European Journal of Neurology 2002, 9: 207–219

EFNS TASK FORCE

EFNS guideline on mild traumatic brain injury: report of an EFNS task force
P. E. Vosa, L. Battistinb, G. Birbamerc, F. Gerstenbrandc, A. Potapovd, T. Prevece, Ch. A. Stepanf,
P. Traubnerg, A. Twijnstrah, L. Vecseii and K. von Wildj
a
Department of Neurology, University Medical Centre Nijmegen, Nijmegen, The Netherlands; bClinica Neurologica I, Padova, Italy; cLudwig
Boltzmann Institute for Restorative Neurology and Neuromodulation, Vienna, Austria; dInstitute of Neurosurgery, Russian Academy of
Medical Sciences, Moscow, Russia; eUniversity Institute of Clinical Neurophysiology, University Medical Centre, Ljubljana, Slovenia;
f
Neurological Hospital Rosenhügel, Vienna, Austria; gDepartment of Neurology, Comenius University School of Medicine, Bratislava, Slovak
Republic; hDepartment of Neurology, University Medical Centre Maastricht, Maastricht, The Netherlands; iDepartment of Neurology,
Szent-Györgyi University Hospital, Szeged, Hungary; and jNeurochirurgische Klinik, Clemens Hospital, Münster, Germany

Keywords: In 1999, a Task Force on Mild Traumatic Brain Injury (MTBI) was set up under the
clinical decision rule, auspices of the European Federation of Neurological Societies. Its aim was to propose
computed tomography, an acceptable uniform nomenclature for MTBI and definition of MTBI, and to
guideline, head injury, develop a set of rules to guide initial management with respect to ancillary
intracranial complication, investigations, hospital admission, observation and follow-up.
mild traumatic brain
injury, risk factors

Received 21 February 2002

Accepted 21 February 2002

reactions. The outcome is almost invariably poor (death

Introduction
or a vegetative state/traumatic apallic syndrome)
That trauma of the head can cause brain injury has long (Table 1) (Gerstenbrand and Lucking, 1970; Frowein
been recognized. Indeed, the term commotio cerebri and Firsching, 1990; Stein and Spettell, 1995).
was used already in the sixteenth century by Ambroise More than 95% of all TBIs are considered mild, with
Pare (cf. Denny-Brown and Russell, 1941; Frowein and moderate and severe TBI together accounting for only
Firsching, 1990). Trauma of the head is a common 5% of cases (Meerhoff et al., 2000). Mortality in MTBI
cause of morbidity and mortality in European coun- is low (between 0.04 and 0.29%) and almost exclusively
tries. The incidence of traumatic brain injury (TBI) caused by intracranial haemorrhage (Klauber et al.,
varies between 229 and 1967 per 100 000, with the 1989). Intracranial haemorrhage (extradural or subdur-
highest incidence occurring in men aged 15–24 years al) that often requires neurosurgical intervention occurs
(Jennett, 1996; Kraus et al., 1996). TBI is the leading in 0.2–3.1% of all MTBI patients and between 6.3 and
cause of death among people younger than 45 years 21% have other intracranial complications [computed
(Jennett, 1996; Kraus et al., 1996). tomography (CT) abnormalities] (Shackford et al.,
Usually, TBI is classified as mild, moderate or severe 1992; Stein and Ross, 1992; Borczuk, 1995; Culotta
(Table 1). There is general agreement that in mild et al., 1996; Dunham et al., 1996; Hsiang et al., 1997;
traumatic brain injury (MTBI) patients have a hospital Haydel et al., 2000; Stiell et al., 2001).
admission Glasgow Coma Score (GCS) of 13–15 Early recognition of symptoms and signs known to
(Teasdale and Jennett, 1974; Williams et al., 1990; increase the risk of development of an intracranial
Gomez et al., 1996; Haydel et al., 2000; Stiell et al., haemorrhage is the key issue of initial management
2001). In moderate TBI, patients have an admission (Haydel et al., 2000; Stiell et al., 2001).
GCS of 9–12, and in severe TBI an admission GCS of 8
or less after resuscitation (Table 1) (Bullock et al.,
Search strategy
1996). A fourth (critical) grade refers to the severest
form of TBI, in which there is evidence of brain stem The Task Force systematically searched the English
damage (with acute midbrain or bulbar syndrome), literature in the MEDLINE database (1966–2001) using
with diminished or no pupillary reactions and decere- the keywords minor head injury, mild head injury, mild
brate motor posturing, or absent pupillary and motor traumatic brain injury, traumatic brain injury and
management. Additional articles were identified from
Correspondence: Dr Pieter E. Vos, University Medical Centre
the bibliographies of the articles retrieved (including
Nijmegen, PO Box 9101, 6500 HB, Nijmegen, The Netherlands also the German language) and from textbooks. Arti-
(fax: + 31 24 354 1122; e-mail: [email protected]). cles were included if they contained data on at least one

