1637
SPECIAL COMMUNICATION
Position Statement: Definition of Traumatic Brain Injury
David K. Menon, MD, PhD, Karen Schwab, PhD, David W. Wright, MD, Andrew I. Maas, MD, PhD, on behalf
of The Demographics and Clinical Assessment Working Group of the International and Interagency Initiative
toward Common Data Elements for Research on Traumatic Brain Injury and Psychological Health
ABSTRACT. Menon DK, Schwab K, Wright DW, Maas AI,
on behalf of The Demographics and Clinical Assessment
Working Group of the International and Interagency Initiative
toward Common Data Elements for Research on Traumatic
Brain Injury and Psychological Health. Position statement: defi-
nition of traumatic brain injury. Arch Phys Med Rehabil 2010;91:
1637-40.
A clear, concise definition of traumatic brain injury (TBI) is
fundamental for reporting, comparison, and interpretation of
studies on TBI. Changing epidemiologic patterns, an increasing
recognition of significance of mild TBI, and a better under-
standing of the subtler neurocognitive neuroaffective deficits
that may result from these injuries make this need even more
critical. The Demographics and Clinical Assessment Working
Group of the International and Interagency Initiative toward
Common Data Elements for Research on Traumatic Brain
Injury and Psychological Health has therefore formed an expert
group that proposes the following definition:
TBI is defined as an alteration in brain function, or other
evidence of brain pathology, caused by an external force.
In this article, we discuss criteria for considering or estab-
lishing a diagnosis of TBI, with a particular focus on the
problems how a diagnosis of TBI can be made when patients
present late after injury and how mild TBI may be differenti-
ated from non-TBI causes with similar symptoms. Technologic
From the University of Cambridge, Cambridge, United Kingdom (Menon); De-
fense and Veterans Brain Injury Center, Washington, DC (Schwab); Emory Univer-
sity School of Medicine, Atlanta, GA (Wright); University Hospital Antwerp, Ant-
werp, Belgium (Maas).
Supported by the National Institute of Neurological Disorders and Stroke (NINDS),
the National Institute on Disability and Rehabilitation Research, the Department of
Veterans Affairs, the Defense and Veterans Brain Injury Center, and the Defense
Centers of Excellence, the Medical Research Council (RG46503), the National
Institute for Health Research, United Kingdom (RG53668), the BOC Professorship of
the Royal College of Anaesthetists (RG42458), the NIH-NINDS (NS 062778A, NS
059032-01, TW 007262-01), the Wallace H. Coulter Foundation, the Division of
Emergency Neurosciences, Department of Emergency Medicine at Emory University,
the NIH-NINDS (NS 42691), and the Flemish Institute for promoting Innovation in
Science and Technology.
No commercial party having a direct financial interest in the results of the research
supporting this article has or will confer a benefit on the authors or on any organi-
zation with which the authors are associated.
Views expressed are those of the authors and do not necessarily reflect those of the
agencies or institutions with which they are affiliated, including the U.S. Department
of Veterans Affairs, the U.S. Department of Defense, the U.S. Department of Health
and Human Services, the National Institutes of Health, the National Institute of
Mental Health, and the Uniformed Services University of the Health Sciences. This
work is not an official document, guidance, or policy of the U.S. Government, nor
should any official endorsement be inferred.
Correspondence to David K. Menon, MD, PhD, Division of Anaesthesia, Univer-
sity of Cambridge, Box 93, Addenbrooke’s Hospital, Cambridge CB2 2QQ, United
Kingdom, Andrew I. R. Maas, MD, PhD, Department of Neurosurgery, University
Hospital Antwerp, Wilrijkstraat 10, 2650 Edegem, Belgium, e-mail:
dkm13@wbic.cam.ac.uk, and e-mail: andrew.maas@uza.be. Reprints are not avail-
able from the authors.
0003-9993/10/9111-00368$36.00/0
doi:10.1016/j.apmr.2010.05.017
advances in magnetic resonance imaging and the development
of biomarkers offer potential for improving diagnostic accu-
racy in these situations.
Key Words: Brain injuries; Diagnosis; differential; Stress
disorder; posttraumatic; Rehabilitation.
