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).

Scalp lesions

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

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. ¹ 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 scalp. ¹ 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. ¹ 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

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). ² Subacute subdural hematomas are isodense (25 to 45 HU), and chronic subdural hematomas are usually hypodense (0 to 25 HU; figure 7). ² 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 attenuation).

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. ³ 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 (figure 8).

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 symptomatic mass.

Contusions

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. ⁴ In both subacute and chronic cerebral contusions, MR has also been found to have superior sensitivity for detection when compared with CT. ⁴ 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. ⁵

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). ⁶ 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. ⁷

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. ⁸ 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. ⁸ Paterakis et al ⁹ 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 behavioral alterations.

Survivors of DAI brain injury may show secondary Wallerian degeneration of the sheared axons. ¹⁰ 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 T2-weighted images.

Conclusion

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. AR