Handbook of Clinical Neurology, Vol.

127 (3rd series)

Traumatic Brain Injury, Part I
J. Grafman and A.M. Salazar, Editors
© 2015 Elsevier B.V. All rights reserved

Chapter 1

Epidemiology of traumatic brain injury

MARK FAUL* AND VICTOR CORONADO
Centers for Disease Control and Prevention, Atlanta, GA, USA

OVERVIEW: IMPORTANCE OF INJURY
AND TRAUMATIC BRAIN INJURY
In 2009, injury was the leading cause of death in the US
for persons aged 1–44 years (CDC, 2009). Because the
burden of injury is concentrated among these younger
and middle age groups, the impact on disability-adjusted
life years lost for injury is approximately 15% in the US.
Meanwhile, the impact of injury on mortality for all age
groups is approximately 10% (Murray and Lopez, 1997).
Injuries are classified into the two categories of uninten-
tional and intentional injuries, or violence-related inju-
ries. For all age groups, unintentional injury is the
fifth leading cause of death, after heart disease, malig-
nant neoplasms, chronic respiratory disease, and cere-
brovascular disease (CDC-WISQARS, 2009). After
combining unintentional injury and violence-related
injury, there were 177,154 total injury deaths in the US
during 2009 (CDC-WISQARS, 2009). The most com-
monly injured body region associated with death was
the head (Barell et al., 2002), and in a recent analysis
it was found that nearly one-third of all injury-related
deaths in the US have at least one diagnosis of traumatic
brain injury (TBI) (CDC-Quickstats, 2010).
OVERALL TRAUMATIC BRAIN
INJURY RATES
The overall incidence rate of TBI in the US for
2002–2006 was 579 per 100 000 persons, or approxi-
mately 1.7 million cases per year (Faul et al., 2010). This
estimate includes all levels of TBI severity. The TBI-
related hospitalization rate in the US was 93.8 per
100 000 persons. In a meta-analysis that included data
from the 1990s and the 2000s, the TBI hospitalization
rate in Europe was calculated to be 235 per 100 000 per-
sons (Tagliaferri et al., 2005). However, methodological
differences and variations in healthcare systems make
comparisons of TBI rates across other countries chal-
lenging. Large variations of TBI rates are found among
European countries (Berga et al., 2005). Most of the dif-
ferences in rates were due to a broader admission criteria
for mild TBI based on different case definitions and
patient inclusion rules in Europe compared to the US
(Berga et al., 2005). Meanwhile, TBI hospitalizations
in Ontario, Canada, have been calculated as 22 per
100 000 persons for females and 52 per 100 000 persons
for males during 2006–2007 (Colantonio et al., 2010).
These differences are based mostly on a different defi-
nition of TBI (see more detailed information below).
Because many developing countries experience a rapid
surge during urbanization, which is associated with a rise
in motor vehicle use, there is an increase in TBI-related
motor vehicle crashes in those developing countries
(WHO, 2006). The TBI incidence rate in developing
nations is generally higher (e.g., India 160 per 100 000
persons and Asia 344 per 100 000, cited in Tagliaferri
et al., 2005) than more developed nations and is pre-
dicted to surpass many diseases as a main cause of death
and disability by the year 2030 (WHO, 2006).
DEFINITIONS
According to the US Centers for Disease Control and
Prevention (CDC), a TBI is caused by a bump, blow,
or jolt to the head or a penetrating head injury that dis-
rupts the normal function of the brain. Not all blows or
jolts to the head result in a TBI. Exposures to blasts, and
the accompanying overpressure wave, are a leading
cause of TBI for active duty military personnel in war
zones (Champion et al., 2009). The severity of a TBI
may range from mild to severe. Signs and symptoms
vary by severity, ranging from loss of consciousness
(LOC) lasting a few seconds to seizures, to coma, or even
death. Much interest, however, has been placed on the

*Correspondence to: Mark Faul, PhD, MA, Centers for Disease Control and Prevention, 4770 Buford Highway, Atlanta, GA, USA.
Tel: +1-770-488-1276, E-mail: mfaul@cdc.gov
4 M. FAUL AND V. CORONADO
lower severity spectrum of TBI, especially in cases who
present with mild TBI (National Center for Injury
Prevention and Control, 2003). The majority of report-
ed TBIs in the US are classified as mild TBI (National
Center for Injury Prevention and Control, 2003).
Research suggests that up to 10% of persons with mild
TBI may present persistent symptoms 1 year after the
injury and in some cases even lifelong disability
(National Center for Injury Prevention and Control,
2003). Patients with mild TBI may present with one or
more of the following signs or symptoms: any period
of observed or self-reported transient confusion, dis-
orientation, or impaired consciousness; any period of
observed or self-reported dysfunction of memory
(amnesia) around the time of injury; observed signs of
other neurologic or neuropsychological dysfunction,
such as seizures acutely following head injury; infants
and very young children may exhibit irritability, lethargy,
or vomiting following head injury; symptoms among
older children and adults such as headache, dizziness,
irritability, fatigue, or poor concentration, when identi-
fied soon after injury, can be used to support the diag-
nosis of mild TBI, but cannot be used to make the
diagnosis in the absence of LOC or altered
consciousness (National Center for Injury Prevention
and Control, 2003). Further research may provide addi-
tional guidance in this area. Any period of observed or
self-reported LOC lasting 30 minutes or less can also
be a symptom of TBI (National Center for Injury
Prevention and Control, 2003).
Based on a clinical definition, the CDC has developed
a standard TBI definition for surveillance purposes. This
CDC definition is based on diagnostic codes from the
International Classification of Disease (ICD) (Marr
and Coronado, 2004). TBI is an outcome of an energy
force transferred to the head according to the CDC def-
inition. Forms of organic brain degeneration, such as
those from congenital sources, stroke or anoxia, are
not classified as a TBI (Traumatic Brain Injury Act,
1996). Although widely used, using administrative or
billing ICD coded databases may not capture all cases
of a particular condition, in this case TBI. The clinical
diagnosis of a disease or injury is not always accurately
reflected in administrative billing codes. The data used
in the diagnosis of a TBI is more detailed and tends to
be more accurate than the data used in a surveillance
system. While a very specific diagnosis is of prime
importance for treatment purposes, surveillance data
systems tend to use multiple proxies as the goal is to
get an estimate of disease burden. For example, in
TBI, Bazarian et al. (2006) compared data obtained from
emergency department (ED) medical records of patients
with mild TBI to the corresponding data obtained from
ICD coded billing records for services rendered in the
ED; and found that the sensitivity, specificity, and pos-
itive predictive value of the ICD coded CDC definition
for TBI was 45.9%, 97.8%, and 23%, respectively. These
findings suggest that estimates based on these ICD
codes do not completely capture mild TBI in an ED set-
ting and that summary estimates should be viewed with
caution.