© 2010 by the American Congress of Rehabilitation
Medicine
D URING THE PAST 50 YEARS, there has been an evolv-
ing consensus in the neurotraumatology community re-
garding the injury mechanisms, disease processes, pathologies,
and clinical outcomes that fit under the umbrella of TBI. This
evolution has included a change in nomenclature from “head
injury” to the more precise “traumatic brain injury.” However,
our understanding of what is included, even in this more
precise terminology, has tended to be implicit rather than
explicit. Such an approach has served us well in epidemiologic
descriptions, clinical management, and research.
However, the past few years have witnessed an increased
awareness of additional injury mechanisms that can cause TBI,
linked substantially (but not exclusively) to modes of injury
associated with military combat.1 In addition, there has been an
attempt to clarify diagnostic criteria for mild TBI,2 an increas-
ing recognition of the impact of mild TBI, and a better under-
standing of the more subtle neurocognitive and neuroaffective
deficits that may result from TBI in general.3 The recognition
of the impact of previously undiagnosed TBI has also been
driven by the development of new biomarkers and imaging
tools.4
This understanding that both milder insults and less typical
presentations now fit under the TBI diagnostic umbrella has
increased the overlap with (and diagnostic confound by) non-
TBI pathologies. These overlapping conditions can result in
diagnostic ambiguity, which may confound precise epidemio-
logic description, appropriate clinical management, and ratio-
nal research strategy development.
In April 2009, the United States Department of Veterans Af-
fairs and Department of Defense issued a Clinical Practice Guide-
line for the management of concussion/mild TBI.5 This Clinical
Practice Guideline included a common definition of TBI, severity
of brain injury stratification, diagnostic criteria, evaluation, treat-
ment, and patient follow-up recommendations. The Clinical Prac-
tice Guideline evaluated the best evidence available, which
provided a pragmatic solution to the problem of diagnostic
categorization and reporting and allowed establishment of ef-
fective clinical protocols and pathways for clinical care.
List of Abbreviations
ACRM American Congress of Rehabilitation Medicine
LOC level of consciousness
MRI magnetic resonance imaging
PTA posttraumatic amnesia
PTSD posttraumatic stress disorder
TBI traumatic brain injury
UK United Kingdom
Arch Phys Med Rehabil Vol 91, November 2010
1638 CDEs: DEFINITION OF TRAUMATIC BRAIN INJURY, Menon
However, despite substantial previous efforts in this area
(some of which are listed in the discussion above, or quoted
later in this article), there continues to be a need for a more
general assessment of the issue. This has recently been ad-
dressed as part of a workshop supported by The Defense
Centers of Excellence for Psychological Health and Traumatic
Brain Injury, the National Institute of Neurological Disorders
and Stroke, the Department of Veterans Affairs, and the Na-
tional Institute on Disability and Rehabilitation Research.4 The
position statement provides the consensus of the experts who
made up The Demographics and Clinical Assessment Working
Group (appendix 1) as part of this workshop.
TBI DEFINITION
TBI is defined as an alteration in brain function, or other
evidence of brain pathology, caused by an external force.
EXPLANATORY NOTES
[A] Alteration in brain function is defined as 1 of the
following clinical signs:
● Any period of loss of or a decreased LOC
● Any loss of memory for events immediately before (retro-
grade amnesia) or after the injury (PTA)
● Neurologic deficits (weakness, loss of balance, change in
vision, dyspraxia paresis/plegia [paralysis], sensory loss,
aphasia, etc.)
● Any alteration in mental state at the time of the injury
(confusion, disorientation, slowed thinking, etc.)
It is important to recognize that factors other than TBI may
be responsible for alterations in mental state at the time of the
injury (eg, pain, posttraumatic shock, medication, alcohol in-
toxication/abuse, and/or recreational drug use). However, these
confounders may be associated with well documented TBI and
present particular diagnostic challenges with mild TBI (where
the evidence of TBI may be subtle). Consequently, the pres-
ence of these confounding factors should not preclude a diag-
nosis of TBI; however, careful clinical review may need to be
used before assigning a given set of clinical findings as being
caused by TBI in such settings. Similarly, focal motor deficits
caused by spinal, plexus, or other peripheral nerve injury may
provide an alternative cause of focal neurologic deficit. This
may be a less common confound, unless the level of conscious-
ness is decreased, but must still be considered before a robust
diagnosis of TBI is possible.
