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0037-198X/06/$-see front matter 2006 Elsevier Inc. All rights reserved. 177
doi:10.1053/j.ro.2006.04.003
178 T.H. Le and A.D. Gean
Imaging Findings
for rapid setting of windows and levels. A narrow window
Scalp Injury
width (W: 80, L: 40) is used to evaluate the brain. A slightly
wider window width (W: 150, L: 75) is used to exaggerate When reviewing CT scans for head trauma, begin by exam-
contrast between extra-axial blood and the adjacent skull. An ining the extracranial structures for evidence of soft-tissue
even wider window (W: 2500, L: 500) is used to evaluate the injury and/or radio-opaque foreign bodies. Scalp injury is a
osseous structures (Figs. 2 and 3). reliable indication of the site of impact. Scalp injury includes
Magnetic resonance imaging (MRI) is recommended for pa- soft-tissue lacerations, subgaleal hematoma, cephalohema-
tients with acute TBI when the neurologic findings are unex- toma, and residual foreign bodies. The subgaleal hematoma
plained by CT. MR is also the modality of choice for subacute is far and away the most common manifestation of scalp
or chronic injury. MR is usually comparable to CT in the injury. It can be recognized as focal soft-tissue swelling lo-
detection of an acute epidural and subdural hematoma.11,12 cated beneath the subcutaneous fibrofatty tissue and above
However, MR is more sensitive to subtle extra-axial collec- the temporalis muscle and calvarium (Fig. 1).
tions, nonhemorrhagic lesions, brainstem injuries, and sub-
arachnoid hemorrhage (SAH) when using fluid-attenuated Skull Fractures
inversion recovery (FLAIR).13,14 Nondisplaced linear fractures of the calvarium can be diffi-
Fluid-attenuated inversion recovery imaging improves the cult to detect on CT when the fracture plane is parallel to the
conspicuity of focal gray matter abnormalities (eg, contu- plane of section. Fortunately, isolated linear skull fractures
sions), white matter abnormalities, shear injuries, and SAH usually do not require treatment unless they are associated
by eliminating (or nulling) the bright cerebrospinal fluid with an epidural hematoma. Surgical treatment is usually
signal. Sagittal and coronal FLAIR images are particularly only indicated for depressed and compound skull fractures,
helpful in the detection of diffuse axonal injury (DAI) involv- both of which are easily detectable on CT (Fig. 2). Depressed
ing the corpus callosum and the fornix, two areas that are skull fractures can be associated with an underlying contu-
difficult to evaluate on routine T2-weighted images. On a sion; therefore, attention to the subadjacent parenchyma is
more cautious note, abnormal high signal in the sulci and essential (Fig. 14).
cisterns of ventilated patients receiving a high inspired oxy- Thin-section (1-mm) CT using a bone algorithm is recom-
gen fraction (0.60) have been observed and should not be mended for the evaluation of fractures in the skull base, orbit,
mistaken for hemorrhage.15 or facial bones. Thin sections are helpful for evaluating the
Gradient-echo imaging is highly sensitive to local magnetic degree of comminution and depression of bone fragments.
Imaging of head trauma 179
Figure 2 Depressed skull fracture with an associated acute epidural hematoma (EDH). (A) Axial CT scan displayed in
bone window shows a right frontal depressed skull fracture (arrowhead). Skull fractures can be associated with an
underlying epidural hematoma (B, arrow) and/or contusion, especially depressed comminuted fractures.
Figure 4 Diagram of the subdural hematoma (SDH) and EDH. The EDH is located above the outer dural layer (ie, the
periosteum), and the SDH is located beneath the inner (meningeal) dural layer. The EDH does not cross sutures. The
SDH does not cross the falx or the tentorium. (Reprinted with permission from Gean AD: Imaging of head trauma.
