2/11/24, 21:42 Traumatic brain injury: Epidemiology, classification, and pathophysiology - UpToDate

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Traumatic brain injury: Epidemiology, classification, and

pathophysiology
AUTHORS: Craig Williamson, MD, MS, Venkatakrishna Rajajee, MBBS
SECTION EDITOR: Michael J Aminoff, MD, DSc
DEPUTY EDITOR: Richard P Goddeau, Jr, DO, FAHA

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Oct 2024.

This topic last updated: May 16, 2023.

INTRODUCTION

Traumatic brain injury (TBI) is a major source of health loss and disability worldwide.
Globally, the annual incidence of TBI is variably estimated at 27 to 69 million [1,2]. Many
survivors live with significant disabilities, resulting in major socioeconomic burden. In 2010,
the economic impact of TBI in the United States was estimated to be $76.5 billion in direct
and indirect costs [3,4].

The focus of this topic is on the epidemiology, pathophysiology, and classification of TBI.
Other aspects of traumatic head injury are discussed separately. (See "Management of acute
moderate and severe traumatic brain injury" and "Acute mild traumatic brain injury
(concussion) in adults" and "Intracranial epidural hematoma in adults" and "Posttraumatic
seizures and epilepsy" and "Subdural hematoma in adults: Etiology, clinical features, and
diagnosis" and "Skull fractures in adults".)

EPIDEMIOLOGY

Definition of TBI — A simple, consistent definition of TBI is critical in estimating its burden.
In 2010, the international interagency initiative toward common data elements for research
in TBI and psychological health proposed a definition of TBI applicable across the spectrum
of injury severity.

This definition states that TBI is an alteration in brain function, or other evidence of brain
pathology, caused by an external force [5]. In this definition, the presence of confounding
factors such as intoxication or medical illness does not preclude a diagnosis of TBI, although
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clinical judgment is used to decide whether the patient's symptoms are a consequence of the
TBI. Additionally, this definition recognizes that clinical symptoms of brain injury may be
delayed or absent, and that "other evidence of brain pathology" can include imaging or
laboratory investigations. The focus of this definition is "brain" rather than "head" injury. The
six categories of external force that may result in TBI include [5]:

● The head being struck by an object

● The head striking an object
● Acceleration/deceleration of the brain without direct external impact
● A foreign body penetrating the brain
● The force from a blast/explosion
● Other forces yet to be defined

Global trends — Estimating the global burden of TBI is challenging. For one, many patients
with TBI, particularly with mild injury, do not seek medical attention. Also, high-quality
epidemiologic data are mostly available from high-income countries, while the majority of
the world's population resides in low- and middle-income countries. Existing data suggest,
however, that the incidence of TBI varies substantially across countries and regions.

The Global Burden of Disease (GBD) study published the following estimates regarding TBI in
2016 [1]:

● Incidence – The global annual incidence was estimated at 27.08 million, with an age-
standardized incidence rate of 369 per 100,000 population [1]. However, one study,
which used open-source epidemiologic data on traffic injuries to model the incidence of
TBI, estimated a worldwide annual TBI incidence of 69 million, higher than the GBD
estimate [2].

● Prevalence – Global TBI prevalence was estimated at 55.5 million, with an age-
standardized prevalence rate of 759 per 100,000 [1].

● Disability burden – TBIs were estimated to result in 8.1 million years of living with
disability worldwide in 2016 (111 per 100,000, age standardized) [1].

● Causes – Overall, falls were the single most common cause of TBI, with road traffic
injuries the second most common cause [1].

● Socio-demographic trends – Studies have reported somewhat conflicting data

regarding socio-demographic trends.

Stratified by socio-demographic index (SDI), the age-standardized incidence rate was

highest in the high-middle category at 468 per 100,000 [1]. While the incidence rate
rose globally by 3.6 percent compared with 1990, it fell by 9.4 percent in countries with

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the highest SDI, rose by 21.8 percent in countries in the middle SDI category, and fell by
9.3 percent in the lowest SDI category. Falls were the single most common cause of TBI
in every SDI category, with road traffic injuries the second most common cause. The
reduction in TBI in high SDI countries is thought to be a result of road safety
regulations.

In another study, the total burden of TBI was found to be three times greater in low- to
middle-income countries compared with high-income countries [2]. In lower-income
countries, 56 percent of TBIs were estimated to be due to traffic accidents compared
with 25 percent in high-income countries. Other trends identified in other studies
include a greater proportion of older TBI patients and falls as a mechanism of injury in
high-income countries, compared with younger patients and traffic accidents as the
primary mechanism of injury in lower-income countries [6-9].

