Imaging of Head Trauma

Tuong H. Le, MD, PhD, and Alisa D. Gean, MD

T raumatic brain injury (TBI) is a leading cause of mortality
and morbidity in the world’s population, especially those
under age 44.1 In the United States alone, the cost of head
Imaging Techniques
Skull films are poor predictors of intracranial pathology and
trauma has been estimated to be over 40 billion dollars an- should not be performed to evaluate adult TBI.6-8 In the low-
nually.2 The National Center for Injury Prevention and Con- risk patient, skull films rarely demonstrate significant find-
trol has estimated that approximately 2% of the entire pop- ings. In the high-risk patients, the lack of abnormality on
ulation of the USA currently lives with disabilities caused by skull films does not exclude major intracranial injury.9 Pa-
TBI.3 TBI accounts for more than 500,000 emergency depart- tients who are at high risk for acute intracranial injury must
ment visits annually.4 The etiologies of head trauma are usu- be imaged by CT. The “scout view” that is obtained with all
ally associated with the patient age. In the elderly population, CT exams can be used as a “pseudoskull film.” In cases of
accidental falls are the most common causes. Motor vehicle suspected child abuse, a skull series may occasionally iden-
crashes are common culprits in young patients. In children, tify a fracture that is not identified on the concomitant CT
abuse and neglect are common reasons. examination. While this finding may not have surgical im-
TBI can be classified into primary and secondary injuries. portance, it, nevertheless, warrants removal of the child from
Primary lesions are the direct result of trauma to the head, the hostile environment.
and secondary lesions arise as complications of primary le- Computed tomography (CT), in the setting of acute trauma,
sions. Clinically, this classification is important because sec- is indicated for severe TBI (GCS ⬍ 8), persistent neurologic
ondary injuries can be preventable, whereas primary injuries, deficit, antegrade amnesia, unexplained asymmetric pupil-
by definition, have already occurred by the time the patient lary response, loss of consciousness more than 5 minutes,
first presents for medical attention. TBI can be further di- depressed skull fracture, penetrating injury, or bleeding dia-
vided according to location (intra- or extra-axial), mecha- thesis or anticoagulation therapy.10 The goal of imaging is to
nism (penetrating/open or blunt/closed), and clinical severity identify treatable injuries to prevent secondary damage. In
(minor, mild, moderate, or severe). The severity of head in- the acute setting, CT is the modality of choice because it is
jury is usually based on the Glasgow Coma Scale (minor: fast, widely available, and highly accurate in the detection of
GCS ⫽ 15; mild: GCS ⱖ 13; moderate: 9 ⱕ GCS ⱕ 12; skull fractures and intracranial hemorrhage. Life-support and
severe: 3 ⱕ GCS ⱕ 8).5 Primary extra-axial lesions include monitoring equipment can easily be accommodated in the
epidural, subdural, subarachnoid, and intraventricular hem- CT scanner suite. In addition, CT is usually superior to MR in
orrhage. Primary intra-axial lesions include cortical contu- revealing skull fractures and radio-opaque foreign bodies.
sions, intracerebral hematomas, axonal shearing injuries, With modern CT scanners, contiguous 3.75- or 5-mm sec-
gray matter injury, and vascular injury. Acute and subacute tions from the skull base to the vertex can be obtained in less
secondary injuries include cerebral edema, ischemia, and than 10 minutes. Thinner 1- or 2.5-mm sections are used to
brain herniation. Chronic secondary lesions include hydro- evaluate the orbits, maxillofacial structures, and skull base.
cephalus, the cerebrospinal fluid (CSF) leak, leptomeningeal With recent advances in multidetector CT (MDCT), thin
cyst, and encephalomalacia. These lesions will be discussed cross-sectional slices can be performed which allowed for
in further detail following a discussion about different meth- high-quality three-dimensional reconstruction. Thinner
ods for imaging TBI. slices also improve the diagnostic accuracy of CT in the eval-
uation of maxillofacial, orbital, and temporal bone fractures.
Intravenous contrast administration should not be per-
University of California, San Francisco, San Francisco General Hospital, San formed because it can both mask and mimic underlying hem-
Francisco, CA. orrhage.