COST: BURDEN OF INJURY
The economic cost of TBI in the US is measured by com-
bining the costs of two major cost categories (Finkelstein
et al., 2006). The first is direct cost and includes the cost
of deaths within and outside of the medical system and
the costs of medical treatments of hospitalized and non-
hospitalized TBI patients. The second category of cost is
called productivity costs. Parts of these costs are lost
wages and fringe benefits due to the incapacity to work
and the absence from the workplace or disability from
the injury. Simply stated, these costs represent a loss
in value of what is being produced after a TBI. Using
year 2000 data, the total annual cost of TBI was esti-
mated to be 60.43 billion US dollars (Finkelstein et al.,
2006). The direct cost of TBI was estimated to be 9.22
billion US dollars and the productivity losses were
51.21 US dollars. The productivity losses associated with
TBI were higher than those associated with any other
injured body region (e.g., other head/neck, spinal cord
injury, vertical column injury, torso, upper extremity,
lower extremity, other/unspecific and system-wide)
(Fig. 1.1).
SEVERITY MEASURES
The most common severity assessment for TBI is the
Glasgow Coma Scale score (GCS) (Teasdale and
Jennett, 1974; Shah and Kelly, 2003). This score is com-
monly used in prehospital settings and in EDs and is the
total of three combined scores: Glasgow Motor, Glas-
gow Verbal, and Glasgow Eye movement. Each compo-
nent of the score identifies the patient’s crude functional
status. It has also been shown to be a useful system in
determining TBI severity (Evans, 2006). Early severity
classification of TBI is based partly on the use of the
GCS, where 80% of all head injuries are mild TBI
(GCS score between 13 and 15) (Kraus and Norjah,
1988), 10% are classified as moderate TBI (GCS score
between 9 and 12), and the remaining 10% are classified
as severe, scoring 8 or less on GCS (Saatman et al., 2008).
Although GCS is more frequently calculated in the ED,
GCS data collected at the injury scene also helps guide
the transport of the patient to the appropriate healthcare
facility (Sasser et al., 2012). However, differences in
injury scene GCS and ED GCS can lead to inaccurate pre-
dictions of TBI severity 15% of the time (Andriessen
 EPIDEMIOLOGY OF TRAUMATIC BRAIN INJURY
Fig. 1.1. The cost of injury by body region. (Data from Finkelstein et al., 2006.)
et al., 2011). Substance use and intubation, as well as
facial swelling, can interfere with an accurate GCS
assessment.
Other severity measures of TBI have been studied but
were deemed unreliable when applied to TBI. Examples
of TBI severity measures include LOC and post-trauma
amnesia (PTA), which are commonly collected on state
surveillance datasets (Marr and Coronado, 2004) and
trauma registries. The LOC has been shown to be an
unreliable predictor of a TBI diagnosis, with studies
showing the presence of LOC and a TBI diagnosis occurs
at different frequencies, such as 32%, (Walker et al.,
2007), 36% (Boswell et al., 2002), and 50% (Dutton
et al., 2011). Another severity measure is PTA which is
measured using units of time of the amnesia after the
injury. Such information is collected from the patient
immediately after the trauma event. Immediate PTA
has also been an unreliable predictor of a diagnosis of
TBI because not every patient has PTA. However, when
present, the duration of PTA is a good indicator of the
extent of cognitive and functional deficits after TBI
(Khan et al., 2003) and it is considered to be a good pre-
dictor of outcome (Alexander, 1995; Bowen et al., 1999;
Nakase-Richardson et al., 2011). Nonetheless, the validity
of self-reported data and the ability of a TBI patient to
recognize their cognitive, behavioral, and emotional
symptoms have been called into question for people sus-
taining a TBI (Sbordone et al., 2000) as up to 25% of
patients change their self-evaluation of symptoms over
a 3 month time period (Gronwall and Wrightson,
1980). Thus, as a measure, PTA, which involves cogni-
tion, has limited usefulness during the diagnosis of TBI.
Because most TBIs are classified as mild, some
researchers have attempted to develop further categori-
zations of mild TBI. An early example to further catego-
ries of mild TBI was made by Esselman and Uomoto
5
(1995), who developed a classification of mild TBI injury
into grades I–IV. Their classification of mild TBI into
graded categories based on severity made use of many
symptoms (amnesia, loss of consciousness, confusion,
anatomic lesions, abbreviated injury scoring, and the
duration of symptoms). Approximately 41 different
classification scales of gradations of mild TBI severity
have been developed (Anderson et al., 2006). Overall,
these progressive efforts have not been integrated into
medical practice because there is no consensus among
experts on the best grading system for mild TBI (Cobb
and Battin, 2004).
EMERGENCY DEPARTMENT RATES
The majority of TBIs are identified in the emergency
department (ED). Of the 1.7 million people in the US
who are annually diagnosed with a TBI, 1 365 000, or
80%, were treated in EDs and released alive (Faul
et al., 2010). TBIs represent 1.4% of all visits seen in
an ED and 4.8% of the total injuries presented in an
ED (Faul et al., 2010). Treatment in the ED begins with
diagnostic procedures. Upon presentation of advanced
symptoms of TBI in an ED, computed tomography
(CT) scans are used to determine visible damage inside
the skull. CT scans are more widely used now to evaluate
TBI in order to increase diagnostic accuracy and to
enhance treatment options (Kuppermann et al., 2009).