Finally, in the Global Neurotrauma Outcomes Study, median age and mechanism of
injury were strongly associated with human development index (HDI) tier across 57
countries [10]. Median patient age in low HDI tier countries was 28 years versus 54
years in very high HDI tier countries. In very high HDI tier countries, 27 percent of TBIs
were due to road traffic collisions as opposed to 62 percent in medium tier and 37
percent in low tier countries.

United States — Few high-quality epidemiologic monitoring studies exist [6]. The GBD study
estimates a TBI incidence of 1.11 million and prevalence of 2.35 million in the United States
in 2016 [1]. Standardized for age, the incidence rate was 333 per 100,000 in 2016, a 3.3
percent reduction from 1990, while the prevalence rate was 605 per 100,000, a 5.7 percent
reduction compared with 1990 [1].

The Centers for Disease Control and Prevention (CDC) estimates that in 2014 there were
approximately 2.53 million emergency department (ED) visits, 288,000 hospitalizations, and
56,800 deaths related to TBI in the United States [11]. These numbers are thought to
underestimate the burden of TBI, since they do not include patients who did not seek
medical attention, received ambulatory care, were seen at Veterans Affairs centers, or were
in the military.

Data from the CDC suggest that older adults bear the brunt of the morbidity and mortality
associated with TBI [12]:

● The highest rates of TBI emergency visits were seen in older adults (≥75 years; 1682 per
100,000 population), the very young (0 to 4 years; 1619 per 100,000), and young adults
(15 to 24 years; 1010 per 100,000).

● The highest rates of TBI-related hospitalizations occurred in the adults ≥75 years (471
per 100,000) compared with adults 65 to 74 years (146 per 100,000), and with adults 55
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to 64 years (90 per 100,000). Rates of TBI-related deaths demonstrate similar age-
related trends.

There was also evidence of a shift in the primary mechanism of TBI in the United States
[4,11,12]. Compared with 2006, the rate of ED visits for TBI in 2014 increased 54 percent from
522 per 100,000 to 802 per 100,000. The largest increase (80 percent) was seen as a result of
falls. Falls were the leading cause of TBI-related injuries, and over half of TBIs due to falls
were in the youngest (0 to 4 years) and oldest (≥75 years) age groups. Rates of TBI-related
deaths resulting from self-harm, including suicide, increased by 17 percent during the study
period while age-adjusted rates of TBI-related hospitalizations due to traffic accidents fell. In
adolescents, sports-related injuries account for a substantial proportion [13]. The proportion
of TBI secondary to violence has risen over the past decade and now accounts for 7 to 10
percent of cases [14].

Lower socioeconomic status, alcohol and drug use, and underlying psychiatric and cognitive
disorders are also risk factors for brain injury [13,15].

TBI is a major problem for the United States military; the Department of Defense reports that
between 2000 and 2019, 413,858 military personnel suffered TBI [16], while 15,262 suffered
TBI in the first three-quarters of 2019 [17].

Moderate and severe TBIs are associated with neurologic and functional impairments. The
prevalence of long-term disability related to TBI in the United States is variably estimated to
be between 3.2 to 5.3 million, or approximately 1 to 2 percent of the population [18,19].

Epidemiologic trends more specific to mild TBI are discussed separately. (See "Acute mild
traumatic brain injury (concussion) in adults", section on 'Epidemiology'.)

CLASSIFICATION

TBI is a heterogeneous disease. There are many different ways to categorize patients in
terms of clinical severity, mechanism of injury, and pathophysiology, each of which may
impact prognosis and treatment.

The best prognostic models ideally include all of the factors described below, as well as age,
medical comorbidity, and laboratory parameters [7,20,21]. However, treatment decisions are
likely best informed by considering these variables individually rather than as a lump score.
Further efforts at improved classification are ongoing, as these may help to refine treatment
approaches [22].

Clinical severity scores — TBI has traditionally been classified using injury severity scores;
the most commonly used is the Glasgow Coma Scale (GCS) ( table 1), which should be

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measured in the emergency department (ED) following resuscitation and in the absence of
sedation [23].

