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Traumatic brain injury: Epidemiology, classification, and

pathophysiology
Author: Venkatakrishna Rajajee, MBBS
Section Editor: Michael J Aminoff, MD, DSc
Deputy Editor: Janet L Wilterdink, MD

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

Literature review current through: Apr 2020. | This topic last updated: Jul 18, 2018.

INTRODUCTION

Traumatic brain injury (TBI) is one of the leading causes of disability in the United States, estimated at
13.5 million individuals [1]. Many survivors live with significant disabilities, resulting in major
socioeconomic burden as well. In 2010, the economic impact of TBI in the United States was
estimated to be $76.5 billion in direct and indirect costs [2,3].

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 "Post-traumatic seizures and epilepsy" and "Subdural
hematoma in adults: Etiology, clinical features, and diagnosis" and "Skull fractures in adults".)

EPIDEMIOLOGY

In 2013, there were approximately 2.5 million emergency department (ED) visits, 282,000
hospitalizations, and 56,000 deaths related to TBI in the United States [4]. TBI contributes to 30
percent of all injury-related deaths in the United States [4]. These numbers are thought to significantly
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. TBI
is a major problem for the United States military; the Department of Defense reports that between
2000 and 2017, 375,230 military personnel suffered TBI [5]. The incidence of TBI varies greatly
across countries and regions, from 811 per 100,000/year in New Zealand to 7.3 per 100,000/year in
Western Europe [6]. The incidence of TBI in countries such as Sweden, Italy, France, and Norway
appears to have decreased over time, while the incidence of TBI in Spain and Taiwan may have
increased [6].

The National Center for Injury Prevention and Control has published data on TBI-related ED visits,
hospitalizations, and deaths in the United States during 2013 [4]:

● The highest rates of TBI were observed in older adults (≥75 years; 2232 per 100,000 population),
very young (0 to 4 years; 1591 per 100,000), and young adults (15 to 24 years; 1081 per
100,000).

● Males had higher rates of TBI (959 per 100,000) than females (811 per 100,000), as is true for
other categories of traumatic injury.

● The most common mechanisms of TBI, adjusted for age, were falls (413 per 100,000), being
struck by an object (142 per 100,000), and motor vehicle crashes (122 per 100,000).

Compared with 2007, the rate of ED visits for TBI increased from 534 per 100,000 to 787 per
100,000, with at least part of the increase attributable to falls in older adults [4]. Falls in older adults
also led to more hospitalizations for TBI: from 357 per 100,000 to 454 per 100,000. The primary
cause of TBI-related death also changed, from motor vehicle crashes in 2007 to intentional self-harm
in 2013. While TBI-related hospitalization as a result of motor vehicle crashes saw a decline after
2007, mostly attributable to a decrease among young adults, an increase in hospitalizations for TBI
related to falls was observed, predominantly in older adults.

Lower socioeconomic status, alcohol and drug use, and underlying psychiatric and cognitive
disorders are also risk factors for head injury [7,8].

In adolescents, sports-related injuries account for a substantial proportion [8]. The proportion of TBI
secondary to violence has risen over the past decade and now accounts for 7 to 10 percent of cases
[9].

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 [10,11].

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 [12-14]. 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 [15].

Clinical severity scores — TBI has traditionally been classified using injury severity scores; the
most commonly used is the Glasgow Coma Scale (GCS) (table 1) [16]. A GCS score of 13 to 15 is
considered mild injury, 9 to 12 is considered moderate injury, and 8 or less is considered severe TBI.

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 [17,18].

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
[19,20]. 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 [21].

Neuroimaging scales — TBI can lead to several pathologic injuries, most of which can be identified
on neuroimaging [15]:

● 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 computed tomography (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) [22]. 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 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 [23].

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 [24]. Multiple systemic
traumatic injuries can further exacerbate brain injury because of associated blood loss, 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 is central to the initial
management of severe head injury. Likewise, the identification, prevention, and treatment of
secondary brain injury is the principle focus of neurointensive care management for patients with
severe TBI. (See "Management of acute moderate and severe traumatic brain injury".)

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 cerebral
edema and swelling.

● 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 typically present with profound coma without elevated intracranial pressure (ICP), and often
 have poor outcome. 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 computed tomography (CT) for
detecting DAI, and the sensitivity of the test declines if delayed from the time of injury [25].

● 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) [23]. (See
"Intracranial epidural hematoma in adults" and "Intracranial epidural hematoma in children:
Clinical features, diagnosis, and management".)

• 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 associated with underlying
cerebral injury (image 4). (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 [26-30]. 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 [31].

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 [26,32-40]:

● 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.

