Because traumatic brain injuries are so common and serious, effective imaging modalities must be used to identify and classify the different types of lesions that can occur due to head trauma. This article reviews the types of brain lesions found in cases of head trauma, their common mechanisms of injury, and their radiographic findings.
2Lt. Waite is a medical student and Dr. Smirniotopoulos is
Professor of Radiology, Neurology, and Biomedical Informatics
and Chairman of the Department of Radiology and Nuclear
Medicine at the Uniformed Services University of the Health
Sciences, Bethesda, MD.
The Head Injury Task Force of the National Institute of
Neurologic Disorders and Strokes estimates that there are 2 million
traumatic brain injuries per year in America; 500,000 of these are
severe enough to require hospital admission. Motor vehicle
accidents cause 51% of all traumatic brain injuries; falls account
for 21%, assaults and violence 12%, and sports and recreation 10%.
Two-thirds of all people sustaining head injuries are less than 30
years of age, and young men are at least twice as likely as women
to be the victim.
Because traumatic brain injuries are so common and serious,
effective imaging modalities need to be implemented to identify and
classify the different types of lesions that can occur due to head
trauma. When evaluating acute head injuries, the time that a study
takes to complete and the consideration of what types of monitoring
equipment can be taken with the patient into the scanner may become
critical. Because of these criteria, computed tomography (CT) has
become the primary modality for evaluating acute head trauma.
Recent technical advances in magnetic resonance imaging (MRI) have
reduced the time required to perform MRI evaluations. However,
there is still a potential problem with ferromagnetic life-support
equipment and the potential for ferromagnetic material in patients'
clothing. The patient's clinical condition, the type of head trauma
lesion suspected, and whether or not it is acute, subacute, or
chronic will determine which imaging modality should be used
initially. In most acute situations, a CT will be performed first,
with an MRI as a supplemental examination in cases in which higher
sensitivity is required (e.g., CT examination fails to account for
the patient's signs and symptoms).
Blunt head trauma can occur without an impact, as the result of
inertial forces such as acceleration and deceleration. The
identification of a scalp lesion signifies an impact or "contact
injury" and may focus your attention on the underlying bone (for
fracture, epidural, etc.; figure 1) and subjacent brain (for a
contusion; figure 2). In addition, the distinction between coup and
countercoup (or contre-coup) contusions relies on knowledge of the
mechanism of injury: coup contusions occur with an impact to the
head, at the site of the impact; whereas countercoup contusions are
opposite the point of impact.
Epidural hematomas usually arise secondary to significant trauma
with associated skull fractures. These are classically described as
presenting with a transient loss of consciousness ("concussion"),
then a lucid interval, followed by delayed neurological symptoms
and loss of consciousness. However, the classic "lucid interval" is
seen in less than half of cases. Epidural hematomas accumulate in
the potential space between the cranial periosteum and the naked
bone of the inner table of the skull. The periosteum delimiting
this space is bound down firmly to the cranium at the sutural
margins. As the head is struck, the calvaria bends inward and
adjacent margins bend outward causing a linear fracture (figures 3
and 4). Fractures have been found to occur in approximately 90% of
patients with epidural hematomas.
When the trauma occurs, a meningeal artery, which is attached
between the inner table and the dura, can be injured. Although
meningeal artery tears are most commonly associated with epidural
hematomas, meningeal veins and dural venous sinuses can also be
injured. The rate of expansion of the hematoma depends on many
factors: 1) whether a vein or artery is involved; 2) if the
transected artery goes into spasm; 3) if the collection of blood is
walled off to create a pseudo-aneurysm; 4) if the epidural
collection drains by the meningeal veins into the diploic veins;
and 5) if the hematoma decompresses through the fracture into the
Rapid arterial bleeding into the epidural space will displace the
adjacent brain. As the pressure in the hematoma gradually rises,
eventually a tamponade at the bleeding site can be produced
(usually only with venous bleeding). Unfortunately, expansion of
the hematoma may lead to cerebral herniation and death.
CT is most commonly used to diagnose epidural hematoma. The CT
appearance of an epidural hematoma depends on the source of the
bleeding (arterial versus venous), the interval between injury and
CT (acute versus chronic), the severity of hemorrhage, and the
degree of clot organization or breakdown. The vast majority of
epidural hematomas appear as biconvex extra-axial masses (figure
5). An acute epidural hematoma usually has homogeneous high
attenuation of whole blood. However, sometimes there is
high-attenuation with a radiolucent "swirl" inside--thought to be
produced by fresh blood from active bleeding invaginating into
dense clotted blood.