The GCS is universally accepted as a tool for TBI classification because of its simplicity,
reproducibility, and predictive value for overall prognosis. However, it is limited by
confounding factors such as medical sedation and paralysis, endotracheal intubation, and
intoxication. These confounding issues are often particularly prominent in patients with a
low GCS score [24,25].

An alternative scoring system, the Full Outline of UnResponsiveness (FOUR) Score, has been
developed in order to attempt to obviate these issues, primarily by including a brainstem
examination [26,27]. However, this lacks the long track record of the GCS in predicting
prognosis and is somewhat more complicated to perform, which may be a barrier for non-
neurologists [28].

Severity classification — A GCS score of 8 or less measured on admission represents severe

TBI, a GCS score of 9 through 12 traditionally has represented moderate TBI, and a GCS score
of 13 through 15 mild TBI.

However, the recognition that more than one-third of patients with TBI and a GCS score of 13
have potentially life-threatening intracranial lesions has led to a reevaluation of this
classification [29,30]. While a revised classification has not been widely adopted, a GCS score
of 9 through 13 likely best represents the TBI population at moderate risk for death or long-
term disability (ie, "potentially severe"). The term "mild TBI" should be reserved for patients
with a GCS score of 14 or 15 who have no major intracranial pathology on imaging. (See
"Acute mild traumatic brain injury (concussion) in adults", section on 'Definitions'.)

The classification of severity based on the GCS reflects both the intensity of care required
during acute hospitalization and long-term outcomes. Transforming Research and Clinical
Knowledge in TBI (TRACK-TBI) is a longitudinal observational study in the United States that
investigated recovery from TBI extending from the acute hospitalization to several years
following injury [31-33]. While most patients with severe (98 percent) and moderate (92
percent) TBI required initial admission to an intensive care unit, patients with severe TBI
were hospitalized for a longer duration overall than patients with moderate TBI (mean 26
versus 15 days, p<0.001) [32]. By contrast, six months following injury, over 90 percent of
patients with mild TBI and no evidence of intracranial pathology on computed tomography
(CT) of the brain were completely independent within the home [31]. The prognosis of
moderate and severe TBI is discussed in detail separately. (See "Management of acute
moderate and severe traumatic brain injury", section on 'Mortality and functional outcomes'.)

Neuroimaging scales — TBI can lead to several pathologic injuries, most of which can be
identified on neuroimaging [22]:

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● Skull fracture
● Epidural hematoma (EDH)
● Subdural hematoma (SDH)
● Subarachnoid hemorrhage (SAH)
● Intraparenchymal hemorrhage
● Cerebral contusion
● Intraventricular hemorrhage
● Focal and diffuse patterns of axonal injury with cerebral edema

Two currently used CT-based grading scales are the Marshall scale and the Rotterdam scale:

● The Marshall scale uses CT findings to classify injuries in six different categories
( table 2) [34]. It is widely used in neurotrauma centers and has been shown to
predict the risk of increased intracranial pressure (ICP) and outcome in adults
accurately, but it lacks reproducibility in patients with multiple types of brain injury.

● The Rotterdam scale is a more recent CT-based classification developed to overcome

the limitations of the Marshall scale ( table 3). It has shown promising early results
but requires broader validation [35].

Other considerations — There are other important considerations for prognosis and
treatment in individuals with severe TBI.

● Different disease mechanisms (eg, closed versus penetrating injuries, blast versus blunt
trauma) may affect the type of pathologic brain injury.

● Extracranial injuries are present in approximately 35 percent of cases [36]. Multiple

systemic traumatic injuries can further exacerbate brain injury because of associated
blood loss, hypotension, hypoxia, and other related complications.

PATHOPHYSIOLOGY

The pathophysiology of TBI-related brain injury is divided into two separate but related
categories: primary brain injury and secondary brain injury.

Current clinical approaches to the management of TBI center around these concepts of
primary and secondary brain injury. Surgical treatment of primary brain injury lesions,
particularly subdural and epidural hematomas, is central to the initial management of severe
head injury. Likewise, the identification, prevention, and treatment of secondary brain injury
is the principal focus of neurointensive care management for patients with severe TBI. (See
"Management of acute moderate and severe traumatic brain injury".)

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Primary brain injury — Primary brain injury occurs at the time of trauma. Common
mechanisms include direct impact, rapid acceleration/deceleration, penetrating injury, and
blast waves. Although these mechanisms are heterogeneous, they all result from external
mechanical forces transferred to intracranial contents. The damage that results includes a
combination of focal contusions and hematomas, as well as shearing of white matter tracts
(diffuse axonal injury [DAI]) along with focal and global cerebral edema.