Approximately 44% of mild TBI cases that present in
the ED are further examined using CT (Bazarian
et al., 2005). Not captured in the TBI ED visits are the
TBIs that are seen in outpatient clinics and the TBIs that
are undiagnosed, which have been reported to be as high
as 89 000 per year (Schootman and Fuortes, 2000). It is
estimated that 11% (Fife, 1987), 61% (Boswell et al.,
2002), and 75% (Kay et al., 1993) of TBIs are undiagnosed,
6 M. FAUL AND V. CORONADO
suggesting that people may not have access to healthcare
or that the public may be unclear of when to seek medical
attention for a mild TBI.
Trends
In the US, emergency department visits for TBI have
steadily increased over time. Using the National Hospital
Ambulatory Medical Care Survey (NHAMCS), the rates
of TBI patients seen at an ED have increased. In 1995 the
regression-adjusted average annual rate of ED TBI visits
was 339 visits per 100 000 persons and this rate grew to
623 visits per 100 000 persons in 2010 (Fig. 1.2). This rep-
resents an overall 84% increase in TBI emergency
department visits during 1995 through 2010. An exami-
nation of the two publications that used the same method
to calculate TBI rates for two different time periods
revealed that TBI-related falls increased from 126 per
100 000 persons for the reporting period of 1995–2001
(Langlois et al., 2004) to 180.2 per 100 000 persons for
the reporting period 2002–2006 (Faul et al., 2010).
Fall-related TBI ED visits comprised 61% of all TBIs
for persons within the age group of 65 years old and
older (Faul et al., 2010). Among many possible explana-
tions for the increase in fall-related TBI is that falls in
older adults occur more frequently due to the increase
in arrhythmias (Bodofsky et al., 2010) and additional
pharmaceutical treatments for chronic disease
(Sanchez et al., 2009). Overall, the large increase in
ED visits requires additional exploration, but it could
be partly attributed to the public’s growing knowledge
of the awareness of TBI as an important public health
injury that requires medical attention (Faul et al.,
2011). More analysis is needed to fully explore the rea-
sons behind the large increase in TBI ED visits.
Fig. 1.2. Traumatic brain injury-related emergency visits. Source: National Hospital Ambulatory Medical Care Survey
(NAMCS).
HOSPITALIZATIONS
In the US, of the 1.7 million people, on average, who are
diagnosed annually with a TBI, 275 000 (16%) were trea-
ted in a hospital setting and were discharged (Faul et al.,
2010). Using surveillance data from 11 states, 74.9% of
the all hospitalized TBI patients had a mild TBI
(Langlois et al., 2003). Another 9.6% of hospitalized
TBI patients were classified as having a moderate or
severe TBI, with 5.7% having an unknown severity score
(Langlois et al., 2003). Although treatment options vary
across hospital settings, the treatment guidelines pro-
mulgated by the Brain Trauma Foundation are the most
widely used guidelines in the US (Brain Trauma
Foundation, 2007). Of all of injury-related hospitaliza-
tions (n ¼ 1 826 548), hospitalizations for TBI constitute
15.1% of the injury burden (n ¼ 275 000) and 0.7% of
all hospitalizations (Faul et al., 2010).
Trends
A 50% decrease in TBI hospitalization rates was
reported (Thurman and Guerrero, 1999) during the years
1980–1995. The authors found that the decrease in hos-
pitalizations was due to fewer people being treated for
less severe TBI in a hospital setting and that more care
was provided in outpatient settings. More recent data
using the National Hospital Discharge Survey (NHDS)
for years 1995–2010 is shown in Figure 1.3. After adjust-
ing the data to fit a regression equation, the rate of TBI
hospitalizations in 1995 was 85 visits per 100 000 persons;
meanwhile this rate rose to 94 per 100 000 persons in
2010. This regression adjusted rate calculation method
reveals a 10.6% increase in TBI hospitalizations. This
finding needs additional exploration. Factors contribut-
ing to the increase in TBI hospitalization rates include an
 EPIDEMIOLOGY OF TRAUMATIC BRAIN INJURY
Fig. 1.3. Traumatic brain injury-related hospitalizations. Source: National Hospital Discharge Survey (NHDS).
overall increase in falls among older adults (Thompson
et al., 2006) and increased use of anticoagulants, which
potentially promotes intracranial bleeding, among older
adults, who after falling are more prone to more severe
TBIs (Cohen et al., 2009). Meanwhile, a 25% decrease in
TBI hospitalizations where motor vehicle traffic was the
cause was found for the period 1986 through 1996 (cited
in Masson et al., 2001). Figure 1.3 illustrates the trends in
TBI hospitalizations over time.
Hospitalization rates also vary by TBI cause. There
was a slight decrease in motor vehicle and traffic-related
TBI during the reporting periods of 1995–2001
(rate ¼ 21.5 per 100 000 persons) (Langlois et al., 2004)
to 2002–2006 (rate ¼ 19.4 per 100 000 persons) (Faul
et al., 2010). Assaults remained the same for both report-
ing periods at 5.2 per 100 000 persons. Meanwhile, fall-
related TBI seen in a hospital setting increased substan-
tially from 17.7 per 100 000 persons to 21.2 per 100 000
persons. Among fall-related injuries, an increase in the
hospitalization rate for older adults was associated with
a decrease in fall-related deaths in a recent Oklahoma-
based study (Fletcher et al., 2007). The authors also noted
that the decrease in falls that result in TBI-related deaths
likely contributes to more people with a TBI disability in
the age group.
DEATHS
Approximately 52 000 US residents die as a result of TBI
annually (Faul et al., 2010). Nearly one-third (Quickstats,
2010) or 30.5% (Faul et al., 2010) of all injury-related
deaths involve a TBI. In trauma centers, where the most
severe TBI patients are treated, mortality has been
reported to be as high as 50% of all trauma-related
deaths (Dutton et al., 2010).
7
Alcohol is a major risk factor in all injuries and
30–50% of all patients hospitalized with trauma are
intoxicated at the time of injury (Lowenfels and
Miller, 1984). Although alcohol is a known risk factor
for the occurrence of nearly all types of injury in adults,
it is disproportionately associated with a TBI (cited in
Shandro et al., 2009). One-quarter to one-half of patients
with acute TBI were intoxicated at the time of injury
(Shandro et al., 2009). Higher concentrations of a
patient’s blood alcohol content have also been associated
with higher mortality than a finding of no alcohol in the
blood (Homer et al., 2006).