Address reprint requests to Alisa D. Gean, MD, Professor of Radiology, CT images must be reviewed using multiple windows and
Neurology, and Neurological Surgery, University of California, San
Francisco, Chief of Neuroradiology, San Francisco General Hospital,
levels. With the widespread utilization of picture archiving
1001 Potrero Avenue, San Francisco, CA 94110. E-mail: agean@ and communication system (PACS), most imaging interpre-
sfghrad.ucsf.edu. tation is now performed on computer workstations, allowing

0037-198X/06/$-see front matter © 2006 Elsevier Inc. All rights reserved. 177
doi:10.1053/j.ro.2006.04.003

Tissue anisotropy is exploited in the new tech- epidural hematoma is a crescent-shaped hyperdense collection con. mistaken for hemorrhage. shear injuries. two areas that are skull fractures can be associated with an underlying contu- difficult to evaluate on routine T2-weighted images. Fortunately. The presence of hemosiderin alters the local magnetic suscepti- bility of tissue. is ferromagnetic. Depressed ing the corpus callosum and the fornix. 1). helpful in the detection of diffuse axonal injury (DAI) involv. white matter abnormalities. both of which are easily detectable on CT (Fig. L: 75) is used to exaggerate When reviewing CT scans for head trauma. due to the inherent inhomogeneity adjacent to the para- nasal sinuses and mastoid air cells. and epidural hematoma. subgaleal hematoma. Gean inhomogeneity caused by the presence of blood.12 cated beneath the subcutaneous fibrofatty tissue and above However. Axial CT often reduced in acute DAI. This limitation is even more problem- atic at high magnetic field strength unless parallel imaging is used. extra-axial collection along the white matter axons. Subjacent to which measures the preferential motion of water molecules the scalp injury is a biconvex. subdural. MR is usually comparable to CT in the injury. isolated linear skull fractures sions). hyperdense. Hemosid- erin. is frequently reduced in compatible with an acute epidural hematoma (#). Imaging Findings for rapid setting of windows and levels. MR is also the modality of choice for subacute is far and away the most common manifestation of scalp or chronic injury. Through its superior sensitivity to foci of acute shearing injury. and sub- arachnoid hemorrhage (SAH) when using fluid-attenuated Skull Fractures inversion recovery (FLAIR). nonhemorrhagic lesions. cisterns of ventilated patients receiving a high inspired oxy. the temporalis muscle and calvarium (Fig.11. The fractional anisotropy (FA). 2 and 3). L: 500) is used to evaluate the injury and/or radio-opaque foreign bodies.D. It can be recognized as focal soft-tissue swelling lo- detection of an acute epidural and subdural hematoma. DWI has especially improved detec- tion of DAI. Anterior to the chronic DAI. MR is more sensitive to subtle extra-axial collec. Scalp injury includes Magnetic resonance imaging (MRI) is recommended for pa. is Figure 1 Subgaleal. sistent with an acute subdural hematoma (arrowhead).16-18 DWI reveals more DAI lesions than fast spin- echo T2-weighted or gradient-echo T2*-weighted images in patients imaged within 48 hours of injury.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. The apparent diffusion coefficient (ADC). begin by exam- contrast between extra-axial blood and the adjacent skull. How- ever. 2).H.15 or facial bones.16 Diffusion-weighted imaging (DWI). The subgaleal hematoma plained by CT. tions. plane of section. On a sion. cephalohema- tients with acute TBI when the neurologic findings are unex. brainstem injuries. Scalp injury is a osseous structures (Figs. and residual foreign bodies. A slightly wider window width (W: 150. reliable indication of the site of impact. . soft-tissue lacerations. and SAH usually do not require treatment unless they are associated by eliminating (or “nulling”) the bright cerebrospinal fluid with an epidural hematoma. Because hemosiderin can persist indefinitely. Thin sections are helpful for evaluating the Gradient-echo imaging is highly sensitive to local magnetic degree of comminution and depression of bone fragments. An ining the extracranial structures for evidence of soft-tissue even wider window (W: 2500.178 T. resulting in areas of signal loss on gradient- echo T2*-weighted images. Le and A. image demonstrates a left parietal subgaleal hematoma (arrow). which measures the ran- dom motion of water molecules in brain tissue.13. A narrow window Scalp Injury width (W: 80. toma. therefore. Surgical treatment is usually signal.60) have been observed and should not be mended for the evaluation of fractures in the skull base. Thin-section (1-mm) CT using a bone algorithm is recom- gen fraction (⬎0. Note that it is superficial to the temporalis muscle (*). nique of diffusion tensor imaging (DTI). has improved the evaluation of TBI. 14). abnormal high signal in the sulci and essential (Fig. which measures the magnitude of water diffusion averaged over a three-dimensional space. contu. its detection on gradient-echo T2*-weighted im- ages allows for improved evaluation of remote injury. L: 40) is used to evaluate the brain. a breakdown product of blood. orbit. gradient-echo images are limited in the evaluation of cortical contusions of the inferior frontotemporal lobes. attention to the subadjacent parenchyma is more cautious note. Sagittal and coronal FLAIR images are particularly only indicated for depressed and compound skull fractures.