● Shearing mechanisms lead to DAI, which is visualized pathologically and on

neuroimaging studies as multiple small lesions seen within white matter tracts
( image 1). Patients with severe DAI may present with coma without elevated
intracranial pressure (ICP). This typically involves the gray-white junction in the
hemispheres, with more severe injuries affecting the corpus callosum and/or midbrain.
Magnetic resonance imaging (MRI; in particular diffusion tensor imaging) is more
sensitive than CT for detecting DAI, and the sensitivity of the test declines if delayed
from the time of injury [37]. While some patients with DAI suffer a poor outcome,
imaging evidence of DAI outside the brainstem is not a reliable predictor of poor
outcome [38,39], and outcomes for DAI within the brainstem can vary substantially
based on the degree of involvement of the ascending reticular activating system (ARAS)
[40].

● Focal cerebral contusions are the most frequently encountered lesions. Contusions are
commonly seen in the basal frontal and temporal areas, which are particularly
susceptible due to direct impact on basal skull surfaces in the setting of
acceleration/deceleration injuries ( image 2). Coalescence of cerebral contusions or a
more severe head injury disrupting intraparenchymal blood vessels may result in an
intraparenchymal hematoma.

● Extra-axial (defined as outside the substance of the brain) hematomas are generally
encountered when forces are distributed to the cranial vault and the most superficial
cerebral layers. These include epidural, subdural, and subarachnoid hemorrhage.

• In adults, epidural hematomas (EDHs) are typically associated with torn dural vessels
such as the middle meningeal artery and are almost always associated with a skull
fracture. EDHs are lenticular shaped and tend not to be associated with underlying
brain damage. For this reason, patients who are found to have EDHs only on CT scan
may have a better prognosis than individuals with other traumatic hemorrhage
types ( image 3) [35]. (See "Intracranial epidural hematoma in adults" and
"Intracranial epidural hematoma in children".)

• Subdural hematomas (SDHs) result from damage to bridging veins, which drain the
cerebral cortical surfaces to dural venous sinuses, or from the blossoming of
superficial cortical contusions. They tend to be crescent shaped and are often
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associated with underlying cerebral injury ( image 4). Because cerebral atrophy
causes stretching of the bridging veins, making them more susceptible to traumatic
injury, SDHs may occur in response to no or minimal trauma in older adults. (See
"Subdural hematoma in adults: Etiology, clinical features, and diagnosis" and
"Intracranial subdural hematoma in children: Epidemiology, anatomy, and
pathophysiology".)

• Subarachnoid hemorrhage (SAH) can occur with disruption of small pial vessels and
commonly occurs in the sylvian fissures and interpeduncular cisterns.
Intraventricular hemorrhage or superficial intracerebral hemorrhage may also
extend into the subarachnoid space. (See "Nonaneurysmal subarachnoid
hemorrhage".)

• Intraventricular hemorrhage is believed to result from tearing of subependymal

veins, or by extension from adjacent intraparenchymal or subarachnoid
hemorrhage. (See "Intraventricular hemorrhage".)

Approximately one-third of patients with severe TBI develop a coagulopathy, which is

associated with an increased risk of hemorrhage enlargement, poor neurologic outcomes,
and death [41-45]. While the coagulopathy may result from existing patient medications such
as warfarin or antiplatelet agents, acute TBI is also thought to produce a coagulopathy
through the systemic release of tissue factor and brain phospholipids into the circulation,
leading to inappropriate intravascular coagulation and a consumptive coagulopathy [46].

Secondary brain injury — Secondary brain injury in TBI is usually considered as a cascade of
molecular injury mechanisms that are initiated at the time of initial trauma and continue for
hours or days. These mechanisms include [41,47-55]:

● Neurotransmitter-mediated excitotoxicity causing glutamate, free-radical injury to cell

membranes
● Electrolyte imbalances
● Mitochondrial dysfunction
● Inflammatory responses
● Apoptosis
● Secondary ischemia from vasospasm, focal microvascular occlusion, vascular injury

These lead, in turn, to neuronal cell death as well as to cerebral edema and increased ICP
that can further exacerbate the brain injury. This injury cascade shares many features of the
ischemic cascade in acute stroke. These various pathways of cellular injury have been the
focus of extensive preclinical work into the development of neuroprotective treatments to
prevent secondary brain injury in TBI. No clinical trials of these strategies have demonstrated
clear benefit in patients.