A TBI can also result in disability and death after hos-
pitalization (Jiang et al., 2002). In their examination of
846 patients with a severe TBI one year after the injury
event they found the following outcomes: good recov-
ery, 32%; moderate disability, 14%; severe disability,
24%; vegetative status, 1%; and death, 29%. It is impor-
tant to note that death does occur during hospitalization
following a TBI.
National surveillance of deaths in the US com-
monly utilizes data from the National Vital Statistics
System where details of each death can be identified.
However, according to Rodriguez et al., the report-
ing accuracy of TBI using death certificates has
been found to produce an undercounting of TBI
(Rodriguez et al., 2006). These authors found that
the sensitivity of death certificate-based surveillance
was 78% and that the majority (62%) of missed cases
was due to listing “multiple trauma” as the cause of
death. They also found that death certificate surveil-
lance was more likely to produce underestimates of
TBI-related deaths during traffic crashes, falls, and
for persons aged 65 years old and older (Rodriguez
et al., 2006).
8 M. FAUL AND V. CORONADO
Trends
TBI mortality rates in the US have been declining since
1989. During 1989–1998, there was an annual average
incidence of 53 288 TBI-associated deaths among US res-
idents (19.4 per 100 000 persons in the population)
(Adekoya et al., 2002). Meanwhile the mortality rate
for the reporting period of 1995–2001 was 18.1 per
100 000 persons in the population (Langlois et al.,
2004) and during 2002–2006 the rates fell to 17.4 per
100 000 persons (Faul et al., 2010). The decline in TBI
mortality is greatest in motor vehicle crashes, where
TBI rates fell from 6.1 per 100 000 persons to a rate of
5.6 per 100 000 persons (Faul et al., 2010). An additional
source of declining deaths was found in assaults, where
rates fell from 2.4 per 100 000 persons during the period
1995–2001 to 2.0 per 100 000 persons during the period
2002–2006. Although the overall number of deaths
declined, the numbers and rates of fall-related TBIs
increased substantially over time from 2.4 per 100 000
persons to 3.3 per 100 000 persons. The rapid increase
in fall-related TBIs among older adults (Thomas et al.,
2008) and prevention programs designed to prevent falls
in older adults have been shown to be effective
(Rubenstein et al., 1990; Fox et al., 2010). An additional
factor that contributed to the survivability of TBI could
be due to physicians’ increasing adherence of established
guidelines for the treatment for severe TBI (Hesdorffer
and Ghajar, 2007). These authors showed that a disre-
gard for the use of the guidelines dropped 50% from
2001 to 2007. Adherence with key parts of the guidelines
includes intracranial pressure monitor insertion, which
rose from 51.6% in 2001 to 77.4% in 2006 and the avoid-
ance in the use of steroids which rose from 53.9% in 2001
to 86% in 2007. An evaluation of the Brain Trauma
Foundation guidelines showed that if there were to be
80% adherence to the guidelines in the treatment of
severe TBI among treating physicians, there would be
an estimated 50% reduction in TBI-related deaths
(Faul et al., 2007).
As noted, many authors have found a decline in TBI-
related deaths. The reasons behind the decline are a com-
bination of policy and law-based interventions and suc-
cessful clinical interventions. An examination of the
Mortality Multiple Cause-of-Death from the National
Vital Statistics System and adjusting the data to fit a
regression equation, the regression-adjusted rate of
TBI deaths in 1995 was 18.8 per 100 000 persons and
16.2 per 100 000 in 2010. This represents a 13.7% decline
in TBI deaths over a 15 year period (Fig. 1.4).
MECHANISM (EXTERNAL CAUSES)
In looking at the causes of TBI in the ED, using the latest
summarized data from CDC (Faul et al., 2010), the
leading causes of TBI are falls (178.4 per 100 000 per-
sons), struck by or against events (92.7 per 100 000
persons), and motor vehicle crashes (74.7 per 100 000
persons). Among the top four mechanistic categories of
injury, assaults are the least common form of TBI (50.6
per 100 000 persons) (Faul et al., 2010) (Fig. 1.5). Because
external cause codes are not completed on all cases,
there are some diagnosed TBIs for which the mechanism
is unknown (69.1 per 100 000 persons). Furthermore,
some TBIs are not captured in healthcare surveillance
systems because people either do not seek treatment or
seek treatment outside of ED or hospital setting.

Fig. 1.4. Traumatic brain injury-related deaths per 100 000 persons. Source: Mortality Multiple Cause-of-Death data from the
National Vital Statistics System.
 EPIDEMIOLOGY OF TRAUMATIC BRAIN INJURY
Fig. 1.5. External cause of traumatic brain injury by age group. (Reproduced from Faul et al., 2010.)
PEAKS WITHIN AGE GROUPS
The incidence rate of TBI across age groups and mech-
anism of injury are highly variable and suggestive of
various lifestyles and activities as people age. During
the early stages and later stages of life, a person’s vul-
nerability to falls is the greatest. In ED visits, TBI
related falls for those aged 0–4 years old is 806.3 per
100 000 persons and 440.2 per 100 000 persons for those
aged 75 years old and older. The majority of people with
fall-related TBIs in this age group were seen in EDs and
discharged without being hospitalized. However, older
adults were hospitalized more often than younger per-
sons. A TBI that occurs when a person is struck by or
against an opposing force occurs most frequently in
the youngest age group of 0–4 years old (rate ¼ 269.3
per 100 000 persons). Motor vehicle crashes are the
most common cause of TBIs in the age groups 15–19
years old and 20–24 years old (respective rates 194.9
and 213.1 per 100 000 persons). Assaults are, overall,
the least frequent of the common mechanistic cause
categories, where rates peak during persons in the
20–24-year-old age group (rate ¼ 160.8 per 100 000
persons) (Faul et al., 2010).
GENDER
Overall, the rate of TBI among males seen in EDs is
547.6 per 100 000 persons and among females is 385.9
per 100 000 persons. Thus, a male is more likely to incur
a TBI compared to a female. For every age group cate-
gory (consisting of 4 years per category), TBI is more
frequent for males than females (Faul et al., 2010).
