Background

Trauma to the head accounts for more deaths and disability in the United States than any other neurologic disorder among individuals younger than the age of 50 years.168,275 More than 50,000 people die each year from brain trauma, about one third of all injury deaths, with approximately 11,000 new cases of spinal cord injury reported during the same time.^{54,57,138,168} Motor vehicle accidents cause approximately half of traumatic brain injuries (TBIs) in the United States, with falls and firearms responsible for most of the remaining cases.^188,275 TBI is a cause of long-term disability that annually affects an estimated 70,000 to 90,000 people.⁵⁴ Public health efforts to prevent the occurrence and mitigate the consequences of TBI have received increased attention in recent years because of the serious outcome and large number of people affected. Alcohol is often a precipitating factor in these injuries.^57,65 The clinical assessment of posttraumatic patients is discussed here, with emphasis on appropriate diagnostic imaging.

Imaging Findings

Brain and Skull Trauma.

Patients with head trauma constitute a large percentage of cases referred for neuroimaging. Imaging of hyperacute trauma (<24 hours) to the skull and brain should begin with MRI or CT, particularly in a patient with neurologic deficit, because the diagnostic yield of plain film radiography does not warrant its use. In the first 24 hours after trauma, CT is the imaging modality of choice rather than MRI. Emergency equipment is more easily used with CT compared with MRI because of the incompatibility of equipment with a strong magnetic field. However, recent advances have resulted in the commercial introduction of more MRI–compatible patient stabilization equipment.^154,207,275

Attenuation of blood in CT scans depends on its constituent components because serum is less dense than protein and red blood cells. Therefore, serum displays less attenuation than brain tissue; the other products of hemorrhage and hematoma exhibit greater attenuation than the brain. Assessment of fractures and penetrating injuries is easily accomplished with CT in most cases and is fast, reliable, and easily accessible in most communities (Fig. 33-1). CT is compatible with patient stabilization devices and monitoring equipment.⁵² Posttraumatic CT protocol should include 5- to 10-mm thick contiguous axial images from the skull base to the vertex with bone, brain, and subdural windows or level settings. Limitations resulting from beam-hardening artifact should be taken into consideration, particularly in the frontal, parietal, occipital, and cerebellar regions. In patients who require assessment of vascular injury, magnetic resonance angiography (MRA), duplex or transcranial ultrasonography, CT with contrast, or conventional catheter angiography is used.^{42,85,154,249}

Magnetic resonance imaging is superior to CT in the demonstration of blood products in acute, subacute, and chronic posttraumatic patients, as well as nonhemorrhagic lesions such as diffuse axonal injury, cortical contusions, white matter shear injury, and brainstem lesions. Within the past 10 years, recognition of a deoxyhemoglobin rim in hyperacute injuries has made MRI a reasonable alternative to CT.²² In addition, MRI is better at visualizing hemorrhages within the brain parenchyma and subcortical gray matter.^85,241 MRI provides direct multiplanar acquisitions in the axial, sagittal, or coronal planes and permits excellent soft-tissue contrast. In imaging hemorrhage or hematoma in the brain, the MRI signal is dependent not only on the length of time that the blood has been present but also on the strength of the magnet. Familiarity with the MRI system is essential in determining the signal characteristics to be expected in the various time stages after trauma.^23,197,248

Blood products are predominantly oxyhemoglobin with a deoxyhemoglobin rim in the hyperacute stage after trauma (<24 hours). Whereas deoxyhemoglobin is more prevalent in the acute stage (24–72 hours), methemoglobin predominates in the subacute or late phase (72 hours–2 weeks). Methemoglobin remains in the central portion of the lesion, and hemosiderin surrounds the periphery after 2 weeks. Eventually, hemosiderin deposition dominates the blood products in the late chronic stage with low signal characteristics on both T1- and T2-weighted images (Table 33-1).*