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However, a critical aspect of ameliorating secondary brain injury after TBI is the avoidance of
secondary brain insults, which would otherwise be well tolerated but can exacerbate
neuronal injury in cells made vulnerable by the initial TBI. Examples include hypotension and
hypoxia (which decrease substrate delivery of oxygen and glucose to injured brain), elevated
ICP/decreased cerebral perfusion pressure (CPP), fever and seizures (which may further
increase metabolic demand), and hyperglycemia (which may exacerbate ongoing injury
mechanisms). (See "Management of acute moderate and severe traumatic brain injury".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the
Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th
grade reading level, and they answer the four or five key questions a patient might have
about a given condition. These articles are best for patients who want a general overview
and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are
longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th
grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to
print or e-mail these topics to your patients. (You can also locate patient education articles
on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

● Basics topics (see "Patient education: Head injury in adults (The Basics)")

SUMMARY

● Definition – Traumatic brain injury (TBI) is defined as an alteration in brain function, or

other evidence of brain pathology, caused by an external force. TBI encompasses a
broad range of pathologic injuries to the brain of varying clinical severity that result
from head trauma. (See 'Definition of TBI' above.)

● Epidemiology – The incidence rate of TBI varies across regions. TBI in high-income
countries has trended toward an older age group, with falls as the primary mechanism
of injury, while TBI in low- and middle-income countries trends toward a younger age
group, with traffic accidents as the primary mechanism of injury. (See 'Epidemiology'
above.)

● Causes – In the United States, TBI-related emergency department (ED) visits,

hospitalizations, and deaths are most common in adults age ≥75 years. Falls have
replaced traffic accidents as the most common mechanism for TBI-related ED visits,
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hospitalizations, and deaths, especially in older adults. Violence and self-harm have also
become more common causes of TBI. (See 'Epidemiology' above.)

● Clinical severity classification – TBI is classically categorized using the Glasgow Coma
Scale (GCS) ( table 1) as mild (GCS score 14 through 15), moderate (GCS score 9
through 13), and severe (GCS score 3 through 8) according to clinical severity. (See
'Clinical severity scores' above.)

● Other classification schemes – TBI can also be classified according to the type and
severity of neuroimaging findings, the mechanism of brain injury, and other variables.
These factors individually, and in the aggregate, influence prognosis and treatment.
(See 'Classification' above.)

● Pathophysiology – The pathophysiology of TBI includes primary and secondary brain

injury:

• The pathoanatomic sequelae of primary TBI include intra- and extraparenchymal

hemorrhages and diffuse axonal injury (DAI). (See 'Primary brain injury' above.)

• Secondary TBI results from a cascade of molecular injury mechanisms, which are
initiated at the time of initial trauma and continue for hours or days. It is likely that
secondary brain injury can be exacerbated by modifiable systemic events such as
decreased cerebral perfusion pressure (CPP), hypoxia, fever, and seizures. (See
'Secondary brain injury' above.)

ACKNOWLEDGMENT

The UpToDate editorial staff acknowledges Nicholas Phan, MD, FRCSC, FACS, and J Claude
Hemphill, III, MD, MAS, who contributed to an earlier version of this topic review.

Use of UpToDate is subject to the Terms of Use.

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Topic 4825 Version 16.0

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GRAPHICS

Glasgow Coma Scale (GCS)

Score

Eye opening

Spontaneous 4

Response to verbal command 3

Response to pain 2

No eye opening 1

Best verbal response

Oriented 5

Confused 4

Inappropriate words 3

Incomprehensible sounds 2

No verbal response 1

Best motor response

Obeys commands 6

Localizing response to pain 5

Withdrawal response to pain 4

Flexion to pain 3

Extension to pain 2

No motor response 1

Total

The GCS is scored between 3 and 15, 3 being the worst and 15 the best. It is composed of three
parameters: best eye response (E), best verbal response (V), and best motor response (M). The
components of the GCS should be recorded individually; for example, E2V3M4 results in a GCS score
of 9.

In the setting of head trauma, a GCS score of 8 or less measured on admission represents severe
traumatic brain injury (TBI).