Imaging of head trauma 179 Figure 2 Depressed skull fracture with an associated acute epidural hematoma (EDH). With MDCT. (open arrow) and fractures of the sphenoid sinus (curved arrow) pacts to the side of the head. Diastasis of the left lambdoid suture poral bone fractures (Fig. and fluid in the middle ear cavity should always raise concern for a temporal bone fracture. thinner section axial imaging can be performed. fication of the mastoid air cells. 3) usually result from direct im. and transverse fractures are perpendic- a longitudinal left temporal bone fracture (arrowheads) with opaci- ular to the long axis of the petrous bone. MDCT with 3D reconstruction can elegantly display complex fractures and they can be generated expeditiously with so- phisticated algorithms. Longitudinal tem. Thin-section (1 to 1. Skull fractures can be associated with an underlying epidural hematoma (B. arrow) and/or contusion. p 63. which can be difficult in intubated or mentally altered pa- tients.20 Complications include conduc. de- pending on their orientation relative to the long axis of the petrous bone. They represent more than 70% and left lateral orbital wall (arrow) are also present. 1994. tive hearing loss from dislocation or fracture of the ossicles. Axial CT scan shows the petrous pyramid. PA. opacification of the mastoid air cells.5 mm) axial and direct coronal CT imaging with bone algorithm recon- struction is recommended for the evaluation of temporal bone fractures. William & Wilkins-Lippincott.) . permission from Gean AD: Imaging of head trauma. Philadelphia. especially depressed comminuted fractures. or in patients with suspected cervical spine injury. Fractures are classified as longitudinal or transverse. (Reprinted with of temporal bone fractures. and coronal reformats may be adequate for interpretation without the need for direct coronal imaging. Longitudinal fractures parallel the long axis of Figure 3 Longitudinal temporal bone fracture. (A) Axial CT scan displayed in “bone window” shows a right frontal depressed skull fracture (arrowhead).19 Temporal Bone Fractures Pneumocephalus.

The EDH is located above the outer dural layer (ie. and facial nerve palsy. extra-axial collection (Fig. 2). The developing hematoma dissects the dura from the inner table of the skull. within a biconvex. Complications in. associated with an overlying skull fracture. and the vertex from injury to the superior sagittal sinus. They typically result from severe crushing blows to the skull. nystagmus. Venous EDHs are less common than arterial EDHs and tend to occur at three classic locations: the poste- rior fossa from rupture of the torcula or transverse sinus. can cross midline. they may occur from stretching or tearing of meningeal arteries without an associ- ated fracture. the EDH clude sensorineural hearing loss. 1994. Mass effect with mottling appearance (“swirl sign”). p 76. biconvex. the acute EDH appears as a well-defined. extra-axial sulcal effacement and midline shift is frequently seen. Primary Head Injury Extra-Axial Injury The epidural hematoma (EDH) occurs in the potential space located between the inner table of the skull and the dura (Fig. the periosteum). 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. tached at sutural margins (Fig. that disrupts the middle meningeal artery. PA. The heterogenous density within this cause the EDH is located in the potential space between the EDH is secondary to mixing of hyperacute (low attenuation) with dura and inner table of the skull. Pa- tients with mixed temporal bone fractures have a high inci- dence of associated intracranial injury.) otorhinorrhea from CSF leak. Left frontal subarachnoid hemor- sutures because the periosteal layer of the dura is firmly at.21 Venous EDHs can be difficult to diagnose on axial imaging but can be readily confirmed on coronal reformatted images. . Trans.H. Gean Figure 4 Diagram of the subdural hematoma (SDH) and EDH.D. and facial palsy are dicts rapid expansion of an arterial EDH is the presence of also common complications. at the vertex. Be. The EDH does not cross sutures.” Axial CT image shows a heterogenous. hyper- dense. They frequently result from a skull frac- ture. Vertigo. Le and A. vascular injury. 4). forming an ovoid mass that displaces the adjacent brain. Williams & Wilkins-Lippincott. sinus is not tightly attached to the sagittal suture. 2). and peri.10 In children. An important imaging finding that pre- lymphatic fistula. and the SDH is located beneath the inner (meningeal) dural layer. However. Mixed or complex temporal low-attenuation areas within the hyperdense hematoma (the bone fractures involve a combination of fracture planes. it rarely crosses cranial acute (high attenuation) blood.180 T. rhage (SAH) is also noted (arrowheads). Philadelphia. On CT. (Reprinted with permission from Gean AD: Imaging of head trauma. usually in the temporal squamosa. fluid collection (black arrow). It is usually Figure 5 EDH “Swirl sign. the middle cranial fossa from disruption of the sphenoparietal sinus. The SDH does not cross the falx or the tentorium.