ª 2002 EFNS 207

208 P. E. Vos et al.

Table 1 Classification of traumatic brain injury

Admission Glasgow Coma Scale Score (GCS) and clinical characteristics modified from the Dutch,
Scandinavian and American classification systems (Teasdale and Jennett, 1974; Stein and Spettell,
Classification 1995; Maas et al., 1997; Ingebrigtsen et al., 2000; Twijnstra et al., 2001)

Mild GCS ¼ 13–15

Category 0 GCS ¼ 15
No LOC, no PTA, ¼ head injury, no TBI
No risk factors
Category 1 GCS ¼ 15
LOC < 30 min, PTA < 1 h
No risk factors
Category 2 GCS ¼ 15 and risk factors present*
Category 3 GCS ¼ 13–14
LOC < 30 min, PTA < 1 h
With or without risk factors present*
Moderate GCS ¼ 9–12
Severe GCS £ 8
Critical GCS ¼ 3–4, with loss of pupillary reactions and absent or decerebrate motor reactions

TBI, traumatic brain injury; GCS, Glasgow Coma Scale; LOC, loss of consciousness; PTA, post-traumatic amnesia. *Risk factors are shown in
Table 2.

of the following: patients classified according to known fracture and extradural haematoma, all types of brain
classification systems (i.e. admission GCS 13–15), injury can be produced by (angular) acceleration of the
outcome data (CT abnormalities, need for neurosurgi- head without impact, provided there is a period of loss
cal intervention, mortality) or management. Articles of consciousness (LOC) (Gennarelli et al., 1982). Thus,
judged to be of historical value were also included. For shear forces generated in the brain upon sudden
the purpose of this report a total of 125 papers were rotation may cause damage to axons and blood vessels
finally included. Additional information can be found (Houlbourn, 1943; Gennarelli, 1983; Grcevic, 1988;
on the European Federation of Neurological Societies Gerstenbrand and Stepan, 2001). Controversy exists on
(EFNS) website. Where appropriate, a classification of whether diffuse brain dysfunction can occur in MTBI
evidence level (EL) was given for interventions, diag- without there being structural damage. Spatz and
nostic tests and grades of recommendation for man- others defined commotio cerebri as a functional distur-
agement according to the neurological management bance without any damage to brain tissue (‘traceless
guidelines of the EFNS (Hughes et al., 2001). disturbances’) (Trotter, 1924; Spatz, 1936). This has
considerable consequences for the terminology used
and is a frequent source of problems in forensic and
Mechanisms of traumatic brain injury
insurance issues after TBI.
Traumatic brain injury is usually the consequence of Brain damage after head injury can also be classified
impact to the head, during which energy (impulse) is by its time course (Teasdale, 1995; Maas et al., 1997).
transmitted to the head, which undergoes sudden Primary damage occurs at the moment of impact and is
acceleration, deceleration or rotation. Head trauma thought to be irreversible. Secondary brain damage
can be closed, blunt, if the skull remains intact, or evolves in hours or days after the injury as a conse-
penetrating if the skull and (often) the dura are quence of systemic (predominantly hypoxia and hypo-
penetrated by sharp objects (including gunshot, knives, tension) or intracranial complications (brain oedema,
screwdrivers, arrows, darts) (Bayston et al., 2000). tentorial or foraminal herniation). Tertiary complica-
Focal damage, or contact injuries, such as skull tions (sepsis, thromboembolic complications, critical
fracture, extradural haematoma, contusion-related sub- illness polyneuropathy) may occur days or weeks after
dural haematoma, cortical contusion, are produced by the trauma as a result of an altered catabolic state or
direct collisional forces acting on the skull, resulting in increased thrombosis because of bed rest, paralysis or
compression of underlying tissue (coup) or of tissue infection (Gerstenbrand, 1977).
remote from the site of the impact (contre coup)
(Pudenz and Shelden, 1946; Sellier and Unterharn-
Classification of MTBI
scheidt, 1963).
Impact to the head per se is not mandatory to evoke Many different terms exist to describe and define MTBI
brain dysfunction or brain damage. Except for skull (Frowein and Firsching, 1990; Williams et al., 1990;

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 Guideline on mild traumatic brain injury 209