TABLE 33-1

BLOOD PRODUCTS

Time after Trauma	Hemoglobin/Hemosiderin	Magnetic Resonance Imaging Signal Characteristics
Hyperacute (<24 hours)	Oxyhemoglobin–deoxyhemoglobin rim	Intermediate T1, high T2, low T2 rim
Acute (24–72 hours)	Deoxyhemoglobin	Intermediate T1, low T2
Subacute early (3–7 days)	Early, intracellular methemoglobin	High T1, low T2
Subacute late (1–2 weeks)	Later, extracellular methemoglobin	High T1, high T2
Chronic early (>2 weeks)	Extracellular methemoglobin with a hemosiderin rim	High central signal in both T1 and T2, low signal rim
Chronic late (>2 months)	Hemosiderin predominates late	Low T1, low T2

Clinical Comments

The most common head injuries result from blunt or nonpenetrating trauma. These injuries frequently induce a temporary or longer loss of consciousness, and the brain may sustain gross damage despite absence of skull fracture or penetrating injury. Skull fractures may indicate the presence of significant trauma; however, the presence or absence of a skull fracture cannot be used to predict the presence or severity of intracranial injury.

Trauma to the head and spine often requires emergency evaluation and treatment performed by an emergency team at the site of injury. It is essential that the injury not be compounded by excessive movement immediately after trauma. The cervical spine must be stabilized before transport. If time allows, a cursory physical and neurologic assessment of the patient is recommended. Evaluating the ABCs (airway, breathing, and circulation) is suggested, and the Glasgow Coma Scale (GCS) is used to assess posttraumatic brain injury. The outcome of the GCS and severity and type of trauma are good predictors of mortality.²⁵⁷ Spinal cord injury may mask injuries below the level of the trauma, particularly in the abdominal region.⁵⁷ Before the arrival of emergency medical transportation, a physician may administer cardiopulmonary resuscitation (CPR), treatment for shock, or other life-sustaining procedures, always avoiding further spinal cord injury. State Good Samaritan laws should be understood before initiating care. Even if a Good Samaritan law is in place, some jurisdictions consider it “gross negligence” to provide care at a level beyond which a person is trained.

Background

By design, the skull is a rigid shell protecting the brain from direct injury. The inner table of the vault has roughened edges, ridges, and bony prominences along the floor of the anterior fossa, sphenoid wings, and petrous pyramids that can contuse the brain surface during the compressive force of a traumatic event.

Cortical contusions or bruises may occur by direct trauma (coup) or by the brain rebounding and striking the skull (contrecoup) from acceleration and deceleration.185,234 A vascular injury must be present for bruising to occur. Parenchymal lesions are found on the surface of the brain in the form of microhemorrhage with edema. Cortical contusions typically are multiple and measure approximately 2 to 4 cm in diameter. About 30% to 50% of these lesions are hemorrhagic.⁵⁴ Cellular disruption is associated with the release of vasoactive substances. The resulting vascular permeability to serum proteins facilitates a progressive increase of interstitial fluid. Over a short period of time, blood and edematous fluid advance within the white matter and into the subdural and subarachnoid spaces, producing a mass pressure effect on adjacent anatomic structures with positive neurologic findings. Approximately 50% to 75% of cortical contusions involve the frontal and temporal lobes, especially the lateral aspects of both lobes and inferior surface of the frontal lobe.⁵⁴ The falx, tentorium, and cranial fossae are especially vulnerable areas.^185,199 Gliding and shearing injuries often are bilateral with tearing of the parasagittal venous structures.^199,224

Imaging Findings

Computed tomography is usually used for initial evaluation of hyperacute cortical contusion because it is fast, reliable, and readily available. Recognition of hyperacute cortical injury is dependent on increased attenuation in the region of the contusion. However, CT has a tendency to underestimate the size of these lesions soon after injury because of isoattenuation with edema and surrounding brain tissue. Repeat scanning often allows complete visualization of original foci and recognition of other sites of involvement. CT also produces beam-hardening artifacts that hamper imaging of more peripheral parenchymal cortical tissue adjacent to the skull.²⁹¹