effacement of the frontoparietal sulci and mild midline shift result- cause the SDH is often associated with parenchymal injury. An acute-on-chronic SDH would have a similar appearance. right. In rapid decompression of the hydroceph- alus. which measures 20 to 30 HU. the radiol- ogist can adjust the window setting readily to avoid this po- tential pitfall (Fig. Other causes of the SDH include rapid decompression of obstruc- tive hydrocephalus. Because of the prominent extra-axial space in the elderly resulting from ce- rebral atrophy. extra-axial collection (Fig. thought to represent active bleeding (Fig. There is also frequently identified along the falx and tentorium. In these pa- tients. The attenuation gradient is are supratentorial and located along the convexity. an isodense phase occurs. and an increased in- cidence of SDH in these patients has been observed. The SDH is uncommonly seen in association with DAI. intravenous contrast administration can be helpful by demonstrating an enhancing capsule or displaced cortical veins. 6).Imaging of head trauma 181 the degree of mass effect seen frequently appears more severe relative to the size of the collection. ing from the SDH mass effect. 5). 1). Subdural hematomas (SDH) are generally venous in origin.” With most viewings and interpreta- tions now performed on computer workstations. 8). A small thin convexity SDH can be difficult to appreciate adjacent to the hyperdense skull unless the images are viewed with a “wide window. relative to normal brain. homoge. Axial CT image shows a large. The collection nous. SDHs are frequently seen layering along the entire hemispheric convexity from the an- terior falx to the posterior falx (Figs. 7). It can be difficult to distinguish from prominent subarach- noid space in patients with cerebral atrophy. the brain surface recedes from the dura quicker than the brain parenchyma can re-expand after being compressed by the distended ventricles. crescent-shaped. They usually arise from laceration of bridging cortical veins during sudden head deceleration. and injury to pial vessels and pacchion- ian granulations. The acute SDH is hyper- dense. Rebleeding during evolution of a SDH ap- pears as a heterogeneous mixture of fresh blood and partially liquefied hematoma (Fig. measuring 50 to 60 Hounsfield Units (HU). . Be. 9). They are secondary to the presence of hemorrhage of different ages. Occasionally. CSF (Fig.23 It is an ominous sign that needs to be followed closely. holohemi- spheric. The attenuation (density) of an acute SDH initially in- creases because of clot retraction. On CT. During the transition from the acute to Figure 6 Rebleeding during evolution of a SDH (surgically con. Because the inner dural layer and arachnoid are not firmly attached. fluid collection with mixed hyperdense (acute) and isodense (hyperacute) blood. The chronic SDH has a low-atten- uation value similar to. the chronic SDH. but slightly higher than.22. A sediment level or “hematocrit effect” may be seen either from rebleeding or in patients with clotting disorders (Fig. Axial CT image demonstrates a large. they may also result from disruption of penetrating branches of super- ficial cerebral arteries. usually between firmed). extra-axial. The density will progressively decrease as protein degradation occurs within the hematoma. increased motion between the brain paren- chyma and the calvarium is permitted. Most has a hyperdense “sediment” level (*). extra-axial fluid collection. Figure 7 SDH with hematocrit level. so-called “swirl sign”). 6 to 10). the acute SDH appears as hyperdense. holohemispheric. right.

(b) extension into the subarachnoid space by a contusion or hematoma. SAH ap- (arrowhead) can be difficult to discriminate from the adjacent pa. Traumatic subarachnoid hemorrhage (SAH) can result from (a) the disruption of small pial vessels.D. consistent with chronic weighted. ter on T1-weighted images (A). displacement of gray matter with white matter “buckling. The acute SDH is isointense to brain on T1-weighted and hypointense on T2-weighted images. At this stage. SAH is very common chronic SDH. During the subacute phase. T1-weighted images demonstrate high signal in- tensity due to the presence of methemoglobin in the subdural collection. 10). FLAIR. de- pending on the biochemical state of hemoglobin. On CT. pears as linear or serpentine areas of high attenuation that renchyma. the SDH with TBI. fluid attenuation inversion recovery (FLAIR) imaging and SDH. such as effacement of sulci. and proton-density T2-weighted imaging. or (c) dif- Figure 9 Isodense subacute SDH. and presence or absence of rebleeding. The MR appearance of a SDH also evolves over time. 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. when the subdural hematoma may be isodense or hypodense on CT scans. and hyperintense to brain paren- head). conform to the morphology of the cerebral sulci and cisterns . 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. Figure 10 Appearance of the chronic SDH on MRI. Gean Figure 8 Chronic SDH and hydrocephalus. Recognition of indirect imaging findings.182 T. The chronic SDH appears hypointense on T1- weighted and hyperintense on T2-weighted images relative to normal brain (Fig. Le and A. 1 to 3 weeks after the acute event. noncommunicating obstructive hydrocephalus. Axial CT image demon. Because of its multiplanar capability.H. The signal intensity of chronic SDH is slightly higher than CSF signal intensity on T1-weighted. During the transition from acute to fusion of intraventricular hemorrhage. clotting capability. It is hypointense to gray and white mat- (white arrowhead) and there is subfalcine herniation (black arrow. an isodense phase occurs. but it rarely causes mass effect.” and midline shift on a noncontrast CT scan can avoid this common pitfall. Mild dilation of the right lateral ventricle is compatible with chyma on T2-weighted images (B-D). The left lateral ventricle is compressed due to the mass effect proton-density MR images. depending on the patient’s hematocrit level.