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), 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: Closed head injury (The Basics)")

SUMMARY

Traumatic brain injury (TBI) encompasses a broad range of pathologic injuries to the brain of varying
clinical severity that result from head trauma.

● In the United States, TBI-related emergency department (ED) visits, hospitalizations, and deaths
are most common in older adults (≥75 years), followed by the very young (0 to 4 years) and
young adults (15 to 24 years). Motor vehicle crashes are no longer the most common
mechanism for TBI-related ED visits, hospitalizations, and deaths, and have been replaced by
falls, especially in older adults. (See 'Epidemiology' above.)

● TBI is classically categorized as mild, moderate, and severe according to clinical severity using
the Glasgow Coma Scale (GCS) (table 1). (See 'Clinical severity scores' above.)

● 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.)

● 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 hypotension, hypoxia,
fever, and seizures. (See 'Secondary brain injury' above.)

ACKNOWLEDGMENT
The editorial staff at UpToDate would like to acknowledge 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 Subscription and License Agreement.

REFERENCES

1. Schiller JS, Lucas JW, Ward BW, Peregoy JA. Summary health statistics for U.S. adults:
National Health Interview Survey, 2010. Vital Health Stat 10 2012; :1.

2. Finkelstein E, Corso P, Miller T. The Incidence and Economic Burden of Injuries in the United St
ates, Oxford University Press, New York 2006.

3. Coronado V, McGuire L, Faul M, et al. Epidemiology and public health issues. In: Brain Injury M
edicine: Principles and Practice, 2nd ed, Zasler ND, Katz DI, Zafonte RD, et al (Eds), Demos M
edical Publishing, New York 2012.

4. Taylor CA, Bell JM, Breiding MJ, Xu L. Traumatic Brain Injury-Related Emergency Department
Visits, Hospitalizations, and Deaths - United States, 2007 and 2013. MMWR Surveill Summ
2017; 66:1.

5. Defense and Veterans Brain Injury Center. DoD Numbers for Traumatic Brain Injury. Departmen
t of Defense, 2017.

6. Li M, Zhao Z, Yu G, Zhang J. Epidemiology of Traumatic Brain Injury over the World: A

Systematic Review. Austin Neurol & Neurosci 2016; 1:1007.

7. Liao CC, Chiu WT, Yeh CC, et al. Risk and outcomes for traumatic brain injury in patients with
mental disorders. J Neurol Neurosurg Psychiatry 2012; 83:1186.

8. Ilie G, Boak A, Adlaf EM, et al. Prevalence and correlates of traumatic brain injuries among
adolescents. JAMA 2013; 309:2550.

9. Butcher I, McHugh GS, Lu J, et al. Prognostic value of cause of injury in traumatic brain injury:
results from the IMPACT study. J Neurotrauma 2007; 24:281.

10. Thurman DJ, Alverson C, Dunn KA, et al. Traumatic brain injury in the United States: A public
health perspective. J Head Trauma Rehabil 1999; 14:602.
11. Zaloshnja E, Miller T, Langlois JA, Selassie AW. Prevalence of long-term disability from
traumatic brain injury in the civilian population of the United States, 2005. J Head Trauma
Rehabil 2008; 23:394.

12. Steyerberg EW, Mushkudiani N, Perel P, et al. Predicting outcome after traumatic brain injury:
development and international validation of prognostic scores based on admission
characteristics. PLoS Med 2008; 5:e165; discussion e165.

13. Menon D, Harrison D. Prognostic modelling in traumatic brain injury. BMJ 2008; 336:397.

14. MRC CRASH Trial Collaborators, Perel P, Arango M, et al. Predicting outcome after traumatic
brain injury: practical prognostic models based on large cohort of international patients. BMJ
2008; 336:425.

15. Saatman KE, Duhaime AC, Bullock R, et al. Classification of traumatic brain injury for targeted
therapies. J Neurotrauma 2008; 25:719.

16. Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale.
Lancet 1974; 2:81.

17. Balestreri M, Czosnyka M, Chatfield DA, et al. Predictive value of Glasgow Coma Scale after
brain trauma: change in trend over the past ten years. J Neurol Neurosurg Psychiatry 2004;
75:161.

18. Stocchetti N, Pagan F, Calappi E, et al. Inaccurate early assessment of neurological severity in
head injury. J Neurotrauma 2004; 21:1131.

19. Stead LG, Wijdicks EF, Bhagra A, et al. Validation of a new coma scale, the FOUR score, in the
emergency department. Neurocrit Care 2009; 10:50.

20. Wijdicks EF, Bamlet WR, Maramattom BV, et al. Validation of a new coma scale: The FOUR
score. Ann Neurol 2005; 58:585.