A subacute epidural hematoma is characterized by a homogenous,
hyperdense collection of blood due to clotting of the hematoma.
Chronic epidural hema-tomas often appear partially or totally
lucent due to the breakdown of blood products within the hematoma.
Most epidural hematomas present acutely, either due to the
associated fracture or from acute expansion of the hematoma causing
secondary effects (e.g., herniation). In hypotensive patients,
fluid resuscitation may restore normal blood pressure that then
leads to a delayed accumulation and presentation. Most patients
with true chronic epidural hematomas have had a delayed clinical
presentation due either to the small size of the extra-axial
hematoma, or from slower accumulation of hematoma volume caused by
venous (rather than arterial) bleeding.
Subdural hematomas (SDH) are accumulations of blood in the
potential space between the dura and the arachnoid. This space is
actually "epiarachnoid"--a term that will never catch on, but one
that accurately localizes the mass. In absolute terms, the subdural
blood is actually accumulating within the dural border layer of the
meningeal dura, in a natural cleavage plane. Clinically, the
presentation varies from nonspecific headache or nonlocalizing
signs and symptoms, such as lethargy or confusion. A lumbar
puncture is usually negative (the blood is not in the subarachnoid
space) and an electroencephalogram may show low voltage (the clot
"insulates" the brain from the scalp electrodes). Subdural
hematomas may present over a broad spectrum of time intervals. They
can be classified as acute (<1 week old), subacute (7 to 22 days
old), or chronic
(more than 22 days old). Capsule formation surrounding the hematoma
can also help to differentiate between acute and chronic subdural
hematomas. In general, subdural hematomas are crescent-shaped
(concave toward the brain), cross the sutures, and extend over a
larger area than do epidural hematomas of comparable volumes
(figure 6). Subdural ("epiarachnoid") hematomas may also layer
against the dural reflections of the falx and the
tentorium--appearing on CT as dural thickening.
CT is usually the first choice in the evaluation of subdural
hematomas, primarily for the rapidity with which a study can be
obtained. CT can also be three to five times less expensive than
MR. The appearance of subdural hematomas on CT depends upon the age
of the hematoma. Acute subdural hematomas are typically hyperdense
compared with the brain (50 to 100 HU).
Subacute subdural hematomas are isodense (25 to 45 HU), and chronic
subdural hematomas are usually hypodense (0 to 25 HU; figure 7).
Of course, all of these situations may be complicated by rebleeding
(which elevates attenuation) or associated arachnoid tears that
allow admixture of cerebrospinal fluid (which lowers
Acute subdural hematomas due to child abuse may be found
primarily within the interhemispheric fissure (figures 7 and 8). It
is thought that tearing of bridging veins from an
acceleration-deceleration injury (either from whiplash or child
abuse) causes a portion of these.
In comparison, some acute subdural hematomas are more lateral and
are most often due to a combination of venous, pial arterial
injury, or direct brain contusion and laceration.
MR has an advantages over CT because of multiplanar (especially
coronal) imaging and because subacute subdural hematomas may be
difficult to detect on CT if they are thin and isodense to the
brain. Subacute subdural hematomas are often hyperintense to brain
on T1-weighted images and may be variable compared with brain on
T2-weighted images. Chronic subdural hematomas can have a varied
signal on T1-weighted images, ranging from hypointense to
isointense, but are usually hyperintense on T2-weighted images
Rebleeding into the subdural space occurs in 10% to 30% of cases
and can complicate chronic subdural hematomas. Due to increasing
tension from the hematoma, the bridging veins are stretched across
the subdural hematoma and eventually rupture. Also, the neomembrane
that forms around a chronic subdural hematoma is composed of
fragile, newly formed capillaries and may rupture spontaneously or
with very minor secondary trauma, thus resulting in rebleeding.
This rebleeding into an established chronic subdural hematoma can
lead to mixed attenuation on CT and mixed signal intensity on MR
imaging (figure 9). Rebleeding may also convert a small
well-tolerated (asymptomatic) subacute hematoma into a larger
Contusions of the brain have been classified according to the
mechanism and location of injury into: coup and countercoup. A coup
contusion usually occurs when a moving object collides with a
stationary head, causing the skull to move inward (with or without
fracture) and direct transmission of force damages the underlying
brain tissue. There can be direct mechanical injury to the
underlying vessels, causing extravasation of whole blood from
capillaries with petechial and perivascular hemorrhages. If the
forces are more severe, progressively larger vessels may be
disrupted, and the blood may coalesce into confluent hematomas. In
contrast, countercoup contusions are produced at a location other
than the point of initial impact, usually 180š opposite. This often
occurs when the head and brain are in motion and strike a
stationary object. For example, a fall on the occiput often times
causes countercoup contusions in the anterior temporal lobes and
inferior frontal lobes (orbito-frontal gyri). These different types
of contusions can also occur together causing a mixture of coup and
countercoup contusions in the same patient.