Traditionally, a GCS score of 9 through 12 has represented moderate TBI, and a GCS score of 13
through 15 mild TBI. However, the recognition that more than one-third of patients with TBI and a
GCS score of 13 have potentially life-threatening intracranial lesions has led to a reevaluation of this
classification. While a revised classification has not been widely adopted, a GCS score of 9 through 13
likely best represents the TBI population at moderate risk for death or long-term disability. [1]

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Reference:
1. Godoy DA, Aguilera S, Rabinstein AA. Potentially severe (moderate) traumatic brain injury: A new categorization
proposal. Crit Care Med 2020; 48:1851.

Reproduced with permission from: Teasdale G, Jennett B. Assessment of coma and impaired consciousness: A practical scale.
Lancet 1974; 2:81. Copyright © by the Lancet Ltd. 1974.

Graphic 81854 Version 11.0

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Marshall CT (computed tomography) classification of traumatic brain injury

Category Definition

Diffuse injury I (no No visible intracranial pathology seen on CT scan

visible pathology)

Diffuse injury II Cisterns are present with midline shift of 0-5 mm and/or lesions densities
present; no high or mixed density lesion >25 cm 3 may include bone fragments
and foreign bodies

Diffuse injury III Cisterns compressed or absent with midline shift 0-5 mm; no high or mixed
(swelling) density lesion >25 cm 3

Diffuse injury IV Midline shift >5 mm; no high or mixed density lesion >25 cm 3
(shift)

Evacuated mass Any lesion surgically evacuated

lesion V

Non-evacuated mass High or mixed density lesion >25 cm 3 ; not surgically evacuated
lesion VI

Reproduced with permission from: Adelson PD, Bratton SL, Carney NA, et al. Guidelines for the acute medical management of
severe traumatic brain injury in infants, children, and adolescents. Chapter 1: Introduction. Pediatr Crit Care Med 2003; 4:S2.
Copyright © 2003 Lippincott Williams & Wilkins.

Graphic 67172 Version 11.0

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Rotterdam CT (computed tomography) classification of traumatic brain

injury

Predictor value Score

Basal cisterns

Normal 0

Compressed 1

Absent 2

Midline shift

No shift or shift ≤5 mm 0

Shift >5 mm 1

Epidural mass lesion

Absent 0

Present 1

Intraventricular blood or subarachnoid hemorrhage

Absent 0

Present 1

Sum score Total + 1

Reproduced with permission from: Maas Al, Hukkelhoven CW, Marshall LF, Steyerberg EW. Prediction of outcome in traumatic
brain injury with computed tomographic characteristics: a comparison between the computed tomographic classification and
combinations of computed tomographic predictors. Neurosurgery 2005; 57:1173. Copyright © 2005 Lippincott Williams &
Wilkins.

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Diffuse axonal injury (DAI)

CT scan of the brain showing DAI. Note the deep shearing-type injury in or near the white matter of
the left internal capsule (arrow).

CT: computed tomography.

Reproduced with permission from: J Claude Hemphill II, MD and Nicholas Phan, MD, FRCSC.

Graphic 67573 Version 5.0

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Frontal cerebral contusion

CT scan of the brain depicting cerebral contusions. The basal frontal areas (as shown) are particularly
susceptible.

CT: computed tomography.

Reproduced with permission from: J Claude Hemphill III, MD and Nicholas Phan, MD, FRCSC.

Graphic 53951 Version 4.0

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Traumatic epidural hematoma (EDH)

CT scan demonstrating a right EDH (arrow). Note the lenticular shape.

CT: computed tomography.

Reproduced with permission from: J Claude Hemphill III, MD and Nicholas Phan, MD, FRCSC.

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Traumatic subdural hematoma (SDH)

CT scan showing a left acute SDH (arrow). SDHs are typically crescent shaped. In this case the SDH is
causing significant mass effect and shift of midline structures to the right.

CT: computed tomography.

Reproduced with permission from: J Claude Hemphill III, MD and Nicholas Phan, MD, FRCSC.

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Contributor Disclosures
Craig Williamson, MD, MS Grant/Research/Clinical Trial Support: Xoran [Portable CT scans]. Other
Financial Interest: National Football League [Unaffiliated neurotrauma consultant]. All of the relevant
financial relationships listed have been mitigated. Venkatakrishna Rajajee, MBBS No relevant
financial relationship(s) with ineligible companies to disclose. Michael J Aminoff, MD, DSc No relevant
financial relationship(s) with ineligible companies to disclose. Richard P Goddeau, Jr, DO, FAHA No
relevant financial relationship(s) with ineligible companies to disclose.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these
are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.

Conflict of interest policy

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