Typically, TBI has been diagnosed when the symptoms and
signs are closely temporally related to the insult. However, we
need to recognize that clinical manifestations may be delayed.
This issue is particularly relevant for neuropsychiatric sequelae
(depression, impulsivity, apathy, etc.), which may only be
documented some time after the insult, and may also be the
consequence of non-TBI etiologies. In this context, a diagnosis
of TBI may be dependent on diagnostic tests (see [B] below)
that are undertaken some time after the acute event.
[B] or other evidence of brain pathology: Such evidence
may include visual, neuroradiologic, or laboratory confirmation
of damage to the brain.
Classically, TBI has been defined based on clinical criteria.
However, modern imaging techniques (eg, diffusion tensor
MRI) show increasing sensitivity, and it is possible that other
sensitive biomarkers may be developed in the future. Such
diagnostic techniques may enable a diagnosis of TBI in the
following situations:
● Clinical consequences are subtle or delayed
Arch Phys Med Rehabil Vol 91, November 2010
● Clinical diagnosis is confounded by a difficult context (eg,
battlefield TBI), or
● There is a need to differentiate TBI induced clinical signs
from those with other causes (eg, chemical warfare)
[C] caused by an external force may include any of the
following events:
● The head being struck by an object
● The head striking an object
● The brain undergoing an acceleration/deceleration move-
ment without direct external trauma to the head
● A foreign body penetrating the brain
● Forces generated from events such as a blast or explosion
● Or other force yet to be defined
DISCUSSION
Clear-cut definitions and unambiguous diagnostic criteria are
prerequisites for epidemiology, clinical care, and research in
any disease. Yet little attention has been paid in the literature to
defining TBI, and many clinicians feel that the term is self-
explanatory. The gradual change in terminology from “head
injury” to “traumatic brain injury” reflects the understanding
that it is the damage to the brain that matters, and not so the
damage to scalp or skull. The importance of injury to the brain
in defining TBI is reflected in the proposed definition.
The working group felt that a short and concise definition of
TBI was preferable to a more lengthy description. Agreement
on the essentials of this definition was reached reasonably
quickly. However, there was substantially more discussion
regarding the criteria for defining an “alteration in brain func-
tion.” Clinicians generally prefer hard criteria for establishing
a diagnosis, while surveillance studies tend to target a broader
population in order not to miss potential new cases and to limit
the risk of underreporting. The presence of LOC, PTA, or
neurologic deficits constitutes objective criteria when captured
in a clinical research center with rigorous measurement proto-
cols and trained evaluators. Often, particularly for patients with
mild TBI presenting for care (or screening) sometime after the
injury event, information on LOC, PTA, and other alteration of
consciousness (including confusion) is captured by self-report.
Verification can be difficult. A period of confusion or disori-
entation in the absence of LOC or PTA is considered part of an
alteration of consciousness and may be used to establish a
diagnosis of mild TBI. Most TBIs in sports and in medical
trauma settings have been associated with PTA or periods of
confusion and disorientation. A careful clinical interview is
considered essential to establishing a diagnosis of TBI, partic-
ularly in the absence of clinical or other witnesses. Neverthe-
less, the group felt strongly that a diagnosis of TBI should be
considered when these symptoms are reported, even in the
absence of any of the more objective criteria such as LOC,
PTA, or neurologic deficits. The clearest example is damage
resulting from a small, penetrating object, such as a dart or
shotgun pellet. Clearly, in this context, there is brain damage,
but there may be a total absence of any complaint or clinical
symptom. Conversely, “mental symptoms” may also result
from other causes (eg, pain, posttraumatic shock, medication,
alcohol intoxication, and/or recreational drug use), and their
presence in isolation should not be considered a definitive
proof of TBI.
The working group also considered whether neuropsychiat-
ric sequelae (eg, depression, impulsivity, apathy) as a present-
ing symptom in later phases should be considered evidence of
TBI. Although such sequelae may indeed be caused by TBI, we
felt that using these as criteria for establishing a diagnosis
 CDEs: DEFINITION OF TRAUMATIC BRAIN INJURY, Menon 1639

would constitute a circular argument and was therefore not
appropriate.