IVH can result from retrograde flow of SAH into the ventric- ular system via the fourth ventricular outflow foramina (the reverse mechanism in which IVH can extend into the sub- arachnoid space). especially when a high volume (1 to 2 mL) is ent diffusion coefficient (ADC) was correspondingly reduced (not present. Traumatic intraventricular hemorrhage (IVH) can also occur by one of three mechanisms. In- Figure 11 SAH and IVH secondary to aneurysm rupture. Hemosiderins are best detected on gradient-echo T2*-weighted images. C. deed. sylvian. contre- coup). FLAIR has been shown to be more sensitive mal hyperintensity in the same region (B). A useful clue is the extension of the SAH into adjacent sulci. “effacement” of sulci due to the presence of intrasul- cal SAH may be the only imaging clue of the presence of SAH. Chronic hemorrhage on MR scans may show hemosiderin staining in the subarach- noid space. and circle of Willis) may indicate a ruptured aneurysm. In patients who are found unconscious after an unwitnessed event. suggest- ing recent rupture. IVH usually appears as CSF-hyperdense fluid level. the detection of SAH in key cisterns (basilar. The aneurysm appears pointed. white arrowhead). the appar- imal model. layering within the ventricular system (Fig. .Imaging of head trauma 183 the blood is isointense to CSF on CT. Contrast-en- hanced CT angiography (CTA) is particularly helpful in this situa- tion. The diffusion-weighted than CT in detecting acute subarachnoid hemorrhage in an. or basilar cisterns). Subarachnoid hemorrhage along the convexity or ten- torium can be difficult to differentiate from a SDH.and T2-weighted sequences (“superficial hemo- siderosis”). SAH is common with TBI.and T2-weighted im- corpus callosum on CT (A). In this case. rather than trauma. Common sites for SAH include the sylvian and interpeduncular cisterns. First. 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). Acute subarachnoid hemorrhage may be more difficult to Figure 12 DAI on CT and MR. The FLAIR image demonstrates abnor- ages. SAH may lead to communicating hy- drocephalus by impeding CSF resorption at the level of arachnoid villi. D).14 Subacute subarachnoid hemorrhage may be better shown). The greatest accumulation of SAH tends to occur contralateral to the site of impact (ie. Third. CTA shows a right middle cerebral artery trifurcation aneurysm (D). respectively. which appears as areas of decreased signal inten- sity on T1. Patients with IVH are at risk for developing both communicating and noncommunicating hydrocepha- lus secondary to obstruction at the level of the arachnoid villi or aqueduct. Although IVH may appear “tumefactive” as a cast within the ventricle. contrast-enhanced CT an- giography is recommended as the next step in the patient evaluation (Fig. (A) On CT. 11D). They are also at risk of ependymitis from the irritant effects of the blood. Occasionally. it can result from rotation- ally induced tearing of subependymal veins along the surface of the ventricles. Another mechanism is by direct extension of a parenchymal hematoma into the ventricular system. In Grade II DAI. On CT. (Fig. 11A-C). Note the low attenuation within the splenium of the isointense to brain parenchyma on T1. the corpus callosum detect on conventional MR than on CT because it can be is injured. 11B). Intraventricular hemorrhage (IVH) is seen as a high attenuation fluid level within the occipital horn of the left lateral ventricle (B. the that conform to the morphology of the sulci and cisterns. In such cases. an underlying rup- tured aneurysm must also be considered (B. However. image (DWI) shows a focus of bright signal intensity (C). tiny collections of increased density layering in the acute SAH appears as linear or serpentine areas of high attenuation occipital horns may be the only clue to IVH. if the SAH is identified in certain locations (Sylvian. Occa- sionally. interhemispheric.