Evans, 1992; Pople et al., 1993; Birbamer et al., 1994; 1993; Gomez et al., 1996; Jennett, 1996; Haydel et al.,
Stein and Spettell, 1995; Teasdale, 1995; Culotta et al., 2000; Ingebrigtsen et al., 2000). Likewise, there is no
1996; Gomez et al., 1996; Saab et al., 1996; Arienta uniform duration of coma to define MTBI, and thus any
et al., 1997; Ingebrigtsen et al., 2000 Gerstenbrand and limit set is necessarily arbitrary. The aim of the Task
Stepan, 2001; von Wild and Terwey, 2001). Here, a Force is to align these guidelines with other interna-
classification is proposed based on admission GCS, tional classifications (e.g. Mild Traumatic Brain Injury
trauma history [i.e. the duration of LOC and post- Committee of the American Congress of Rehabilitation
traumatic amnesia (PTA)], neurological findings and Medicine, 1993). There are studies showing that out-
risk factors for intracranial complications. Several come is not adversely affected by a short period of LOC.
subclassifications have been proposed to facilitate In children, a 100% good outcome was found if LOC
initial management decisions (Grade B, recommenda- was less than 15 min (Hahn and McLone, 1993)
tion) (Table 1, and Fig. 1 later). (EL ¼ II). In another study, the number of post-
Recommendation: MTBI is defined as the conse- traumatic subjective complaints, neurocognitive per-
quence of blunt (non-penetrating) impact with sudden formance and pre-existing emotional risk factors did not
acceleration, deceleration or rotation of the head with a correlate with the duration of LOC after MTBI
GCS score of 13–15 on admission to hospital. If the (EL ¼ II) (Ruff and Jurica, 1999). Jennett (1996) stated
duration of LOC is maximally 30 min and PTA is less that a duration of altered consciousness of less than
than 60 min, the outcome is considered good (mortality 15–30 min could be considered as mild (EL ¼ IV).
<1%), especially in the absence of risk factors (mor-
tality approaching 0) (Grade B, recommendation)
PTA
(Table 1).
Post-traumatic (or anterograde) amnesia is the period
of inability to lay down continuous memories (amnesic
Admission GCS
for ongoing events) and is often characterized by
Accurate determination of the admission GCS is confusion (Levin et al., 1979; Tate et al., 2000). A
important because the number of intracranial abnor- distinction is usually made between disorientation and
malities and the need for neurosurgical interventions amnesia because the two do not always disappear at the
are inversely related to the admission GCS (Culotta same time (Tate et al., 2000). The outcome of MTBI
et al., 1996; Gomez et al., 1996). The time between the and return to work are determined more by the
accident and hospital admission can influence the GCS. duration of PTA than by the admission GCS (EL ¼ III)
Recent studies used 24 h as the maximum delay for III) (van der Naalt et al., 1999a). If the PTA is shorter
hospital admission, but this delay is often not men- than 24 h, a good outcome (as measured with the
tioned (Jennett, 1996; Haydel et al., 2000; Stiell et al., Glasgow Outcome Scale) is found in 100% of patients
2001). The GCS is also the most frequently used scoring (EL ¼ II) (van der Naalt et al., 1999a). Retrograde
tool in children; however, it is less appropriate for very amnesia is the loss of memory for the period before the
young children whose motor and verbal skills are not accident.
yet fully developed, and for this reason alternative Recommendation: Post-traumatic amnesia shorter
scales have been developed (Simpson et al., 1991; than 1 h and/or a retrograde amnesia shorter than
Durham et al., 2000). The Paediatric Glasgow Coma 30 min are compatible with MTBI and are associated
Scale uses age-adjusted maximal scores but is based on with a good outcome (Grade B, recommendation).
a 14-point GCS instead of the 15-point GCS (Reilly
et al., 1988).
Risk factors

Several symptoms, signs and risk factors associated

Duration of loss of consciousness
with an increased risk of intracranial injury have been
Verification of whether LOC has occurred and accurate identified (EL ¼ II–III) (see Table 2 for overview)
assessment of the duration of LOC are essential because (Masters et al., 1987; Chan et al., 1990; Arienta et al.,
LOC increases the risk of skull fracture and intracranial 1997; Haydel et al., 2000).
complications (EL ¼ Class III) (Teasdale et al., 1990; Recommendation: Recognition of risk factors is
Stein and Spettell, 1995; Gomez et al., 1996). important and such factors should be included in a
There is little agreement on how long LOC should last classification system to further assess the risk of
for the trauma to be defined as MTBI. Times of 5, 10, immediate complications (extracerebral haematoma)
15–20, or 30 min have been reported (Rimel et al., 1981; (Grade B, recommendation). Moreover, this may
Williams et al., 1990; Evans, 1992; Hahn and McLone, enable assessment of the risk for long-term complaints.

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210 P. E. Vos et al.

Table 2

Risk factors for intracranial complications after mild traumatic

brain injury References

Unclear or ambiguous accident history Masters et al. (1987), Vos et al. (2000)
Continued post-traumatic amnesia* Haydel et al. (2000), Stiell et al. (2001)
Retrograde amnesia longer than 30 min Stiell et al. (2001)
Trauma above the clavicles including clinical signs of Feuerman et al. (1988), Haydel et al. (2000), Masters et al. (1987),
skull fracture (skull base or depressed skull fracture) Stiell et al. (2001), Teasdale et al. (1990)
Severe headache Haydel et al. (2000)
Vomiting Nee et al. (1999), Haydel et al. (2000), Stiell et al. (2001)
Focal neurological deficit Masters et al. (1987), Teasdale et al. (1990)
Seizure Masters et al. (1987)
Age < 2 years Masters et al. (1987), Levin et al. (1992b)
Age > 60** Gomez et al. (1996), Haydel et al. (2000), Stiell et al. (2001)
Coagulation disorders Saab et al. (1996), Stein et al. (1992), Volans (1998)
High-energy accident*** American College of Surgeons (1997), Bartlett et al. (1998), Stiell et al.
(2001)
Intoxication with alcohol/drugs Cardoso and Galbraith (1985), Boyle et al. (1991), Kelly (1995)