One option to address the tensions inherent in this discussion
would be to use different degrees of precision for criteria that
are used for considering and for establishing a diagnosis of
TBI. Criteria used to establish a diagnosis of TBI need to be
etiologically unambiguous and unlikely to be confounded by
non-TBI mechanisms. On the other hand, given the wide range
of neurocognitive and neuropsychiatric sequelae recognized as
resulting from TBI, it would be important to consider TBI as a
potential cause in such settings and to use less ambiguous
diagnostic criteria or biomarkers to consolidate such a potential
diagnosis. Not adopting this latter approach may mean that we
miss the opportunity to detect significant epidemiologic rela-
tionships and could mean that options for morbidity reduction
(through injury prevention or early therapy) might never be
investigated.
Nomenclature and definitions are most likely to be a problem
in mild TBI. The criteria we present under [A] Alteration in
brain function are compatible with the diagnostic criteria for
mild TBI presented by the ACRM.6 In a thoughtful analysis,
Ruff et al2 recently examined the current diagnostic schemes
for TBI and addressed potential confounds in these criteria and
how non-TBI mechanisms may present with similar symptom-
atology (table 1).
In addition to the confounds discussed in table 1, Ruff2
addresses the importance of excluding a diagnosis of mild TBI,
as specified by both the ACRM and the World Health Orga-
nization.7 However, it is important to note that these exclusions
mainly focus on preventing patients with moderate or severe
TBI being diagnosed as having mild TBI. In contrast, these
authoritative guidelines provide very little guidance on how
mild TBI may be differentiated from non-TBI causes of similar
symptoms. Such distinction of TBI from non-TBI pathology is
particularly relevant to the high reported incidence of mild
blast TBI in military personnel returning from combat.8 Inci-
dence of exposure to blast is high in such persons, and blast
TBI is now recognized as a specific entity within the broad
spectrum of TBI. However, many soldiers only present late,
and others are identified by routine self-screening. There is an
impression that the incidence of reported mild blast TBI may
be substantially higher in U.S. military personnel than UK
military personnel.9,10 However, caution is needed before this
statement can be accepted, because the difference may be a
result of different approaches to screening, definition, and/or
reporting. For example, 1 report from the United States quotes
a 59% incidence of blast TBI,9 while a UK article reports an
overall blast injury incidence of 3.7%.10 However a closer
examination of the 2 data sources shows that direct compari-
sons are inappropriate. The denominator for the U.S. data9 are
survivors of acute battlefield injuries admitted to a tertiary
center in the United States after evacuation from the theater of
war, all of whom had documented blast injury, and had a
diagnosis of TBI based on comprehensive assessment. On the
other hand, the UK data address acute assessment of injury
severity in the theater of war, and the denominator includes a
high percentage of fatal casualties.10 Differences in reporting
therefore need to be considered carefully and reconciled before
rational comparisons are possible to confirm or exclude real
differences in TBI incidence. Agreement on definitions, screen-
ing procedures, and criteria for establishing a diagnosis of TBI
are required to promote consistency in reporting.
Symptoms associated with mild blast TBI may overlap to a
considerable degree with those of PTSD, unassociated with
TBI.11 Such overlap is driven by, and contributes to, several
ambiguities. It may simply be that, given the context in these
patients, a diagnosis of blast TBI may be more accessible than
one of PTSD.12 However, it is also possible that blast TBI may
overlap with, and be a cause of PTSD. Stein and McAllister13
recently provided a thoughtful analysis of these 2 conditions,
particularly in the context of military TBI. Surprisingly, the
mechanism (emotional vs biomechanical) and locus (head vs
other regions) of injury are weak determinants of whether a
person develops PTSD, persistent postconcussive symptoms,
or both. The most important determinant of the risk of devel-
oping both conditions may be reduced cognitive reserve (either
premorbid or related to recent mechanical or psychologic
trauma). The overlap between the 2 conditions is further sup-
ported by a commonality of neuropathology. For example,
various studies have reported a reduction in hippocampal vol-

Table 1: Potential Confounders in the Diagnosis of Mild TBI2

Confounder Comments

PTA vs LOC
Immediate vs delayed LOC
Experienced vs reported
symptoms
PTA vs psychogenic amnesia
LOC and PTA caused by drugs
Hard neurology vs soft
symptoms
Self-reported LOC will often include the period of PTA.