Magnetic resonance imaging typically demonstrates contusion in the hyperacute stage, particularly if gradient echo and fluid-attenuated inversion recovery (FLAIR) protocols are used.185,225,226 MRI is particularly sensitive to surrounding edema and peripheral cortical foci that may be overlooked on CT. However, many facilities are not equipped with MRI-compatible emergency equipment. In addition, claustrophobia, sedation to reduce motion, and large body habitus must be taken into consideration if MRI is performed instead of CT. MRI is ideal for evaluation of cortical contusions in later stages when emergency equipment is no longer needed.^23,185 The signal intensity of cortical contusion is similar to other blood products produced by trauma (see Table 33-1). Cortical contusion often is associated with other intracranial lesions, such as subdural hematoma (Fig. 33-2). SPECT scans are being used occasionally for diagnosis of cortical contusion. SPECT scanning also has been used in a monitoring role to follow patients with TBI.¹⁴¹

Clinical Comments

Focal neurologic deficits are late-appearing clinical findings. Confusion, focal cerebral dysfunction, seizures, and personality changes are seen more frequently early in cases of cortical contusion.

Background

Epidural hematomas may occur within the spine or skull when blood accumulates between the dura and surrounding bone. If the arteries are torn because of a severe shear trauma separating the dura from the bone, blood may accumulate rapidly in the potential space created by this injury. If there is venous compromise, a slower, more chronic pattern may result. The middle meningeal artery is most commonly involved after skull trauma, although the ethmoidal artery or sinuses (superior sagittal, transverse, or sigmoidal) may be traumatized depending on the exact site of trauma. Although a small percentage of epidural hematomas are bilateral (<10%), the great majority exhibit skull fractures (>90%). The calvarial periosteum (dura layer) is bound down at the suture margins, creating an anatomic boundary to hemorrhage.^152,199

There are numerous causes for spinal epidural bleeding other than high-impact trauma. Spinal epidural hematoma often occurs in conjunction with disk herniation because of involvement of the epidural venous plexus and may be responsible for neural effacement. MRI signal characteristics of disk versus blood must be thoroughly explored because a space-occupying lesion caused by blood resolves quicker than disk debris. This characteristic may clarify the rapid resolution of “sequestered” disk herniations that are, in reality, spinal epidural hematomas.⁹⁴ In addition, thrombolysis, anticoagulation therapy, lumbar puncture, spinal epidural injections, hypertension, and blood dyscrasias may result in spinal epidural hematoma with compromise of neural structures caused by mass effect. These conditions produce symptoms similar to disk herniation, including back pain, numbness or paresthesias, lower extremity weakness, and incontinence (both urinary and fecal).¹⁵²

Imaging Findings

Imaging of both intracranial and spinal epidural hematomas usually begins with CT, although MRI is also diagnostic in stable patients and in facilities equipped with MRI-compatible emergency and stabilization equipment. MRI is particularly useful in evaluating spinal epidural hematoma and its consequences with surrounding neural structures. In the brain, considerable midline shift, large hematoma volume, signs of active bleeding (mixed density clot on CT), and the presence of other associated lesions suggest a poor prognosis after skull trauma. These imaging findings are correlated with clinical signs such as age, coma, papillary abnormalities, and GCS or motor score to help determine an outcome.199,208,233,267 The hematoma typically is lentiform shaped and hyperdense on CT, although less dense areas occur in regions where there is serum or recent bleeding (Fig. 33-3). The area of hematoma usually is homogeneously hyperdense 72 hours after cessation of bleeding. Signal characteristics in MRI scans are typical of other forms of hematoma (see Table 33-1).

Clinical Comments

A transient loss of consciousness may occur with intervals of mental lucidity. Palsy of cranial nerve III may be present and is a sign of cerebral herniation. Somnolence, sleepiness, or unnatural drowsiness 24 to 96 hours after injury constitutes a medical emergency.