*Continued post-traumatic amnesia may be interpreted as a GCS verbal reaction of 4 and hence may be defined as GCS < 15. **The Canadian
CT head rule found age above 65 to be a risk factor (Stiell et al., 2001). ***According to Advanced Trauma Life Support principles, a high-energy
(vehicle) accident is defined as initial speed >64 km/h, major auto-deformity, intrusion into passenger compartment >30 cm, extrication time
from vehicle >20 min, falls >6 m, roll over, auto–pedestrian accidents, or motor cycle crash >32 km/h or with separation of rider and bike
(American College of Surgeons Committee on Trauma, 1997; Bartlett et al., 1998).

visualized on CT and that are likely to be the result of

Complications
the head trauma (Grade C, recommendation).
This definition of intracranial complication affects
Intracranial abnormalities
short- and long-term management issues and makes it
The various cranial, extracerebral and intracerebral possible to relate short- and long-term complications
complications of (mild) TBI can be divided into to intracranial abnormalities present after MTBI. CT
abnormalities that (often) need neurosurgical interven- findings can also predict the absence of late disease
tion (extracerebral haematoma, depressed skull frac- progression. In a study in 2032 patients, no neurolog-
ture, growing skull fracture) and those that cannot ical deterioration occurred and no haematoma was
be treated neurosurgically (contusion zones, brain found when the findings of CT performed within 24 h
oedema, diffuse injury, small haemorrhages, traumatic were normal (EL ¼ Class II) (Dunham et al., 1996).
subarachnoid haemorrhage, pneumocephalus) (Teas- Recommendation: MTBI may produce a variety of
dale et al., 1990; Lloyd et al., 1997; Ingebrigtsen et al., (intra)cranial abnormalities that can be divided into
2000). CT is very sensitive for the detection of those that can be neurosurgically treated and those that
extracerebral haematoma and other intracranial cannot. CT is the gold standard for the detection of
abnormalities, although no formal CT classification intracranial abnormalities and is a safe method for
for MTBI exists, and the sensitivity and specificity and home triage (Livingston et al., 1991; Dunham et al.,
the interrater and intrarater variability of the various 1996) (Grade B, recommendation).
intracranial CT abnormalities are not known. The
percentage of patients with intracranial abnormalities
Neurosurgical intervention
varies with the definitions used, the clinical inclusion
criteria and the radiography method used (Stein and The probability of neurosurgical intervention after
Spettell, 1995; Culotta et al., 1996). Reported rates MTBI is between 0.2 and 3.1%. Neurosurgical inter-
vary between 3 and 13% in patients with an admission vention is defined in different studies as craniotomy or
GCS of 15 and between 25 and 37.5% in patients with craniectomy for haematoma evacuation or explora-
an admission GCS of 13 (Stein and Ross, 1992; tion, elevation of depressed skull fracture, intracranial
Culotta et al., 1996; Dunham et al., 1996; Stiell et al., pressure monitoring, intubation for head injury, ag-
2001). gressive medical treatment or not specified (Stein and
Recommendation: The term intracranial complication Ross, 1992; Culotta et al., 1996; Gomez et al., 1996;
includes all cranial, extracerebral, and intracerebral Haydel et al., 2000; Stiell et al., 2001). An extradural,
abnormalities in relation to head trauma that can be or epidural, haematoma is a collection of blood

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 Guideline on mild traumatic brain injury 211