The rate ratio is largest for gender in the 10–14-year-old
age group (304.1 per 100 000 persons for females and
913.4 per 100 000 persons for males) and is almost at par-
ity for those in the 75 years old and older age group
(927.2 per 100 000 persons for females and 940.1 per
100 000 persons for males) (Faul et al., 2010).
9
RACE
Among ED visits the black racial group has the highest
rate of TBI, with a reported rate of 568.7 per 100 000 per-
sons, followed by the white racial group (456.6 per
100 000 persons) and then the American Indian, Alaskan
Native, Asian, or Pacific Islander group with a rate of
345.3 per 100 000 persons (Faul et al., 2010). For all racial
groups, the highest rate of TBI occurs in the 0–4 age
group. For hospitalizations the black racial group has
the highest rate of TBI, with a reported rate of 78.7
per 100 000 persons, followed by the white racial group
(69.8 per 100 000 persons) and then the American Indian,
Alaskan Native, Asian or Pacific Islander group with a
rate of 58.2 per 100 000 persons (Faul et al., 2010). The
rate of death is highest among the white racial group
(17.7 per 100 000 persons), closely followed by the black
racial group (17.3 per 100 000 persons). The lowest death
rate was found within the American Indian, Alaskan
Native, Asian or Pacific Islander group with a rate of
11.2 per 100 000 persons (Faul et al., 2010).
TRAUMATIC BRAIN INJURY
IN THE MILITARY
In recent years the public has become more aware that
TBI is an important public health issue, in part due to
exposure to images of brain injured veterans from the
war in Iraq and Afganistan. In fact, TBI has been labeled
as the “signature injury” of the war in Iraq (Hoge et al.,
2008). This public exposure, along with some high pro-
file TBI cases, may have influenced the general public
to seek medical treatment following a TBI.
TBI among US military personnel is a critical health
concern for active military personnel and for the vet-
erans of the recent conflicts. According to a Defense
and Veterans Brain Injury Center (DVBIC) analysis of
surveillance data released by the Department of
Defense, 33 149 US military personnel were diagnosed
with a TBI in 2011 alone. This number includes service
10 M. FAUL AND V. CORONADO
members from the Army, Navy, Marine Corps, Air
Force, and from the active duty and reserve components
of the National Guard. The US Department of Veterans
Affairs (VA) estimates that of the 771,874 veterans
sought care from a VA Medical Center from the start
of conflict in October 1, 2001 to December 31, 2011. Also,
a total of 59,218 veterans from Operation Enduring
Freedom and Operation Iraqi Freedom were evaluated
or treated for a condition possibly related to a TBI
(cited directly from Report to Congress, June 2013
(CDC, NIH, DoD, and VA Leadership Panel, 2013)).
DISABILITY
Traumatic brain injury (TBI) is a major cause of disabil-
ity in the US (Kraus et al., 1987). This disability can man-
ifest as cognitive deficits leading to the inability or
reduced ability to work and perform daily activities
and may be associated with an increased need for ongo-
ing medical care, rehabilitation, support, and services
(Zaloshnja et al., 2005). It is estimated that the preva-
lence of TBI-related disability ranged from 2.5 to 6.5 mil-
lion people in the US (Consensus Conference, 1999).
Examination of longitudinal data produced prevalence
estimates of 3.17 million (Zaloshnja et al., 2005), which
suggested that approximately 1.1% of the US population
lives with a TBI-related disability.
People with TBI-related disabilities have been associ-
ated with shorter lifespans (Zaloshnja et al., 2005).
Ventura et al. (2009) found that the lifespan of people
with TBI-related disabilities was reduced by approxi-
mately 8 years for individuals with TBI. The risk of death
after a TBI has been estimated as 7 times greater than
that of the general population in the first year after injury
(Selassie et al., 2005) and 5.3 times greater than that of
the population over an average of 7 years after injury
(Brown et al., 2004). Conditions that promote a shorter
lifespan among those persons with a TBI were seizures,
sepsis, digestive conditions, pneumonia, and other respi-
ratory conditions, as well as external causes and uninten-
tional injury (Harrison-Felix et al., 2006). Prior to this
finding, TBI was identified to be a major cause of epi-
lepsy (Bruns and Hauser, 2003) and such conditions
are associated with cell death in the brain (Liou
et al., 2003).
ALZHEIMER’S DISEASE AND EPILEPSY
The association between TBI and Alzheimer’s disease
has been controversial. Some studies have shown a link-
age while others have not (summarized in Jellinger,
2004). More research is needed before an association
can be made between a TBI and degenerative neurologic
diseases. However, an increased duration of PTA has
been associated with a heightened risk for TBI
complications such as post-traumatic epilepsy
(Chadwick, 2005). In a study of nearly 4500 TBI
patients, it was found that seizures are one of the risks
following a mild, moderate, or severe TBI. The risk of
seizures occurred in approximately 4% of the population
who had a previous TBI, but it was most common for
those who had a severe TBI (Annegers and Coan,
2000). However, epilepsy has been shown to increase
to 45–53% when there is a penetrating TBI (Raymont
et al., 2010).
In general, it has been suggested that TBI may cause a
biological vulnerability to Axis I and Axis II psychiatric
illness in some individuals (Koponen et al., 2002). These
authors found that the most common Axis I disorder
after traumatic brain injury was major depression
(27%) and the most common Axis II disorder was avoid-
ance (15%). The increased risk of psychiatric disorders
appears to be related to the extent of damage to the tem-
poral and frontal lobes (Zhang and Sachdev, 2003). One
predominant theory behind these associations is that the
brain contains a certain amount of cognitive reserve
where new pathways are built upon existing damaged
pathways (Stern, 2002). In theory, TBI reduces this cog-
nitive reserve (Stern, 2002) or “brain reserve” (Satz,
1993) resulting in a potentially increased vulnerability
to future disease (Stern, 2002). Recently, and anecdot-
ally, a prolonged history of TBI has been linked with a
condition called chronic traumatic encephalopathy
(CTE) among athletes. CTE was first seen in boxers
who experienced cumulative head trauma from repeated
punches. The symptoms included diminished cognition,
altered mood, behavior, and poor motor skills. This con-
dition has also been reported in professional football
players, and in 2005, the histopathological findings of
CTE were also reported among football players
(Omalu et al., 2005). Because emerging evidence sug-
gests that CTE is an outcome of prolonged TBI, this topic
will be discussed in detail in later chapters of this book.