Background

Subdural hematomas are caused more frequently by venous rather than arterial damage and are often self-limiting because of the slow bleeding process. However, if the hematoma is large, mass pressure effect may take place, shifting cerebral structures and causing edema in the parenchyma of the brain, resulting in a poor clinical outcome. In addition, the possibility of herniation exists with large subdural hematomas or with hematomas that continue to enlarge after injury. Subdural hematomas arise deep to the dura but external to the arachnoid membrane, and the untreated hematoma may become subacute or chronic. Acute subdural hematoma is more common in older age groups because the veins are less resilient and more easily damaged. Patients taking anticoagulants and patients with alcoholism are also prone to acute subdural hematoma.^{139,224,275,281}

Imaging Findings

Magnetic resonance imaging is more accurate than CT in assessing the size of a subdural hematoma and its effect on surrounding parenchymal tissue (Fig. 33-4).²²⁴ Nonetheless, CT frequently is the imaging modality used because of accessibility, rapid acquisition, and compatibility with emergency equipment. On CT scans, increased density is visualized along the inner table of the skull, most commonly in the parietal region (see Fig. 33-3, B). Small hematomas may be difficult to visualize, and adjustment of the window level or width between usual bone and soft-tissue windows may be necessary. Edema is not as easily perceived with CT as MRI. False-negative CT findings may occur as the result of a high-convexity lesion, beam-hardening artifact, or volume averaging with the high density of calvarium obscuring flat “en plaque” hematomas. Approximately 38% of small subdural hematomas are missed on CT.⁵⁴ Cerebral edema should be suspected and MRI accomplished if midline shift has occurred.^{85,154,173,224,248} A blood-fluid level is seen occasionally.

Background

Extravasation of blood deep to the arachnoid and above the pia mater is defined as subarachnoid hematoma and is most frequently caused by trauma, although this type of hematoma is often caused by vascular compromise, particularly aneurysm and arteriovenous malformation (AVM). Laceration of the microvessels in the superficial portion of the subarachnoid space causes subarachnoid hemorrhage (SAH). Posttraumatic SAH may be benign. However, a communicating hydrocephalus may develop because of obstruction of the arachnoid villi or a noncommunicating hydrocephalus because there is a blood barrier for cerebrospinal fluid (CSF) flow through the third or fourth ventricle. Vasospasm and subsequent cerebral ischemia is another complication of traumatic SAH.^42,57,293 The clinical prognosis is dependent on the volume of blood in the subarachnoid space.

Imaging Findings

Computed tomography is an extremely sensitive test for SAH, particularly during the first 12 hours, although 1 hour is necessary for enough clot retraction to take place for sufficient protein concentration to become hyperdense. Within the past 10 years, it has become possible to demonstrate parenchymal and SAH on MRI with confidence. Studies have shown that FLAIR MRI sequences allow visualization of acute SAH better than CT or other MRI pulse sequences, particularly in the posterior fossa because of beam-hardening artifacts in CT.22,45,92,194,245 Recognition of the deoxyhemoglobin border surrounding areas of oxyhemoglobin in T2-weighted MRI acquisitions also has made it possible to image blood products in hyperacute patients.²² SAH may extend into the basilar cisterns, resulting in hyperdensity on unenhanced CT, and hydrocephalus may occur (see Fig. 33-3, C). Thin-slice CT must be performed to recognize small bleeds; blood may be isodense with brain tissue if the hematocrit levels are below 30%.219,239 An extremely small percentage of patients have false-negative CT or MRI scan findings. Lumbar puncture is indicated in patients who exhibit symptoms of SAH who have negative CT or MRI examination findings.²⁶⁸ It must be remembered that lumbar punctures often are falsely negative in the first 12 hours after injury.^68,219,239