Philadelphia, PA, Williams & Wilkins-Lippincott, 1994, p 76.)
otorhinorrhea from CSF leak, and facial nerve palsy. Trans- tached at sutural margins (Fig. 4). However, at the vertex,
verse temporal bone fractures typically derive from direct where the periosteum that forms the outer wall of the sagittal
impacts to the occiput or frontal region. Complications in- sinus is not tightly attached to the sagittal suture, the EDH
clude sensorineural hearing loss, vascular injury, and peri- can cross midline. An important imaging finding that pre-
lymphatic fistula. Vertigo, nystagmus, and facial palsy are dicts rapid expansion of an arterial EDH is the presence of
also common complications. Mixed or complex temporal low-attenuation areas within the hyperdense hematoma (the
bone fractures involve a combination of fracture planes. They
typically result from severe crushing blows to the skull. Pa-
tients with mixed temporal bone fractures have a high inci-
dence of associated intracranial injury.
Figure 8 Chronic SDH and hydrocephalus. Axial CT image demon- Figure 10 Appearance of the chronic SDH on MRI. The chronic SDH
strates a left frontal extra-axial fluid collection (*) that has a lower is always slightly higher in signal intensity than CSF on T1-
attenuation than the brain parenchyma, consistent with chronic weighted, fluid attenuation inversion recovery (FLAIR) imaging and
SDH. The left lateral ventricle is compressed due to the mass effect proton-density MR images. It is hypointense to gray and white mat-
(white arrowhead) and there is subfalcine herniation (black arrow- ter on T1-weighted images (A), and hyperintense to brain paren-
head). Mild dilation of the right lateral ventricle is compatible with chyma on T2-weighted images (B-D).
noncommunicating obstructive hydrocephalus.
1 to 3 weeks after the acute event, depending on the patients
hematocrit level, clotting capability, and presence or absence
of rebleeding. Recognition of indirect imaging findings, such
as effacement of sulci, displacement of gray matter with white
matter buckling, and midline shift on a noncontrast CT
scan can avoid this common pitfall.
The MR appearance of a SDH also evolves over time, de-
pending on the biochemical state of hemoglobin. The acute
SDH is isointense to brain on T1-weighted and hypointense
on T2-weighted images. During the subacute phase, when
the subdural hematoma may be isodense or hypodense on
CT scans, T1-weighted images demonstrate high signal in-
tensity due to the presence of methemoglobin in the subdural
collection. The chronic SDH appears hypointense on T1-
weighted and hyperintense on T2-weighted images relative
to normal brain (Fig. 10). The signal intensity of chronic SDH
is slightly higher than CSF signal intensity on T1-weighted,
FLAIR, and proton-density T2-weighted imaging. Because of
its multiplanar capability, MR is useful in identifying convex-
ity and vertex hematomas that might not be detected on axial
CT scans because of the similar attenuation of the adjacent
bone.
Traumatic subarachnoid hemorrhage (SAH) can result from
(a) the disruption of small pial vessels; (b) extension into the
subarachnoid space by a contusion or hematoma; or (c) dif-
Figure 9 Isodense subacute SDH. During the transition from acute to fusion of intraventricular hemorrhage. SAH is very common
chronic SDH, an isodense phase occurs. At this stage, the SDH with TBI, but it rarely causes mass effect. On CT, SAH ap-
(arrowhead) can be difficult to discriminate from the adjacent pa- pears as linear or serpentine areas of high attenuation that
renchyma. conform to the morphology of the cerebral sulci and cisterns
Imaging of head trauma 183
(Fig. 11A-C). Common sites for SAH include the sylvian and
interpeduncular cisterns. The greatest accumulation of SAH
tends to occur contralateral to the site of impact (ie, contre-
coup). Subarachnoid hemorrhage along the convexity or ten-
torium can be difficult to differentiate from a SDH. A useful
clue is the extension of the SAH into adjacent sulci. Occa-
sionally, effacement of sulci due to the presence of intrasul-
cal SAH may be the only imaging clue of the presence of SAH.
In patients who are found unconscious after an unwitnessed
event, the detection of SAH in key cisterns (basilar, sylvian,
and circle of Willis) may indicate a ruptured aneurysm,
rather than trauma. In such cases, contrast-enhanced CT an-
giography is recommended as the next step in the patient
evaluation (Fig. 11D).