REHABILITATION
Reliable national estimates of people needing rehabilita-
tion services following a TBI are not available. However,
using unrelated studies combined with national esti-
mates of people hospitalized with a TBI, an estimate
can be constructed. Given that two studies estimated
the need for rehabilitative services following a TBI
requiring hospitalization was 15% (Willer et al., 1990)
and 30% (Thurman et al., 1999), and that the number
of people hospitalized for TBI was 275 000 (Faul et al.,
2010), the estimated average annual need for TBI reha-
bilitation services is 61 875. Rehabilitation is important
following a TBI because subtle neurobehavioral deficits
can be missed without a thorough evaluation during
 EPIDEMIOLOGY OF TRAUMATIC BRAIN INJURY
clinical treatment. These problems are later recognized
and perhaps dealt with through rehabilitation. Because
many patients require rehabilitation for an extended
period of time and because insurance reimbursement
drives rehabilitation practices and policies that number
could be a substantial underestimate of prolonged,
cumulative service needs.
CONCLUSIONS
TBI is a public health problem affecting persons of all
ages regardless of sex and other demographic character-
istics. Most of the causes are preventable and the cause
of TBI appears to be highly dependent on the age of the
person. Thus, a person’s risk exposure to a TBI is suscep-
tible to life changes. For example, younger and older
people have a disproportionate amount of fall-related
TBI mostly because of strength and stability issues.
Meanwhile, TBIs associated with motor vehicle crashes
occur when a driver is least experienced with motor vehi-
cle operation. Better diagnostic tools are currently being
tested by the military and those tools will likely lead to
better diagnosis among civilians.
As the overall incident rate for TBI continues to rise,
more targeted prevention practices will likely become
more important. Prevention efforts such as seat belt
usage and the institution of state laws lowering the legal
limits of blood alcohol concentration of those operating
a motorized vehicle have likely contributed to a large
decrease in TBI-related deaths over time. However,
more can be done, such as better protective equipment
for athletes and mandatory helmet use for motorcycle
drivers. In recognition that older adults are more suscep-
tible to fall-related TBI, strength classes targeting older
populations have been developed and administered. It is
also clear that better epidemiology to help identify more
salient risk factors will lead to an enhanced understand-
ing of the causes of TBI so that more targeted prevention
practices can be created.
DISCLAIMER
“The findings and conclusions in this report are those of
the author(s) and do not necessarily represent the official
position of the Centers for Disease Control and Preven-
tion/the Agency for Toxic Substances and Disease
Registry.”
REFERENCES
Adekoya N, Thurman DJ, White DD et al. (2002). Surveillance
for traumatic brain injury deaths – United States,
1989–1998. MMWR Surveill Summ 51: 1–14.
Alexander MP (1995). Mild traumatic brain injury: pathophys-
iology, natural history, and clinical management.
Neurology 45: 1253–1260.
11
Anderson T, Heitger M, Macleod AD (2006). Concussion and
mild head injury. Pract Neurol 6: 342–357.
Andriessen TM, Horn J, Franschman G et al. (2011).
Epidemiology, severity classification, and outcome of
moderate and severe traumatic brain injury: a prospective
multicenter study. J Neurotrauma 28: 2019–2031.
Annegers JF, Coan SP (2000). The risks of epilepsy after trau-
matic brain injury. Seizure 9: 453–457.
Barell V, Aharonson-Daniel L, Fingerhut LA et al. (2002). An
introduction to the Barell body region by nature of injury
diagnosis matrix. Inj Prev 8 (2): 91–96.
Bazarian JJ, McClung J, Cheng YT et al. (2005). Emergency
department management of mild traumatic brain injury in
the USA. Emerg Med J 22 (7): 473–477.
Bazarian JJ, Veazie P, Mookerjee S et al. (2006). Accuracy of
mild traumatic brain injury case ascertainment using ICD-9
codes. Acad Emerg Med 13: 31–38.
Berga J, Tagliaferri F, Servadeib F (2005). Cost of trauma in
Europe. Eur J Neurol 12 (Suppl. 1): 85–90.
Bodofsky E, Schindelheim A, Milcarek B et al. (2010).
Increase in TBI discharges and associated diagnoses in
the U.S., 2001–2007 Brain Injury. Conference: 8th
World Congress on Brain Injury of the International
Brain Injury Association Washington, DC United States,
24, pp. 184–185.
Boswell JE, McErlean M, Verdile VP (2002). Prevalence of
traumatic brain injury in an ED population. Am J Emerg
Med 20: 177–180.
Bowen AY, Chamberlain AM, Tennent A et al. (1999). The
persistence of mood disorders following traumatic brain
injury: a 1 year follow-up. Brain Inj 13: 547–553.
Brain Trauma Foundation (2007). Guidelines for the manage-
ment of severe traumatic brain injury. J Neurotrauma 24
(Suppl. 1): S1-S106.
Brown AW, Leibson CL, Malec JF et al. (2004). Long-term
survival after traumatic brain injury: a population-based
analysis. NeuroRehabilitation 19: 37–43.
Bruns J, Hauser WA (2003). The epidemiology of traumatic
brain injury: a review. Epilepsia 44 (Suppl. 10): 2–10.
CDC, NIH, DoD, VA Leadership Panel (2013). Report to
Congress on Traumatic Brain Injury in the United States:
Understanding the Public Health Problem among Current
and Former Military Personnel. Centers for Disease
Control and Prevention (CDC), the National Institutes of
Health (NIH), the Department of Defense (DoD), and the
Department of Veterans Affairs (VA). Available at: http://
www.nashia.org/pdf/report-to-congress-on-traumatic-brain-
injury-2013-a.pdf (accessed July 26, 2014).
Centers for Disease Control and Prevention National Center
for Injury Prevention and Control (2003). Report to
Congress on mild traumatic brain injury in the United
States: steps to prevent a serious public health problem.
Centers for Disease Control and Prevention, Atlanta
(GA). Available at: http://www.cdc.gov/ncipc/pub-res/
mtbi/report.htm. Accessed January 16, 2012.
