. N Engl J Med 2012; 366: 819–26.
29) Makdissi M, McCror y P, Ugoni A, et al. A prospec –
tive study of post- concussive outcomes after re –
turn to play in Australian football. Am J Spor ts Med
2009; 37: 877–83.
30) McCror y P. Spor ts concussion and the risk of chro –
nic neurological impairment. Clin J Spor t Med 2011;
21: 6–12.
31) De Beaumont L, Théoret H, Mongeon D et al. Brain
function decline in healthy retired athletes who
sustained their last spor ts concussion in early
adulthood. Brain 2009; 132: 695–708.
32) Guskiewicz KM, Marshall SW, Bailes J, et al. Asso –
ciation between recurrent concussion and late-life
cognitive impairment in retired professional foot –
ball players. Neurosurger y 2005; 57: 719–26.
33) Verghese PB, Castello JM, Holtzman DM. Apolipo –
protein E in Alzheimer’s Disease and other neuro –
logical disorders. Lancet Neurol 2011; 10: 241–52.
34) Liberman J, Stewart W, Wesnes K, et al. Apolipopro –
tein E epsilon 4 and shor t-term recover y from
predominantly mild head injury. Neurology 2002;
58: 1038–4 4.
35) McKee AC, Cantu RC, Nowinski CJ, et al. Chronic
traumatic encephalopathy in athletes: progressive
tauopathy after repetitive head injury. J Neuropa –
thol Exp Neurol 2009; 68: 709–35.
36) Friedmann G, Froom P, Sazbon L, et al. Apolipopro –
tein E- epsilon 4 genotype predicts a poor outcome
after head injur y. Neurology 1999; 52: 244–8.
37) Zhou W et al. Meta-analysis of APOE E4 allele and
outcome after traumatic brain injury J Neurotrauma
2008; 25: 279–90.
38) Teasdale G, Murray G, Nicoll JA. The association
between APOE β4, age and outcome after head in –
jur y: a prospective cohor t study. Brain 2005; 128:
2 5 5 6 – 61 .
39) Nicoll JA, Rober ts GW, Graham DI. Apolipoprotein
E β4 allele is associated with deposition of amyloid
ß protein following head injur y. Nature Med 1995;
1 : 1 3 5 – 7.
40) McCror y P, Berkovic SF. Second-impact syndrome.
Neurology 1998; 50: 677–8.
41) McCror y P, Davis G, Makdissi M. Second-impact
syndrome or cerebral swelling after spor ting head
injur y. Curr Spor ts Med Rep 2012; 11: 21–3.
42) Vernet O, Lutz N, Rilliet B. Die Betreuung des kindli –
chen Schädelhirntraumas. Paediatrica 2004; 15:
4 7.
43) http://www.swiss-icehockey.ch/SIH/medical/de/
medkomm_concussion.php (accessed Agust 23
rd
2012).
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 No. 1 2013
Formation continue
Informations complémentaires
Auteurs
Burkhard Simma , Department of Pediatrics Academic Teaching Hospital Landeskrankenhaus Feldkirch Daniela Jonas Prof. Dr. med. Jürg Lütschg , Universitäts-Kinderklinik beider Basel (UKBB) Andreas Nydegger