Acute subarachnoid hemorrhage may be more difficult to
Figure 12 DAI on CT and MR. In Grade II DAI, the corpus callosum
detect on conventional MR than on CT because it can be
is injured. Note the low attenuation within the splenium of the
isointense to brain parenchyma on T1- and T2-weighted im-
corpus callosum on CT (A). The FLAIR image demonstrates abnor-
ages. However, FLAIR has been shown to be more sensitive mal hyperintensity in the same region (B). The diffusion-weighted
than CT in detecting acute subarachnoid hemorrhage in an- image (DWI) shows a focus of bright signal intensity (C); the appar-
imal model, especially when a high volume (1 to 2 mL) is ent diffusion coefficient (ADC) was correspondingly reduced (not
present.14 Subacute subarachnoid hemorrhage may be better shown). The T2*-weighted image gradient-echo image shows scat-
appreciated on MR because of its high signal intensity when tered foci of susceptibility staining (signal loss) (D).
184 T.H. Le and A.D. Gean
Vascular Injury
Vascular injuries are mentioned here because they are causes of
both intra- and extra-axial injuries, including the cause of hema-
tomas and subarachnoid hemorrhages. Additional traumatic
vascular injuries include the arterial dissection, pseudoaneu-
rysm, and arteriovenous fistula. Arterial injuries are usually re-
Figure 15 Nonhemorrhagic contusion on CT. Axial CT image dem- lated to skull base fractures. The most often injured artery is the
onstrates an ill-defined area of low attenuation within the right internal carotid artery, especially at sites of fixation, where it
temporal lobe (arrow). The low attenuation is due to edema from
enters the carotid canal at the base of the petrous bone, and at its
the nonhemorrhagic contusion. The inferior temporal lobe is com-
monly injured because of its proximity to the petrous ridge.
wing, and the frontal lobes above the cribriform plate, planum
sphenoidale, and lesser sphenoid wing are commonly affected
(Fig. 13). Contusions are associated with a better prognosis than
DAI, unless they are accompanied by brainstem injury or signif-
icant mass effect. Contusions can also occur at the margins of
depressed skull fractures (Fig. 14). The cerebellum is involved
less than 10% of the time.30
On CT, nonhemorrhagic contusions are difficult to detect
initially until the development of associated edema (Fig. 15).
Hemorrhagic contusions are more easily identified and ap-
pear as foci of high attenuation within superficial gray matter
(Fig. 14). They may be surrounded by larger areas of low
attenuation from the associated vasogenic edema. As the con-
tusion evolves, the characteristic salt and pepper pattern of
mixed areas of hypodensity and hyperdensity becomes more
apparent. Contusions with severe mass effect may require
surgical decompression to prevent secondary injury.
On MRI, contusions appear as ill-defined areas of variable
signal intensity on both T1- and T2-weighted images, depend-
ing on the age of the lesions (Fig. 13). They are limited to the
surface and often have a gyral morphology. Hemosiderin from
an old contusion leads to decreased signal intensity on T2- and
especially T2*-weighted images, especially at higher field Figure 16 Intracerebral hematoma. (A) Axial CT shows a hyperdense
lesion within the right putamen. The surrounding low attenuation is
strengths. The signal loss can persist indefinitely and serves as an
due to vasogenic edema. (B) On the T1-weighted image, the periph-
important marker of prior hemorrhage.
ery of the hematoma is hyperintense due to the presence of methe-
The intracerebral hematoma is the most common cause of moglobin. (C) The hematoma is also hyperintense on the T2-
clinical deterioration in patients who have experienced a lucid weighted image due the presence of extracellular methemoglobin.
interval after the initial injury. In contrast to the common con- (D) Gradient-echo T2*-weighted image shows a surrounding he-
tusion described above, the intracerebral hematoma is due to mosiderin rim, which is dark due to local magnetic susceptibility
shear-induced hemorrhage from the rupture of small intrapa- inhomogeneity.
186 T.H. Le and A.D. Gean
Acknowledgments
We thank the residents, fellows, and attendings from the
Neuroradiology Section of the Department of Radiology,
University of California, San Francisco for continuing effort
in submitting interesting cases to the teaching file server
(http://tfserver.ucsf.edu). Some of the cases presented in this
article were the products of their effort.
Figure 21 Leptomeningeal cyst. Lateral radiograph of the skull dem-
onstrates a large lytic (lucent) lesion with scalloped margins located
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