Centers for Disease Control and Prevention, QuickStats
(2010). Injury and Traumatic Brain Injury (TBI)-Related
Death Rates, by Age Group – United States, 2006.
MMWR 59: 303.
12 M. FAUL AND V. CORONADO
Chadwick D (2005). Adult onset epilepsies. E-epilepsy –
Library of articles, National Society for Epilepsy.
Champion HR, Holcomb JB, Young LA (2009). Injuries from
explosions. J Trauma 66: 1468–1476.
Cobb S, Battin B (2004). Second-impact syndrome. J Sch Nurs
20: 262–267.
Cohen DB, Rinker C, Wilberger JE (2009). Traumatic brain
injury in anticoagulated patients. J Trauma 60: 553–557.
Colantonio A, Saverino C, Zagorski B et al. (2010).
Hospitalizations and emergency department visits for
TBI in Ontario. Can J Neurol Sci 37: 783–790.
Consensus Conference (1999). Rehabilitation of persons with
traumatic brain injury. NIH Consensus Development Panel
on Rehabilitation of Persons with Traumatic Brain Injury.
JAMA 282: 974–983.
Dutton RP, Stansbury LG, Leone S et al. (2010). Trauma mor-
tality in mature trauma systems: are we doing better? An
analysis of trauma mortality patterns, 1997–2008.
J Trauma 69: 620–626.
Dutton RP, Prior K, Cohen R et al. (2011). Diagnosing mild
traumatic brain injury: where are we now? J Trauma 70:
554–558.
Esselman PC, Uomoto JM (1995). Classification of the spec-
trum of mild traumatic brain injury. Brain Inj 9: 417–424.
Evans RW (2006). Neurology and Trauma, Oxford University
Press.
Faul M, Wald MM, Rutland-Brown W et al. (2007). Using a
cost–benefit analysis to estimate outcomes of a clinical
treatment guideline: testing the brain trauma foundation
guidelines for the treatment of severe traumatic brain
injury. J Trauma Injury 63: 1271–1278.
Faul M, Xu L, Wald MM et al. (2010). Traumatic Brain Injury
in the United States: Emergency Department Visits,
Hospitalizations and Deaths 2002–2006. Centers for
Disease Control and Prevention. National Center for
Injury Prevention and Control, Atlanta, GA.
Faul M, Xu L, Wald MM et al. (2011). Increase in TBI in
the United States: is awareness of TBI contributing to
an increase in reported cases? Federal Interagency
Conference on Traumatic Brain Injury, Washington DC,
June 13–15, 2011.
Finkelstein E, Corso PS, Miller TR (2006). The Incidence and
Economic Burden of Injuries in the United States, Oxford
University Press, New York, NY.
Fletcher AE, Khalid S, Mallonee S (2007). The epidemiology
of severe traumatic brain injury among persons 65 years of
age and older in Oklahoma, 1992–2003. Brain Inj 21:
691–699.
Fox PJ, Vazquez L, Tonner C et al. (2010). A randomized trial
of a multifaceted intervention to reduce falls among
community-dwelling adults. Health Educ Behav 37:
831–848.
Gronwall D, Wrightson P (1980). Duration of post-traumatic
amnesia after mild head injury. J Clin Neuropsychol 2:
51–60.
Harrison-Felix C, Whiteneck G, DeVivo MJ et al. (2006).
Causes of death following 1 year postinjury among
individuals with traumatic brain injury. J Head Trauma
Rehabil 21: 22–33.
Hesdorffer DC, Ghajar J (2007). Marked improvement in
adherence to traumatic brain injury guidelines in United
States trauma centers. J Trauma 63: 841–848.
Hoge CW, McGurk D, Thomas JL et al. (2008). Mild traumatic
brain injury in U.S. soldiers returning from Iraq. N Engl J
Med 358: 453–463.
Homer CNT, Tremblay LN, Rizoli SB et al. (2006).
Association between alcohol and mortality in patients
with severe traumatic head injury. Arch Surg 141:
1185–1191.
Jellinger KA (2004). Head injury and dementia. Curr Opin
Neurol 17: 719–723.
Jiang JY, Gao GY, Li WP et al. (2002). Early indicators of
prognosis in 846 cases of severe traumatic brain injury.
J Neurotrauma 19: 869–874.
Kay T, Harrington DE, Adams R et al. (1993). Definition of
mild traumatic brain injury. J Head Trauma
Rehabilitation 8 (3): 86–87.
Khan F, Baguley IJ, Cameron ID (2003). Rehabilitation after
traumatic brain injury. Med J Aust 178: 290–295.
Koponen S, Taiminen T, Portin R (2002). Axis I and II psychi-
atric disorders after traumatic brain injury: a 30-year
follow-up study. Am J Psychiatry 159: 1315–1321.
Kraus JF, Nourjah P (1988). The epidemiology of mild,
uncomplicated brain injury. J Trauma 28: 1637–1643.
Kraus JF, Fife D, Conroy C (1987). Pediatric brain injuries: the
nature, clinical course, and early outcomes in a defined
United States population. Pediatrics 79: 501.
Kuppermann N, Holmes JF, Dayan PS et al. (2009). Pediatric
Emergency Care Applied Research Network (PECARN).
Identification of children at very low risk of clinically-
important brain injuries after head trauma: a prospective
cohort study. Lancet 374: 1160–1170.
Langlois JA, Kegler SR, Butler JA et al. (2003). Traumatic
brain injury-related hospital discharges results from a
14-state surveillance system, 1997. MMWR 52: 1–18.
Langlois JA, Rutland-Brown W, Thomas KE (2004).
Traumatic Brain Injury in the United States: Emergency
Department Visits, Hospitalizations, and Deaths.
Department of Health and Human Services (US), Centers
for Disease Control and Prevention, National Center for
Injury Prevention and Control, Atlanta, GA.
Liou AKF, Clark RS, Henshall DC et al. (2003). To die or
not to die for neurons in ischemia, traumatic brain injury
and epilepsy: a review on the stress-activated signaling
pathways and apoptotic pathways. Prog Neurobiol 69:
103–142.