Background

Blunt trauma to the internal carotid, middle cerebral, and anterior cerebral arteries is more commonly the cause of brain ischemia than injuries to other arteries. The external carotid, vertebral, and subclavian arteries are not common sites of injury; posttraumatic brain ischemia and penetrating injuries cause most damage to these arteries. Fractures at the base of the skull and mandible are frequently encountered with traumatic carotid injuries.^43,65,84,293

With relatively minor trauma, disruption of the vascular intima leads to a hemodynamic situation that is ideal for platelet deposition and thrombus formation. The thrombus eventually may occlude the entire vascular lumen, resulting in cerebral ischemia and infarction. In addition, traumatic disturbance of atherosclerotic plaque may give rise to an embolus.

Higher force trauma may lead to more complete tearing of the intima, resulting in dissecting aneurysm as pulsatile high-pressure blood forces its way between the intima and media.82,293 Whereas dissecting extracranial aneurysms are most commonly found in the cervical portion of the internal carotid as it enters the skull, intracranial aneurysms most frequently occur at branches of the middle cerebral artery. Turbulence may cause the aneurysm to enlarge with thrombus formation and possible distal embolization.⁸²

Imaging Findings

Vascular injuries may be examined by MRA, catheter angiography, duplex ultrasonography, transcranial Doppler ultrasonography, and SPECT.141,212,241,247,251 MRA is noninvasive and presents a viable alternative to conventional catheter angiography. Reconstruction of thin-slice two- or three-dimensional time-of-flight axial images using “flow phenomena” allows visualization of the vessel with an angiographic appearance. Phase contrast studies provide information about volume and velocity of blood flow. The key finding in MRA of an intimal tear with dissection is demonstration of the intimal flap that separates the true from the false lumen of the vessel. The lumen may be narrowed with increased signal within the entirety of the lumen or in the periluminal region.* Catheter angiography reveals an irregular narrowing of the vessel or the classic “string sign,” and the intimal flap also may be visualized. Total occlusion from hematoma or thrombus causes interruption of signal on MRA and flow void on angiography.^83,291 Duplex and transcranial ultrasonography rapidly is becoming more common because it is fast, inexpensive, sensitive, and noninvasive.^247,251

Background

A pseudoaneurysm, or “false” aneurysm, is created by rupture of all three arterial walls (intima, media, and adventitia), although egress of blood flow from the vessel is contained initially by surrounding fibrous tissue in the adventitia. These lesions may extravasate blood into the surrounding tissues, which may gradually or abruptly increase in size, resulting in pressure on surrounding structures. Pseudoaneurysm of the vertebral artery is usually observed at the C1 -C2 level. Rupture or distal embolization may take place.²⁴⁹ Catheterization (particularly in patients undergoing anticoagulant therapy or antiplatelet medication), rotational trauma, and infection may be causative factors for pseudoaneurysm.7,105,125 Treatment includes duplex-guided compression (peripheral extracranial vessels), thrombin injection, and surgical repair.³⁷

Imaging Findings

Duplex and transcranial Doppler ultrasonography are becoming increasingly more reliable in early diagnosis of traumatic pseudoaneurysms. Various bone windows are being used for transcranial Doppler. For example, the temporal bone is thin and can be used as a window to reveal segments of the middle cerebral, internal carotid, anterior cerebral, and anterior communicating arteries. The ophthalmic artery is visible through the orbital window and the basilar artery by the suboccipital approach.^130,212,215

The ability of transcranial Doppler ultrasonography and phase contrast MRI to measure volume and velocity of blood flow is particularly useful. However, patients undergoing surgery should have MRA or catheter angiography. MRA is a practical alternative to catheter angiography when patients are allergic to contrast dye, have renal insufficiency, or desire a noninvasive examination.²⁴⁸ Accuracy for carotid stenosis is virtually assured if MRA and ultrasound findings correlate. Nonetheless, if there is no correlation between MRA and ultrasonography, conventional angiography should be done, if possible.⁷³