21. Eken C, Kartal M, Bacanli A, Eray O. Comparison of the Full Outline of Unresponsiveness
Score Coma Scale and the Glasgow Coma Scale in an emergency setting population. Eur J
Emerg Med 2009; 16:29.

22. Marshall LF, Marshall SB, Klauber MR, et al. The diagnosis of head injury requires a
classification based on computed axial tomography. J Neurotrauma 1992; 9 Suppl 1:S287.

23. Maas AI, 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.

24. Maas AI, Stocchetti N, Bullock R. Moderate and severe traumatic brain injury in adults. Lancet
Neurol 2008; 7:728.

25. Moen KG, Skandsen T, Folvik M, et al. A longitudinal MRI study of traumatic axonal injury in
patients with moderate and severe traumatic brain injury. J Neurol Neurosurg Psychiatry 2012;
83:1193.

26. Harhangi BS, Kompanje EJ, Leebeek FW, Maas AI. Coagulation disorders after traumatic brain
injury. Acta Neurochir (Wien) 2008; 150:165.

27. Allard CB, Scarpelini S, Rhind SG, et al. Abnormal coagulation tests are associated with
progression of traumatic intracranial hemorrhage. J Trauma 2009; 67:959.

28. Wafaisade A, Lefering R, Tjardes T, et al. Acute coagulopathy in isolated blunt traumatic brain
injury. Neurocrit Care 2010; 12:211.

29. Stein SC, Young GS, Talucci RC, et al. Delayed brain injury after head trauma: significance of
coagulopathy. Neurosurgery 1992; 30:160.

30. Murray GD, Butcher I, McHugh GS, et al. Multivariable prognostic analysis in traumatic brain
injury: results from the IMPACT study. J Neurotrauma 2007; 24:329.

31. Zehtabchi S, Soghoian S, Liu Y, et al. The association of coagulopathy and traumatic brain
injury in patients with isolated head injury. Resuscitation 2008; 76:52.

32. Büki A, Koizumi H, Povlishock JT. Moderate posttraumatic hypothermia decreases early
calpain-mediated proteolysis and concomitant cytoskeletal compromise in traumatic axonal
injury. Exp Neurol 1999; 159:319.

33. Coles JP, Minhas PS, Fryer TD, et al. Effect of hyperventilation on cerebral blood flow in
traumatic head injury: clinical relevance and monitoring correlates. Crit Care Med 2002;
30:1950.

34. Diringer MN, Videen TO, Yundt K, et al. Regional cerebrovascular and metabolic effects of
hyperventilation after severe traumatic brain injury. J Neurosurg 2002; 96:103.

35. Kroemer G, Galluzzi L, Brenner C. Mitochondrial membrane permeabilization in cell death.

Physiol Rev 2007; 87:99.
 36. Morganti-Kossmann MC, Rancan M, Stahel PF, Kossmann T. Inflammatory response in acute
traumatic brain injury: a double-edged sword. Curr Opin Crit Care 2002; 8:101.

37. Oertel M, Boscardin WJ, Obrist WD, et al. Posttraumatic vasospasm: the epidemiology, severity,
and time course of an underestimated phenomenon: a prospective study performed in 299
patients. J Neurosurg 2005; 103:812.

38. Vespa P, Bergsneider M, Hattori N, et al. Metabolic crisis without brain ischemia is common
after traumatic brain injury: a combined microdialysis and positron emission tomography study. J
Cereb Blood Flow Metab 2005; 25:763.

39. Yi JH, Hazell AS. Excitotoxic mechanisms and the role of astrocytic glutamate transporters in
traumatic brain injury. Neurochem Int 2006; 48:394.

40. Stein SC, Chen XH, Sinson GP, Smith DH. Intravascular coagulation: a major secondary insult
in nonfatal traumatic brain injury. J Neurosurg 2002; 97:1373.

Topic 4825 Version 12.0

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. A score of 13 or higher correlates with mild brain injury,
a score of 9 to 12 correlates with moderate injury, and a score of 8 or less represents severe brain injury.

Graphic 81854 Version 7.0

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 density lesion >25
(swelling) 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 High or mixed density lesion >25 cm 3; not surgically evacuated

mass 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

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.

Graphic 70406 Version 13.0

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

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

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.

Graphic 56200 Version 5.0

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.

Graphic 68102 Version 5.0

Contributor Disclosures
Venkatakrishna Rajajee, MBBS Nothing to disclose Michael J Aminoff, MD, DSc Equity Ownership/Stock
Options: Trust [The portfolio may include medical or drug companies]. Equity Ownership/Stock Options
(Spouse): Trust [The portfolio may include medical or drug companies]. Janet L Wilterdink, MD Nothing to
disclose

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