gliosis. The conspicuity of DAI on MR eventually diminishes as the damaged axons degenerate and the edema resolves. Petechial hemorrhage causes a central hy- pointensity on T2-weighed images and hyperintensity on T1- weighted images as a result of intracellular methemoglobin in the subacute stage. The cortical contusions is a focal brain lesion primarily involv- ing superficial gray matter. Newer imaging methods. The temporal lobes tions of brain tissue. only about 20% of DAI lesions contain suffi.17 However. . Gean sensitivity to blood products. petechial hemorrhages at the gray–white pressed right temporal skull fracture (arrowhead).26 Spin-echo T2- weighted MR techniques. Common find. temporal contusions are also noted. Regions of the brain that are in close contact Intra-Axial Injury with the rough surface on the inner skull table are commonly Diffuse Axonal Injury (DAI) results from rotational accelera.27-29 On MR. is of special interest because it tends to be underdiagnosed by current imaging techniques. especially FLAIR imaging. The para- sagittal regions of the frontal lobes and periventricular re- gions of the temporal lobes are commonly affected. DAI. provides increased success at explaining neurologic def- icits after trauma and predicting long-term outcome. In severe DAI. Grade I DAI involves only the periph- eral gray–white junctions of the lobar white matter. lobes. hemosiderin. the incidence of DAI is thought to be underesti- mated.” an adjacent right frontal surface contusion is revealed Unfortunately. can de- tect many nonhemorrhagic foci of DAI but still underesti- mate the true extent of traumatic white matter damage. and less so. with more severe trauma have DAI involving the lobar white weighted image demonstrates abnormal T1 shortening (increased matter as well as the corpus callosum. There is as. which occurs in about half of all severe head trauma cases. rior body and splenium (Fig. Small bilateral callosum.H. midbrain. windowing.184 T.24. 12). have shown potential in improving the de- tection of white matter injury in both acute and chronic DAI. pathologic studies demonstrate that only a minority of DAI lesions is associated with hemorrhage. The corpus callosum is sociated decreased signal on the gradient-echo images due to the susceptible to DAI because the falx prevents displacement of presence of hemosiderin (B).D. Patients Figure 13 Cortical contusion near the skull base. DAI is characterized by loss or above the petrous bone or posterior to the greater sphenoid severe impairment of consciousness beginning at the mo- ment of direct impact. and there- fore. and edema. A small left temporal SDH with associated pneumo- cient hemorrhage to be detectable on CT. such as DWI and DTI with 3D tractography. which can persist indefi- nitely on gradient-echo T2*-weighted images (Fig. the parasagittal convexity. in addition to the lobar white matter and corpus tion of methemoglobin. These areas include the orbitofrontal and temporal tion and deceleration forces that produce shearing deforma. Clinically. nonhemorrhagic DAI lesions appear as multiple small foci of increased signal on T2-weighted images (Fig. Le and A. The location of the of DAI tends to correlate with the severity of the trauma. (B) Using “brain junction of the cerebral hemispheres and corpus callosum. Through its better cephalus is also noted (arrows). 12D). the dorsolateral images demonstrate mixed heterogenous signal due to a combina. with relative sparing of the underly- ing white matter. DAI in the chronic stage can result in overwhelming cognitive and psychiatric problems. Residual findings may include nonspecific atrophy. Even with MR. or hemosiderin staining. MRI is clearly superior to CT for detecting DAI. particularly the poste- signal intensity) involving the right orbitofrontal lobe. (A) Sagittal T1. The FLAIR (C) and T2-weighted (D) the cerebral hemispheres. Axial CT image displayed with “bone windowing” reveals a nonde- ings include small.17. (A) rhages associated with axonal shearing injury.25 CT is mostly limited to depicting the small focal hemor- Figure 14 Contusion at the margins of depressed skull fractures. The af- fected areas of the brain are often distant from the site of direct impact. is affected. affected. gradient-echo T2*-weighted MR demonstrates more DAI lesions than CT. 12) and as decreased signal on T1-weighted images within the white matter. (arrowhead).