between the dura and skull bone, often as a result of a gically is potentially the most threatening complication
ruptured meningeal middle artery in close relation to a after MTBI (Grade B, recommendation). An extradural
temporal bone fracture or at other sites as a result of haematoma can be easily identified with CT, which
torn dural vessels or oozing from the skull bone should be carried out urgently (Grade B, recommen-
(including the fossa posterior) (Frowein and Firsching, dation).
1990). Although such haematomas are probably pre- Recommendation: The primary goal of initial man-
sent from the moment of impact and visible on CT as agement in MTBI is to identify the patients at risk of
collections of blood, there is often a delay (lucid intracranial abnormalities and especially those that
interval) between the trauma and the moment the may need neurosurgical intervention. Use of a clin-
extradural haematoma enlarges and becomes sympto- ical decision scheme based on risk factors may
matic (usually within 6 h) (Knuckey et al., 1989; Smith facilitate this process (Grade B, recommendation)
and Miller, 1991). The lower the admission GCS, the (see Fig. 1).
higher the risk of an intracranial extracerebral haema-
toma (Teasdale et al., 1990; Stein and Spettell, 1995;
Seizures
Gomez et al., 1996). The frequency of extracerebral
haematoma (extradural or subdural) has been estima- Patients with MTBI have only a slightly increased risk
ted to range from 1 in 31 370 in fully conscious of developing post-traumatic seizures including early
patients without a history of altered consciousness to 1 post-traumatic seizures (a seizure occurring in the first
in 8 (12.7%) in patients with a hospital admission week) (Schierhout and Roberts, 1997; Annegers et al.,
GCS of 13 (Teasdale et al., 1990; Culotta et al., 1996). 1998). Prophylactic antiepileptic treatment is not war-
In a meta-analysis of 10 studies in which at least 50% ranted. A systematic review of randomized controlled
of the patients underwent CT, the weighted mean trials including 2036 patients showed that prophylactic
frequency of intracranial haemorrhage after MTBI antiepileptic treatment did not reduce mortality, neu-
was 0.083% [95% confidence interval (CI): 0.03– rological disability or late seizures (EL ¼ I) (Schierhout
0.13%] (Hofman et al., 2000). and Roberts, 1998). If recurrent seizures occur, treat-
The mortality of MTBI, after systemic (multiple) ment is probably necessary and alternative explanations
injuries are excluded, is very low and almost exclu- (i.e. delayed haematoma, Wernicke–Korsakoff syn-
sively caused by the late or missed diagnosis of drome, alcohol withdrawal or electrolyte disturbances)
deterioration in patients with an intracranial haemor- should be taken into account.
rhage (specifically an extradural haematoma) Recommendation: There is insufficient proof for
(EL ¼ II–III) (Mendelow et al., 1979; Klauber et al., prophylactic antiepileptic treatment after an early
1989; Shackford et al., 1992; Culotta et al., 1996; seizure (Grade A).
Dunham et al., 1996; Gomez et al., 1996; Jennett,
1996; Servadei et al., 2001; Stiell et al., 2001). The
Skull base fracture
prognosis of extradural haematoma is good, especially
when it is detected early in fully conscious patients and A skull base or temporal bone fracture or open
surgery is performed as soon as possible (Paterniti fracture increases the risk of cerebrospinal fluid (CSF)
et al., 1994; Servadei et al., 1995; Servadei, 1997). leakage and CSF fistula formation (Dagi et al., 1983;
However, when rapid neurological deterioration occurs Brodie, 1997; Brodie and Thompson, 1997). The
or when patients are already in coma, mortality rises reported incidence of CSF leakage after basal skull
sharply with the delay between deterioration and fracture varies from approximately 10 to 20%, and the
surgery (EL ¼ III) (Mendelow et al., 1979; Seelig incidence of bacterial meningitis from 2 to 50% (Leech
et al., 1984; Servadei, 1997). and Paterson, 1973; Dagi et al., 1983; Helling et al.,
The growing skull fracture has a very low frequency 1988; Marion, 1991; Brodie, 1997; Brodie and Thomp-
of 0.05–0.6%. It is most likely to occur in children son, 1997). The role of antibiotic prophylaxis in open
younger than 6 years, when a dural tear beneath a skull or basilar skull fractures remains controversial; the
fracture is present and systolic–diastolic pulsations conclusions of two recent meta-analyses on the
result in widening of the fracture margins and inter- prophylactic use of antibiotics were contradictory
position of leptomeninges or brain tissue into the (Demetriades et al., 1992; Brodie, 1997; Villalobos
fracture. It is mentioned here as a long-term compli- et al., 1998).
cation that occurs if early diagnosis and intervention Recommendation: There is insufficient proof for
are deferred. prophylactic antibiotic treatment against meningitis in
Recommendation: The extracerebral haemorrhage patients with clinical signs of a skull base fracture,
(extradural haematoma) that can be treated neurosur- and a definitive study of prophylactic administration

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212 P. E. Vos et al.

Figure 1 Decision scheme for initial management in mild traumatic brain injury (modified from the Dutch and Scandinavian guidelines)
(Ingebrigtsen et al., 2000; Twijnstra et al., 2001). GCS, Glasgow Coma Scale; LOC, loss of consciousness; PTA, post-traumatic amnesia;
TBI, traumatic brain injury; CT, computed tomography; MRI, magnetic resonance imaging. *Risk factors are shown in Table 2. **If
CT availability is limited, conventional skull radiography can be performed but the sensitivity and specificity for intracranial abnormalities
is low.

of antibiotics for post-traumatic CSF fistula has yet

Patients on anticoagulation
to be performed (Grade C) (Working Party of the
British Society for Antimicrobial Chemotherapy, Recommendation: All patients with head injury should
1994). be questioned about the use of anticoagulation therapy