Lowenfels AB, Miller TT (1984). Alcohol and trauma. Ann
Emerg Med 13: 1056–1060.
Marr A, Coronado V (Eds.), (2004). Central Nervous System
Injury Surveillance Data Submission Standards–2002,
Centers for Disease Control and Prevention, National
Center for Injury Prevention and Control, Atlanta, GA.
Masson F, Thicoipe M, Aye P et al. (2001). Epidemiology of
severe brain injuries: a prospective population-based study.
J Trauma 51: 481–489.
Murray CL, Lopez AD (1997). Global mortality, disability,
and the contribution of risk factors: Global Burden of
Disease Study. Lancet 349: 1436–1442.
 EPIDEMIOLOGY OF TRAUMATIC BRAIN INJURY
Nakase-Richardson R, Sherer M, Seel RT et al. (2011). Utility
of post-traumatic amnesia in predicting 1-year productivity
following traumatic brain injury: comparison of the Russell
and Mississippi PTA classification intervals. J Neurol
Neurosurg Psychiatry 82: 494–499.
National Vital Statistics System (2009). National Center
for Health Statistics. Centers for Disease Control
and Prevention. http://www.cdc.gov/nchs/data_access/
Vitalstatsonline.htm \l “Mortality_Multiple” Multiple
Cause of Death Data File within National Vital Statistics
System, public use data. Microdata accessed 6 October
2014: http://www.cdc.gov/nchs/deaths.htm.
Omalu BI, DeKosky ST, Minster RL et al. (2005). Chronic
traumatic encephalopathy in a National Football League
player. Neurosurgery 57: 128–134.
Raymont V, Salazar AM, Lipsky R et al. (2010). Correlates of
posttraumatic epilepsy 35 years following combat brain
injury. Neurology 75: 224–229.
Rodriguez SR, Mallonee S, Archer P et al. (2006).
Evaluation of death certificate-based surveillance for trau-
matic brain injury – Oklahoma 2002. Public Health Rep
121: 282–289.
Rubenstein LZ, Robbins AS, Josephson KR et al. (1990). The
value of assessing falls in an elderly population: a random-
ized clinical trial. Ann Intern Med 113: 308–316.
Saatman KE, Duhaime A, Bullock R et al. (2008).
Classification of traumatic brain injury for targeted thera-
pies. and Workshop Scientific team and Advisory Panel
Members. J Neurotrauma 25: 719–738.
Sanchez A, Krafty R, Weiss H et al. (2009). Trends in sur-
vival and early functional outcomes at hospital dis-
charge associated with severe adult traumatic brain
injuries: an analysis of the Pennsylvania Trauma
Outcome Study Database, 1998–2007. J Head Trauma
Rehabil. 24: 408.
Sasser SM, Hunt RC, Faul M et al. (2012). Guidelines for field
triage of injured patients recommendations of the National
Expert Panel on Field Triage, 2011. MMWR Recomm Rep
61: 1–20.
Satz P (1993). Brain reserve capacity on symptom onset after
brain injury: a formulation and review of evidence for
threshold theory. Neuropsychology 7: 273–295.
Sbordone RJ, Seyranian GD, Ruff RM (2000). The use of sig-
nificant others to enhance the detection of malingerers from
traumatically brain-injured patients. Arch Clin
Neuropsychol 15 (6): 465–477.
Schootman M, Fuortes LJ (2000). Ambulatory care for trau-
matic brain injuries in the US, 1995–1997. Brain Inj 14:
373–381.
13
Selassie AW, McCarthy ML, Ferguson PL et al. (2005). Risk
of posthospitalization mortality among persons with trau-
matic brain injury, South Carolina 1999–2001. J Head
Trauma Rehabil 20: 257–269.
Shah SM, Kelly KM (2003). Emergency Neurology:
Principles and Practice, Cambridge University Press,
Cambridge, UK.
Shandro JR, Rivara FP, Wang J et al. (2009). Alcohol and risk
of mortality in patients with traumatic brain injury.
J Trauma 66: 1584–1590.
Stern Y (2002). Cognitive reserve and Alzheimer disease.
Alzheimer Dis Assoc Disord 20: 112–117.
Tagliaferri F, Compagnone C, Korsic M et al. (2005).
A systematic review of brain injury epidemiology in
Europe. Acta Neurochir 148: 255–268.
Teasdale G, Jennett B (1974). Assessment of coma and
impaired consciousness: a practical scale. Lancet 2: 81–84.
Thomas KE, Stevens JA, Sarmiento K (2008). Fall-related trau-
matic brain injury deaths and hospitalizations among older
adults – United States, 2005. J Safety Res 39: 269–272.
Thompson HJ, McCormick WC, Kagan SH (2006). Traumatic
brain injury in older adults: epidemiology, outcomes, and
future implications. J Am Geriatr Soc 54: 1590–1595.
Thurman D, Guerrero J (1999). Trends in hospitalization
associated with traumatic brain injury. JAMA 282:
954–957.
Thurman DJ, Alverson C, Dunn KA et al. (1999). Traumatic
brain injury in the United States: a public health perspec-
tive. J Head Trauma Rehabil 14: 602–615.
Traumatic Brain Injury Act of 1996 (PL 104–66).
Ventura T, Harrison-Felix C, Carlson N et al. (2009). Postacute
mortality following traumatic brain injury: a population
based study. Arch Phys Med Rehabil 91: 20–29.
Walker R, Cole JE, Logan TK et al. (2007). Screening sub-
stance abuse treatment clients for traumatic brain injury:
prevalence and characteristics. J Head Trauma Rehabil
22: 360–367.
Willer B, Abosch S, Dahmer E (1990). Epidemiology of dis-
ability from traumatic brain injury, in neurobehavioral
sequelae of TBI, Taylor and Francis, London.
World Health Organization (2006). Projections of Mortality
and Burden of Disease to 2030: Deaths by Income
Group, WHO, Geneva.
Zaloshnja E, Miller T, Langlois JA et al. (2005). Prevalence
of long-term disability from traumatic brain injury in the
civilian population of the United States. J Head Trauma
Rehabil 23: 394–400.
Zhang Q, Sachdev PS (2003). Psychotic disorder and traumatic
brain injury. Curr Psychiatry Rep 5: 197–201.