Vascular Injury Vascular injuries are mentioned here because they are causes of both intra. which is dark due to local magnetic susceptibility shear-induced hemorrhage from the rupture of small intrapa. contusions appear as ill-defined areas of variable signal intensity on both T1. (A) Axial CT shows a hyperdense lesion within the right putamen. (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. intracerebral hematomas tend to have less surrounding edema than cortical contusions. wing. (D) Gradient-echo T2*-weighted image shows a surrounding he- tusion described above. and arteriovenous fistula. pseudoaneu- rysm. including the cause of hema- tomas and subarachnoid hemorrhages. . the intracerebral hematoma is due to mosiderin rim. Hemosiderin from an old contusion leads to decreased signal intensity on T2.and T2-weighted images. The cerebellum is involved less than 10% of the time. Axial CT image dem. 13). unless they are accompanied by brainstem injury or signif- icant mass effect. They may be surrounded by larger areas of low attenuation from the associated vasogenic edema. As the con- tusion evolves. Additional traumatic vascular injuries include the arterial dissection. where it temporal lobe (arrow). nonhemorrhagic contusions are difficult to detect initially until the development of associated edema (Fig. 13). Indeed. lated to skull base fractures. includ- ing contusions and DAI. inhomogeneity.and especially T2*-weighted images. Hemorrhagic contusions are more easily identified and ap- pear as foci of high attenuation within superficial gray matter (Fig. delayed hemorrhage is a common cause of clinical deterioration during the first several days after head trauma. On MRI. 14). 16).30 On CT. Contusions are associated with a better prognosis than DAI. depend- ing on the age of the lesions (Fig. the periph- important marker of prior hemorrhage. and at its the nonhemorrhagic contusion. Arterial injuries are usually re- Figure 15 Nonhemorrhagic contusion on CT. interval after the initial injury. The signal loss can persist indefinitely and serves as an due to vasogenic edema. especially at sites of fixation. The inferior temporal lobe is com- monly injured because of its proximity to the petrous ridge. The low attenuation is due to edema from enters the carotid canal at the base of the petrous bone. especially in patients who are uncon- scious at the time of injury. and the frontal lobes above the cribriform plate. 14). especially at higher field Figure 16 Intracerebral hematoma. Contusions with severe mass effect may require surgical decompression to prevent secondary injury.and extra-axial injuries. The surrounding low attenuation is strengths.Imaging of head trauma 185 renchymal blood vessels. 15). They are limited to the surface and often have a “gyral” morphology. The most often injured artery is the onstrates an ill-defined area of low attenuation within the right internal carotid artery. however. hemorrhage in basal ganglia should alert the radiologist that an underlying hypertensive bleed may be the culprit (Fig. In contrast to the common con. and lesser sphenoid wing are commonly affected (Fig. Because the bleeding occurs into areas of relatively normal brain. (B) On the T1-weighted image. planum sphenoidale. Symptoms typically result from the mass effect associated with an expanding hematoma. the characteristic “salt and pepper” pattern of mixed areas of hypodensity and hyperdensity becomes more apparent. Contusions can also occur at the margins of depressed skull fractures (Fig. ery of the hematoma is hyperintense due to the presence of methe- The intracerebral hematoma is the most common cause of moglobin. Intracerebral hematomas are often associated with skull fractures and other primary neuronal lesions. Involvement of the basal ganglia has been de- scribed. Most trau- matic intracerebral hematomas are located in the frontotempo- ral white matter.

they rarely lead to the formation of an EDH. preseptal soft-tissue swelling. CCF can present as an enlarged superior ophthalmic vein. in tissue fluid (cerebral or cytotoxic edema). magnetic resonance angiography onstrates effacement of the cerebral sulci and cisterns and Figure 18 Acquired carotid cavernous fistula (CCF). However. which is best seen on T1-weighted with fat suppression (Fig. Therefore. Patients are often exit from the cavernous sinus beneath the anterior clinoid pro. Again. The dural fistula generally drains via the meningeal veins. T1-weighted MR image performed and ophthalmic examination is not performed. resulting in venous engorgement of the cavernous sinus (Fig. a CCF can be overlooked if a detailed clinical history Figure 17 Carotid dissection. 18) and its draining branches: the ipsilateral superior ophthalmic vein and inferior petrosal sinus.H. The acquired carotid cavernous fistula (CCF) typically results from full-thickness arterial injury. 17). caused by laceration of the middle meningeal artery with result- sents a subacute intramural hematoma. and extraocular muscle enlarge- ment. Skull base fractures. The high signal repre. Le and A. MR findings of vascular injury include (a) the presence of an intramural hematoma. Other findings include proptosis. Conventional angiograms Diffuse cerebral swelling arises from an increase in cerebral remain the gold standard for confirmation and delineation of the blood volume (hyperemia). tinnitus. should alert the radiologist to search for associated cavernous carotid injury. (b) intimal flap with dissection. especially those involving the sphenoid bone. CTA demonstrates asym- metric enhancement of the right cav- ernous sinus secondary to abnormally enlarged venous channels (black ar- rows). Gean and MDCT angiography serve as important screening tools in the evaluation of patients with suspected vascular injury. An associated parenchymal infarction supplied by Acute the injured vessel may also be seen. or an increase vascular dissection and may also show spasm or pseudoaneu. asymptomatic or present with nonspecific complaints such as cess. Another cause of CCF is the rupture of a cavernous carotid aneurysm. ant meningeal artery to meningeal vein fistula formation.D. and (c) Secondary Head Injury absence of a normal vascular flow void secondary to slow flow or occlusion. definitive diagnosis often requires selective carotid angiography with rapid filming to demonstrate the site of communication. usually adventitia of the left internal carotid artery. cavernous si- nus. The findings may be bilateral because venous channels connect the cavernous sinuses. The injury leads to commu- nication between the cavernous portion of the internal carotid artery and the surrounding venous plexus. Patients can present with findings weeks or even months after the initial trauma. On imaging. with fat suppression shows a hyperintense crescent beneath the Another traumatic vascular injury is the dural fistula.186 T. vasogenic edema. therefore. and/or petrosal sinus. Imaging dem- rysm formation. .