ª 2002 EFNS European Journal of Neurology 9, 207–219

 Guideline on mild traumatic brain injury 213

(Grade C, recommendation). All patients with head ion. This model showed 100% (95% CI: 95–100%)
injury on anticoagulation therapy should have their sensitivity for intracranial complications. Application
INR checked and the indication for anticoagulation of the criteria would have resulted in a CT ordering
reviewed (Grade C). These patients should be admitted proportion of 78% (or reduced use of CT of 22%)
for neurological observation (Grade C, recommenda- (Haydel et al., 2000).
tion) (Saab et al., 1996). If CT demonstrates an In the Canadian prospective cohort study involving
intracranial haematoma, the INR should be corrected 3121 patients, 250 patients (8%) had clinically import-
immediately. (Over-)anticoagulation can be best cor- ant brain injury and 31 (1%) required neurosurgical
rected with fresh frozen plasma and vitamin K. If intervention. Five high-risk factors (failure to reach
spontaneous coagulation disorders or additional injur- GCS of 15 within 2 h, suspected open skull fracture,
ies with bleeding exist consultation with a coagulation any signs of basal skull fracture, vomiting >2 episodes
specialist should be sought (Grade C, recommenda- or age >65 years) were derived which had 100%
tion). sensitivity (95% CI: 92–100%) for predicting the need
for neurosurgical intervention (Stiell et al., 2001).
Interestingly, this would lead to a CT ordering propor-
Ancillary investigations
tion of 32%. In addition, two medium-risk factors
(amnesia before impact >30 min and dangerous mech-
Skull radiography versus CT
anism of injury) were 98.4% sensitive (95% CI 96–
The diagnostic value of plain skull radiography is 99%) and 49.6% specific for predicting clinically
debated. Because earlier studies showed that radio- important brain damage. This would lead to a CT
graphic evidence of a skull fracture increases the risk of ordering proportion of 54%. Both studies concluded
intracranial haemorrhage, skull radiography was used that in patients with MTBI the use of CT can be safely
as the principle triage tool on which management limited to those who have certain clinical findings
decisions were based (EL ¼ Class III) (Mendelow et al., (Haydel et al., 2000; Stiell et al., 2001).
1983; Masters et al., 1987; Teasdale et al., 1990; Nee Recommendation: CT is considered a gold standard
et al., 1999). However, recent studies comparing skull for the detection of life threatening (and other intra-
radiography with CT showed a low sensitivity and cranial) abnormalities after MTBI and recommended in
specificity of the presence of a skull fracture on skull those with documented LOC and/or PTA and consid-
radiographs for intracranial haemorrhage (Borczuk, ered mandatory in all patients with certain clinical
1995). A meta-analysis confirmed that skull radiogra- findings (GCS ¼ 13–14, presence of risk factors) (Grade
phy is of little value in the initial assessment of MTBI B, recommendation).
(EL ¼ I) (Hofman et al., 2000). On the basis of studies
in which at least 50% of patients had a CT of the brain,
MRI
the estimated sensitivity of radiographic evidence of
skull fracture for a diagnosis of intracranial haemor- Cerebral magnetic resonance imaging (MRI) is not
rhage was only 0.38 with a corresponding specificity of routinely used in TBI, although in the acute stage
0.95 (Hofman et al., 2000). (within 3 days of injury) MRI is more sensitive than CT
Recommendation: Skull radiography is of insufficient for detecting intracranial abnormalities (Wilson et al.,
value in the detection of intracranial abnormalities in 1988; Yokota et al., 1991; Levin et al., 1992a; van der
patients with MTBI (Grade A, recommendation). Naalt et al., 1999b). Diffusion tensor imaging may
reveal abnormalities not detected by conventional MRI
(Wieshmann et al., 1999; Rugg-Gunn et al., 2001).
CT
The relationship between intracranial abnormalities
Two large prospective studies investigated a clinical on MRI and outcome is not entirely clear, and more
decision rule for use of CT to demonstrate the need for research is needed (Voller et al., 2001). When early
neurosurgical intervention or clinically important brain MRI (within 21 days from the injury) and late MRI
injury after MTBI (Haydel et al., 2000; Stiell et al., (between 5 and 18 months) findings were compared in
2001). In a prospective study involving 1429 patients patients with mild, moderate or severe TBI, measures of
with minor head injury (minor head injury in this study neuropsychological outcome correlated with late MRI
defined as LOC and an admission GCS of 15), seven findings only (Wilson et al., 1988).
predictors (headache, vomiting, seizure, PTA, trauma Recommendation: MRI may be of value for the
above the clavicles, drug or alcohol intoxication, or age detection of structural brain damage in patients without
over 60 years) were retrieved after chi-square analysis CT abnormalities, and especially in those with long-
and determination of likelihood ratios for each criter- term complaints (Grade B, recommendation).