Contusions (both coup and countercoup) may be evaluated on CT;
however MR is far more sensitive. Typically, CT is dependent on the
red-cell extravasation and identifies contusions as punctate or
streak high-attenuation areas in the cortex (figure 2). Although MR
can be more sensitive, sometimes gradient-recalled echo (GRE)
images are needed to bring out magnetic susceptibility changes from
small (petechial) collections of blood. Another problem with CT
evaluation is that high-density blood on the surface of the brain,
immediately adjacent to the high-density skull, can go undiagnosed,
and may be overlooked when there are associated extra-axial
collections in contact with brain (figure 10).
An acute contusion may not be visualized easily on T1-weighted
images. However, proton-density, T2-weighted and especially GRE
images have high sensitivity to increased water (extravasated
plasma and edema) from contusions. T2-weighted and GRE images are
also very sensitive to the associated hypointensity caused by
magnetic susceptibility from the hemorrhagic components of
contusions that make these lesions much more readily visible.
Coronal MR imaging is very helpful in identifying contusions in the
inferior frontal and temporal regions--areas that are difficult to
evaluate with CT because of streaking artifacts from bone at the
base of the skull.
In both subacute and chronic cerebral contusions, MR has also been
found to have superior sensitivity for detection when compared with
Several days after the injury, the deoxyhemoglobin in the contusion
oxidizes to methemoglobin, which has high signal intensity on
T1-weighted images, making identification even easier.
Diffuse axonal injury
When an acceleration/deceleration-type traumatic injury occurs,
one cerebral hemisphere is put into motion in relation to the other
hemisphere. At this time, shearing stresses are produced along the
axons, primarily in the white matter that connects the two
hemispheres. These indirect mechanical forces can "break the
connections" by transecting axons and cause shearing of the small
white matter vessels, producing deep and small petechial
hemorrhages (figures 11 and 12).
This type of trauma occurs most often with very rapid
accelerations/decelerations to those who are involved in motor
vehicle accidents. The "classic" diffuse axonal injury (DAI) occurs
when a "red-light runner" hits another vehicle broadside. Coronal
plane forces, often with an angular velocity, are applied rapidly
to the occupants of the vehicle. Typically, the patient has an
immediate loss of consciousness and often remains in a persistent
vegetative state. The lesions in DAI commonly occur in four
locations: 1) corpus callosum (undersurface); 2) brain stem
(dorsolateral mid-brain, figure 13); 3) basal ganglia/internal
capsule; and 4) corticomedullary junctures.
T2-weighted MR imaging is far more sensitive than CT for
detecting the secondary changes of edema and hemorrhage caused by
DAI, although both imaging modalities most likely underestimate the
true extent of DAI.
Hemorrhagic and grossly nonhemorrhagic DAI have been shown to be
visible only using MR imaging and not visible with CT in
approximately 30% of cases.
Paterakis et al
reported that the presence of hemorrhagic DAI-type injuries and the
association with traumatic space-occupying lesions is a poor
prognostic indicator. While nonhemorrhagic DAI-type injuries may
not signify a poor clinical outcome, they may, nonetheless, be
associated with more subtle higher-level mental status changes and
Survivors of DAI brain injury may show secondary Wallerian
degeneration of the sheared axons.
As the axons degenerate, the brain slowly atrophies, causing
enlargement of the sulci and ventricles. As a result, the white
matter loses volume with scattered areas of hyperintense signal on
The mechanism of injury (for example, acceleration-deceleration
or falling) usually determines the type of brain lesion that will
occur with head trauma. Epidural hematomas are commonly produced by
significant head trauma that typically produces an overlying skull
fracture. Acceleration-deceleration forces, such as motor-vehicle
accidents or child abuse, can cause both subdural hematomas and
diffuse axonal injury. Contusions are surface lesions. Coup
contusions are usually due a moving object colliding with a
stationary head. In contrast, countercoup contusions can be
produced when a moving head collides with a stationary object.
Shearing injuries are deep to the surface, sparing the cortical
gray matter with most lesions in the white matter, brainstem, and
basal ganglia. The type of brain hemorrhage can determine which
imaging modality should be used in the acute, subacute, or chronic
setting in order to optimize medical treatment.