the be seen on imaging (Fig. 8). displacement of the brainstem can cause compression of the contralateral cerebral peduncle against the tentorium (“Ker- nohan’s notch”). 4th ventricular outflow by SAH. An acute SDH overlies the tentorium (arrows). trapping the callosomarginal branches of the ACA. the third cranial nerve is compressed. the brain herniates either upward or downward. As mentioned above. Coronal CT cister- nography performed before (A) and after (B) intrathecal contrast demonstrates a meningocele and suspected bony defect involving the left cribriform plate with contrast leakage into the upper left nasal vault (arrowhead). On CT. sequelae ventricle due to mass effect and enlargement of the contralat.Imaging of head trauma 187 (ACA) are displaced to the contralateral side. Infarction or ischemia can complicate TBI as a result of in- fuse decrease in attenuation of the cerebral hemispheres with loss of creased intracranial pressure or mass effect on cerebral vas- gray–white differentiation. result of cerebral dys-autoregulation. and may lead to ACA infarction. midline under the falx cerebri. but it can also be a potential seizure focus. the cingulate gyrus is displaced across the ular outflow foramina (Fig. Compression of the ipsilateral Encephalomalacia is a common. In uncal herniation. The cerebellum and brainstem are usually ary to impaired CSF reabsorption at the level of the arachnoid spared in cerebral edema and may appear hyperintense rela. of prior parenchyma injury. the gray–white differentiation is lost. 8). Downward herniation of the cerebrum manifests as effacement of the suprasellar and perimesence- phalic cisterns. Noncontrast CT scan in an infant ward herniation. Upward herniation typically occurs with large posterior fossa hematomas that displace portions of the cerebellum and vermis through the tentorial incisura. with diffuse cerebral edema following strangulation. Occasionally. Hyperemia is thought to be the tively. Effacement of the ambient and lateral suprasellar cisterns is an important clue of the presence of uncal herniation. but nonspecific. In cerebral edema. leading to peduncular infarction or hemor- rhage. the medial temporal lobe is displaced over the free margin of the tentorium. The mass effect of the hematoma can also cause downward herniation of the cerebellar tonsils through the foramen magnum. which is in con. respec- compression of the ventricles. the most common hydrocephalus via compression of the aqueduct and ventric- form of herniation. Mass effect from cerebral Brain herniation occurs secondary to mass effect produced herniation or a hematoma can also cause noncommunicating by other causes. 19). these patients present with a “blown pupil” and ipsilateral hemiparesis. Sparing of the brainstem and cerebellum culature by herniation or hematoma. uncal herniation and tonsillar herniation can cause ischemia in the territory of the posterior cerebral artery and the posterior inferior cerebellar artery distributions. In severe cases. In addition to ACA causes these structures to appear dense relative to the rest of the infarction secondary to the subfalcine herniation described brain. There is a dif. traumatic hydrocephalus occurs second- ation is preserved. In subfalcine herniation. It may be clinically asymptom- eral ventricle due to obstruction of the foramen of Monro can atic. villi or secondary to obstruction of the cerebral aqueduct and tive to the affected cerebral hemispheres (Fig. The anterior cerebral arteries imaging appearance consists of an area of low attenuation Figure 20 CSF leak. . above. In transtentorial herniation. Chronic trast to cerebral hyperemia where the gray–white differenti. and cerebral edema usually occurs secondary to tissue hypoxia. Inferior displacement of the pineal calcifica- tion is an additional imaging clue for the presence of down- Figure 19 Diffuse cerebral edema.

Stimac GK. However. ischemia. Orrison WW. University of California. cranial CT and MR in closed head injury evaluation. and hernia- tion. further improve the neuroradiological evaluation of traumatic brain injury and enhance our understanding of the pathophysio- logical manifestations of head trauma.H. Toronto. CSF otorrhea may be noted. 4. Radionuclide cisternography is highly 11. et al: Annual summary of from Gean AD: Imaging of head trauma. Gentry LR. mass effect. Encephalomalacia within the orbitofrontal 5. Woodcock RJ Jr. Hackney DB: Skull radiography in the evaluation of acute head trauma: skull base fracture. Williams vital statistics—2001. 1992 3. Do HM. American Society of identify treatable injuries to prevent secondary damage. Le and A. Masters SJ: Evaluation of head trauma: efficacy of skull films. Zee CS. Loop JW: The utility and futility of radiographic skull exami- lobes is characteristic of remote traumatic injury. 1998 meningeal infection. with volume loss. 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