ª 2002 EFNS European Journal of Neurology 9, 207–219

214 P. E. Vos et al.

evaluated for surgical trauma (EL ¼ III) (American

PET and SPECT
College of Surgeons Committeee on Trauma, 1997).
Positron emission tomography (PET) and technetium Proper triage includes assessing the airways, breathing,
99m
-hexa-methylpropyleneamineoxime single photon and circulation, and also the cervical spine. A neurolog-
emission computed tomography (SPECT) may show ical examination is obligatory and should include level of
abnormalities in the acute and chronic stages when CT consciousness, presence of anterograde or retrograde
or MRI and neurological examination do not show amnesia and/or disorientation, higher cognitive func-
damage (Ichise et al., 1994; Jacobs et al., 1994; Ruff tions, presence of focal neurological deficit (asymmetri-
et al., 1994). Normal findings for SPECT performed cal motor reactions or reflexes, unilateral paresis or
within 1–4 weeks of mild and moderate TBI were cranial nerve deficit), pupillary responses, blood pressure
predictive of a good outcome after 1 year, with a and pulse rate (Valadka and Narayan, 1996; Ingebrigt-
negative predictive value of 97% (Jacobs et al., 1994). sen et al., 2000; Tate et al., 2000). In addition, the
The specificity of abnormal findings, however, has been presence of frontal lobe signs, cerebellar symptoms or
questioned (Alexander, 1998). A similar pattern of sensory deficits should be actively investigated.
hypometabolism in the frontopolar and lateral tem- Recommendation: All patients with TBI should
poral cortices and the basal ganglia has been reported undergo a neurological examination, in addition to a
among patients with depression but no injury (Dolan surgical examination. Furthermore, obtaining accurate
et al., 1994; Mayberg, 1994). history (including medication), preferably with infor-
Recommendation: No recommendations for the use mation being obtained from a witness of the accident or
of PET or SPECT in the initial phase after MTBI can personnel involved in first-aid procedures outside the
be given at present. hospital, is important to ascertain the circumstances
under which the accident took place and to assess the
duration of LOC and amnesia (Grade C, recommenda-
Biochemical markers of traumatic brain injury
tion).
Brain-specific proteins, in particular S100B and neur- The key issue in daily practice remains the question
one-specific enolase, may be released into the circulation whether patients should be routinely admitted but not
after TBI. Serum levels of S100B are higher in patients necessarily undergo CT of the head or whether patients
with intracranial pathology and correlate with clinical should be admitted selectively but undergo CT of the
outcome and the severity of primary and secondary head. MTBI category 2 and 3 patients should be
brain damage (EL ¼ II) (Raabe et al., 1999; Romner evaluated with CT (EL ¼ III) (Teasdale et al., 1990;
et al., 2000). Undetectable serum levels of S100B are Shackford et al., 1992; Stein and Ross, 1992). An
predictive of normal intracranial findings on CT, and algorithm for the initial management of MTBI is given
thus S100B could be used to select patients for CT after in Fig. 1.
MTBI (EL ¼ Class I) (Romner et al., 2000). However, Recommendations: Hospitals should have a protocol
these results have to be confirmed in large prospective for resuscitation and triage of patients with MTBI
studies. In the future, this may be of relevance in the (Grade C). Category 2 and 3 patients should be
medico–legal context, to prove that the acute symptoms admitted to a neurotrauma centre. All children with
and signs and/or the long-term disability or neuropsy- MTBI should be seen by a paediatrician or a child
chological impairments after MTBI are indeed a conse- neurologist (Grade C). CT is recommended for cate-
quence of structural brain damage or of psychological gory 1 patients and is mandatory for all category 2 and
stress in reaction to the event, alcohol intoxication, pre- 3 patients (see Fig. 1) (Grade B, recommendation).* If
existent disorders, systemic injury or other causes (see CT findings are normal, adult category 1 patients can
also Romner et al., 2000). be discharged. Head injury warning instructions should
Recommendation: The study of biochemical markers be given to the patient and family members. Compli-
of MTBI is of considerable interest (especially the ance is greater if both verbal and written instructions
negative predictive value of normal serum concentra- are given (EL ¼ III) (de Louw et al., 1994; Valadka
tions for the absence of intracranial abnormalities), but and Narayan, 1996; Ingebrigtsen et al., 2000). A repeat
at present no recommendations can be given and more CT should be considered if the admission CT findings
research is needed (Grade B, recommendation). were abnormal or if risk factors are present (Table 2)
(Grade C, recommendation).
Initial patient management
*If CT availability is limited, conventional skull radiography can be
According to the Advanced Trauma Life Support performed but the sensitivity and specificity for intracranial abnor-
guidelines, any patient with head injury should be malities is low.