If the onset of LOC is delayed until sometime after injury and neuroimaging studies have
excluded any evidence of structural damage, it may be less likely that the LOC is a
consequence of TBI.*
PTA may conceal LOC in first-person reports—it may be important to ask for LOC that was
reported to the patient, rather than whether the patient experienced it. Conversely, patients
may report events that have been related to them, and this may conceal PTA.
Acute stress disorder or PTSD may be responsible for partial amnesia surrounding the events of
injury. Preserved memory for the events of the accident (ie, no PTA), associated with amnesia
for events that begins some time after the injury, may be accounted for in part or fully by
stress or by medication administered after the injury.
Alcohol or recreational drugs that are on board at the time of the injury, or medication
administered after the injury, may result in gaps in memory.
While a focal neurologic deficit (transient or persistent) or a new-onset seizure provides strong
objective evidence of CNS injury, other neurologic findings that underpin a diagnosis of mild
TBI (fatigue, sleep disorders, headache, etc.) are less specific and may be accounted for by
stress, anxiety, PTSD, or depression.

Abbreviation: CNS, central nervous system.

*This consideration should apply only to mild TBI, with no imaging evidence of intracranial pathology. A delayed onset of LOC after possible
TBI may indicate development of a delayed intracranial space occupying lesion, classically an extradural hematoma, or may be attributable
to a seizure. These issues need careful consideration before any conclusion is drawn regarding the significance of the onset of LOC.

Arch Phys Med Rehabil Vol 91, November 2010

1640 CDEs: DEFINITION OF TRAUMATIC BRAIN INJURY, Menon
ume, detected by MRI, not only in patients with TBI but also
in patients with PTSD.14,15 It remains unclear whether the
degree of hippocampal volume loss in TBI is related to TBI
severity.14,16 Uncertainty therefore exists whether these
changes in PTSD are purely secondary to the condition itself,
or perhaps represent evidence that subjects diagnosed as PTSD
with structural MRI changes may have been exposed to greater
external forces at the time of injury than originally presumed.
The discussion in the previous paragraph emphasizes the
difficulty in finding a criterion standard test to make a diagnosis
of mild TBI, particularly when confounding diagnoses are
possible. It is clear that the acquisition of epidemiologic pre-
cision will need to be a process rather than an event and will
depend on the correlations of symptomatology with (admit-
tedly as yet unestablished) imaging and other diagnostic tests to
provide post hoc categorization of patients. A comparative
long-term combined military and civilian study, in which pa-
tients with mild TBI (both blast and nonblast) and patients
diagnosed with PTSD are followed up over time with sequen-
tial imaging, biomarker measurement, and cognitive assess-
ment, may result in greater diagnostic precision and better
development of research strategy.
APPENDIX 1
Members of The Demographics and Clinical Assessment
Working Group of the International and Interagency
Initiative toward Common Data Elements for Research
on Traumatic Brain Injury and Psychological Health
This is an interagency initiative involving the National In-
stitute of Neurological Disorders and Stroke (NINDS), the
National Institute on Disability and Rehabilitation Research
(NIDRR), the Department of Veterans Affairs (VA), the De-
fense and Veterans Brain Injury Center (DVBIC) and the
Defense Centers of Excellence (DCoE). The membership of
the working group is:
P. David Adelson, MD; Phoenix Children’s Neuroscience In-
stitute, Phoenix, Arizona
Tom Balkin, PhD; Walter Reed Army Institute of Research,
Washington, District of Columbia
Ross Bullock, MD; University of Miami Miller School of
Medicine, Miami, Florida
Doortje C. Engel, MD, PhD; University Hospital Heidelberg,
Germany
Wayne Gordon, PhD; Mount Sinai School of Medicine, New
York, New York
Cindy Harrison-Felix, PhD; Craig Hospital, Englewood, Col-
orado
Jean Langlois, ScD; Department of Veterans Affairs, Rehabil-
itation Research and Development Service, Washington,
District of Columbia
Henry Lew, MD, PhD; Veterans Brain Injury Center and
Department of Physical Medicine and Rehabilitation, Vir-
ginia Commonwealth University School of Medicine,
Richmond, Virginia
Andrew Maas, MD, PhD; University Hospital Antwerp, Bel-
gium
David Menon, MD, PhD; University of Cambridge, United
Kingdom
Claudia Robertson, MD; Baylor College of Medicine, Houston,
Texas
Karen Schwab, PhD; Defense and Veterans Brain Injury Cen-
ter, Washington, District of Columbia
Arch Phys Med Rehabil Vol 91, November 2010
Nancy Temkin, PhD; University of Washington, Seattle,
Washington
Alex Valadka, MD; Seton Brain and Spine Institute, Austin,
Texas
Mieke Verfaellie, PhD; Boston Veterans Affairs Health Care
System and Boston University School of Medicine, Bos-
ton, Massachusetts
Mark Wainwright, MD; Northwestern University, Chicago,
Illinois
David Wright, MD; Emory University School of Medicine,
Atlanta, Georgia
References
1. Kochanek PM, Bauman RA, Long JB, Dixon CR, Jenkins LW. A
critical problem begging for new insight and new therapies. J Neu-
rotrauma 2009;26:813-4.
2. Ruff RM, Iverson GL, Barth JT, Bush SS, Broshek DK, NAN
Policy and Planning Committee. Recommendations for diag-
nosing a mild traumatic brain injury: a National Academy of
Neuropsychology Education paper. Arch Clin Neuropsychol
2009;24:3-10.
3. Silver JM, McAllister TW, Arciniegas DB. Depression and cog-
nitive complaints following mild traumatic brain injury. Am J
Psychiatry 2009;166:653-61.
4. National Institute of Neurological Disorders and Stroke (NINDS)
CDE Project. NINDS Common Data Elements. 2010. Available
at: http://www.commondataelements.ninds.nih.gov/TBI.aspx. Ac-
cessed September 28, 2010.
5. Department of Veterans Affairs and Department of Defense. Clin-
ical Practice Guideline: Management of Concussion/mild Trau-
matic Brain Injury. 2009. Available at: http://www.healthquality.
va.gov/mtbi/concussion_mtbi_full_1_0.pdf. Accessed on Septem-
ber 28, 2010.
6. ACRM; Mild Traumatic Brain Injury Committee. Definition of
mild traumatic brain injury. J Head Trauma Rehabil 1993;8:86-7.
7. Carroll LJ, Cassidy JD, Holm L, Kraus J, Cornado VG. Method-
ological issues and research recommendations for mild traumatic
brain injury: the WHO Collaborating Task Force on Mild Trau-
matic Brain Injury. J Rehabil Med 2004;(Suppl 43):113-25.
8. Ling G, Bandak F, Armonda R, Grant G, Ecklund J. Explosive
blast neurotrauma. J Neurotrauma 2009;26:815-25.
9. Okie S. Traumatic brain injury in the war zone. N Engl J Med
2005;352:2043-7.
10. Ramasamy A, Harrison SE, Clasper JC, Stewart MP. Injuries from
roadside improvised explosive devices. J Trauma 2008;65:910-4.
11. Hoge CW, McGurk D, Thomas JL, Cox AL, Engel CC, Castro
CA. Mild traumatic brain injury in U.S. soldiers returning from
Iraq. N Engl J Med 2008;358:453-63.
12. Bryant RA. Disentangling mild traumatic brain injury and stress
reactions. N Engl J Med 2008;358:525-7.
13. Stein MB, McAllister TW. Exploring the convergence of post-
traumatic stress disorder and mild traumatic brain injury. Am J
Psychiatry 2009;166:768-76.
14. Di Stefano G, Bachevalier J, Levin HS, Song JX, Scheibel RS,
Fletcher JM. Volume of focal brain lesions and hippocampal
formation in relation to memory function after closed head injury
in children. J Neurol Neurosurg Psychiatry 2000;69:210-6.
15. Geuze E, Vermetten E, Bremner JD. MR-based in vivo hippocam-
pal volumetrics: 2. Findings in neuropsychiatric disorders. Mol
Psychiatry 2005;10:160-84.
16. Jorge RE, Acion L, Starkstein SE, Magnotta V. Hippocampal
volume and mood disorders after traumatic brain injury. Biol
Psychiatry 2007;62:332-8.