ª 2002 EFNS European Journal of Neurology 9, 207–219

 Guideline on mild traumatic brain injury 215

on the number of post-traumatic complaints and

Clinical observation
quality of life 6 months after the trauma (de Kruijk,
Another issue is the necessity for and duration of 2001). Graded resumption of activities after discharge
neurological observation after MTBI. Patients in cat- and follow-up may beneficially influence the recovery
egory 1 can be discharged home with head injury process (EL ¼ IV) (Alexander, 1995; Kibby and Long,
warning instructions if CT findings are normal (appen- 1997; Ingebrigtsen et al., 1998).
dix to appear on the website of the EFNS: http:// Recommendation: No recommendations can be
www.efns.org/) (Warren and Kissoon, 1989; Ward given for the need for or duration of bed rest.
et al., 1992; Valadka and Narayan, 1996). Patients in Graded resumption of activities (including return to
categories 2 or 3 should preferably be admitted to work) is probably the best strategy (Grade B,
hospital for observation, although the necessity of this recommendation).
can be questioned in some patients in category 2 (e.g.
patients older then 60 years of age who are not on
Follow-up
anticoagulation therapy). Scandinavian guidelines
recommend an observation period of minimally 12 h, It has been shown that regular specialized outpatient
whereas other guidelines recommend a period of 24 h follow-up visits are effective in reducing social morbid-
or longer (Masters et al., 1987; Bartlett et al., 1998; ity and the severity of symptoms after MTBI (Wade
American Academy of Pediatrics, 1999; Ingebrigtsen et al., 1998). In a large randomized controlled trial,
et al., 2000; Twijnstra et al., 2001). The main goal of patients with a PTA shorter than 7 days and who
clinical observation is to detect, at an early stage, the received specialist intervention had significantly less
development of extradural or subdural haematoma or social disability and fewer post-concussion symptoms
diffuse cerebral oedema. A secondary goal is to deter- 6 months after injury than those who did not receive
mine the duration of PTA. An extradural haematoma the service (EL ¼ II) (Wade et al., 1998).
usually develops within 6 h, and thus the initial CT may Recommendation: It is recommended that all patients
be false negative when performed very early (within in MTBI category 3 who have been admitted to hospital
1 h) (Frowein et al., 1989; Smith and Miller, 1991; should be seen at least once in the outpatient clinic
Servadei et al., 1995). Repeated neurological observa- approximately 1–2 weeks after discharge (Grade C)
tion (see above) is therefore obligatory for the timely (Wade et al., 1998). Patients who are discharged
detection of clinical deterioration and other neurolog- immediately with head injury instructions should con-
ical deficits (such as sensory deficits, frontal lobe signs, tact their general practitioners, who can decide to refer
cerebellar symptoms, etc.). the patient to the neurologist if complaints persist
Recommendation: A repeat neurological examination (Grade C, recommendation).
should be carried out, its frequency being dependent Most patients return to work despite having com-
on the clinical condition of the patient and the plaints (van der Naalt et al., 1999a). Typical post-
presence of CT abnormalities. For instance, the traumatic complaints are headache, dizziness, fatigue,
patient should be examined every 15–30 min and if irritability, anxiety, insomnia, photophobia, phonopho-
no complications or deterioration occurs, every 1–2 h. bia, and memory and concentration disturbances
The use of a neurological checklist may be helpful to (Dikmen et al., 1986; Evans, 1992; Binder, 1997).
document the neurological condition and its course. If Post-traumatic complaints usually occur in the first
deterioration occurs, possible intracranial causes 6–12 weeks after the trauma and tend to disappear
should be evaluated with (repeated) CT (Grade C, by 6 months; however, in 7–8% of patients the post-
recommendation). traumatic complaints become chronic (Fenton et al.,
1993; Bohnen et al., 1994; Dikmen et al., 1994, 1995;
Binder, 1997). Follow-up visits in this patient group are
Bed rest
determined by the presence and persistence of post-
No randomized trials exist on the value and duration traumatic complaints such as headache, dizziness, poor
of bed rest and on the duration of sick leave after concentration and memory disturbances.
MTBI. A survey among various European hospitals Recommendation: Neuropsychological examination
showed major differences in management with regard may be useful after 6 months in patients with persistent
to the ordering (and duration) of bed rest, home complaints, to determine whether these complaints are
observation, sick leave and follow-up examination organic in nature or the result of pre-morbid person-
(de Kruijk et al., 2001). A study in which patients were ality, anxiety, psychological stress in reaction to the
randomized for complete bed rest (for a period of event, other pre-existent disorders or other causes
6 days) versus no bed rest showed no treatment effect (Grade C, recommendation) (Alexander, 1995).

ª 2002 EFNS European Journal of Neurology 9, 207–219

216 P. E. Vos et al.

Conclusions Arienta C, Caroli M, Balbi S (1997). Management of head-

injured patients in the emergency department: a practical
The guidelines presented in this paper incorporate protocol. Surg Neurol 48:213–219.
extensive use of CT. Moreover, the use of a clinical Bartlett J, Kett-White R, Mendelow AD et al. (1998).
decision rule for CT and hospital admission after MTBI Recommendations from the Society of British Neurological
Surgeons. Br J Neurosurg 12:349–352.
may increase the use of CT compared with other
Bayston R, de Louvois J, Brown EM et al. (2000). Use of
existing protocols. There is no agreement in the antibiotics in penetrating craniocerebral injuries. ‘Infection
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patients should be admitted but only a few undergo CT Binder LM (1997). A review of mild head trauma. Part II:
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(Stiell et al., 2001; Twijnstra et al., 2001). A strategy
457.
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outcome of mild head injury: results from a controlled
CT as the gold standard. Therefore, the value of clinical
postal survey. Brain Inj 8:701–708.
risk factors in predicting early and late sequelae Borczuk P (1995). Predictors of intracranial injury in patients
(complaints, neuropsychological disturbances) should with mild head trauma. Ann Emerg Med 25:731–736.
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84:608–610.
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Brodie HA (1997). Prophylactic antibiotics for posttraumatic
negatively affecting clinical outcome. If feasible, this cerebrospinal fluid fistulae. A meta-analysis. Arch Otolar-
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