General Imaging Characteristics of Hemorrhage

The appearance of ICH by CT can vary depending on the age of the hemorrhage and the hemoglobin level. The attenuation of blood is typically based on the protein content of which hemoglobin contributes a major portion. Therefore, the appearance of hyperacute/acute blood is easily detected on CT in patients with normal hemoglobin levels (approximately 15 g/dL) and typically appears as a hyperattenuating mass. This is because, immediately following extravasation, clot formation occurs with a progressive increase in attenuation over 72 hours due to increased hemoglobin concentration and separation of low-density serum. On the other hand, in anemic patients with hemoglobin less than 10 g/dL, acute hemorrhage can appear isoattenuating to the brain and can make detection difficult. Subsequently, following breakdown and hemolysis, the attenuation of the clot decreases until it becomes nearly isoattenuating to cerebrospinal fluid (CSF) by approximately 2 months. In the emergency setting, one should be aware of the “swirl” sign with unretracted clot appearing hypoattenuating and resembling a whirlpool; this may indicate active bleeding and typically occurs in a post-traumatic setting. It is important to recognize this sign, as prompt surgical evacuation may be required. The amount of mass effect on nearby tissues will depend on the size and location of the hemorrhage as well as the amount of secondary vasogenic edema that develops.

Administration of intravenous contrast material is usually not necessary for CT evaluation of ICH. If contrast is given, intra-axial hemorrhage can demonstrate an enhancing ring that is usually due to reactive changes and formation of a vascularized capsule, which typically occurs 5 to 7 days after the event and can last up to 6 months. Subacute and chronic extra-axial hematomas can also demonstrate peripheral enhancement usually due to reactive changes and granulation tissue formation. Unexpected areas of enhancement should raise concern, as active bleeding can appear as contrast pooling.

MR imaging has greatly revolutionized the evaluation of intracranial hemorrhage. The evolution of hemorrhage from the hyperacute to the chronic stage will have corresponding signal changes on T1-weighted images (T1WI), T2-weighted images (T2WI), fluid attenuated inversion recovery (FLAIR) images, and gradient-echo sequences. These properties can assist in detection and understanding of the time course of the injury. While beyond the scope of this chapter, description of the physics of the signal characteristics of blood products on MR is generally based on the paramagnetic effects of iron and the diamagnetic effects of protein in the hemoglobin molecule. The usual signal characteristics of hemorrhage and the general time course over which they evolve is summarized in Table 1-1.

Epidural Hemorrhage

Epidural hematoma is the term generally applied to hemorrhage that forms between the inner table of the calvarium and the outer layer of the dura due to its masslike behavior. More than 90% are associated with fractures in the temporoparietal, frontal, and parieto-occipital regions. CT is usually the most efficient method for evaluation of this type of hemorrhage. Epidural hematoma typically has a hyperdense, biconvex, or lens-shaped appearance. It may cross the midline but does not cross sutures (since the dura has its attachment at the sutures). This might not hold true if a fracture disrupts the suture. There is usually an arterial source, commonly due to tear of the middle meningeal artery and much less commonly (less than 10%) due to tear of the middle meningeal vein, diploic vein, or venous sinus (Figs. 1-1 and 1-2). The classic clinical presentation describes a patient with a “lucid” interval, although the incidence of this finding varies from 5% to 50% in the literature. Prompt identification of an epidural hematoma is critical, as evacuation or early reevaluation may be required. Management is based on clinical status, and therefore alert and oriented patients with small hematomas may be safely observed. The timing of follow-up CT depends on patient condition, but, generally, the first CT scan may be obtained in 6 to 8 hours and, if the patient is stable, follow-up may be extended to 24 hours or more afterward.

Figure 1-1 Epidural hematoma. A, CT shows usual biconvex, hyperdense acute epidural hematoma causing effacement of sulci and lateral ventricles and shift of midline structures. B, CT volume-rendered image shows nondisplaced fracture at vertex involving coronal suture. C, Coronal multiplanar reconstruction shows biconvex epidural hematoma crossing midline over the superior sagittal sinus.

Subdural Collections

Subdural hematoma (SDH) is the term generally applied to hemorrhage that collects in the potential space between the inner layer of the dura and the arachnoid membrane. It is typically the result of trauma (motor vehicle collision, assaults, and falls, the latter especially in the elderly population), causing tear of the bridging vein(s), and has a hyperattenuating, crescentic appearance overlying the cerebral hemisphere (Fig. 1-3). These hemorrhages can cross sutures and may track along the falx and tentorium but do not cross the midline. Inward displacement of the cortical vessels may be noted on a contrast-enhanced scan. There is a high association with subarachnoid hemorrhage. Acute SDHs thicker than 2 cm, seen with other parenchymal injuries, are associated with greater than 50% mortality. As the SDH evolves to the subacute (5 days to 3 weeks) and then chronic (more than 3 weeks) stage, it decreases in attenuation, becoming isodense to the brain and finally to CSF. Subacute SDH can have a layered appearance due to separation of formed elements from serum. Subacute hemorrhages may be relatively inconspicuous when isodense, and therefore it is especially important to recognize signs of mass effect, such as sulcal effacement, asymmetry of lateral ventricles, and shift of midline structures, as well as sulci that do not extend to the skull (Fig. 1-4). Bilateral isoattenuating SDHs can be especially challenging since findings are symmetric. Beware of this, particularly in the elderly patient who does not have generous sulci and ventricles. At this stage, the SDH should be conspicuous on MR imaging, especially on FLAIR sequences. A subacute SDH may also be very conspicuous on T1-weighted images due to the hyperintensity of methemoglobin.

Figure 1-3 Subdural hematoma. Mixed density layered pattern due to recurrent hemorrhages. Image (arrow) shows one method of measuring midline shift.

Figure 1-4 Isodense subdural hematoma. A, Sulcal effacement and midline shift to the right are clues to the presence of a left-sided subdural hematoma. B, Re-expansion of left Sylvian fissure and reduction in midline shift following evacuation.

Chronic subdural hematomas are collections that have been present for more than 3 weeks. Even a chronic hematoma may present in the emergency setting; for example, in a patient prone to repeated falls, brought in because of a change in mental status. On both CT and MR, these collections typically have a crescentic shape and may demonstrate enhancing septations and membranes surrounding the collection after contrast administration. Calcification of chronic SDH can occur and be quite extensive (Fig. 1-5). Areas of hyperdensity within a larger hypodense SDH may indicate an acute component due to recurrent bleeding, an “acute on chronic subdural hemorrhage.” Mixed density collections may also be acute, due to active bleeding or CSF accumulation due to tear of the arachnoid membrane. Chronic SDH is usually isointense to CSF on both T1WI and T2WI, but the appearance can be variable depending on any recurrent bleeding within the collection. The FLAIR sequence is typically very sensitive for detection of chronic SDH due to hyperintensity based on protein content. Hemosiderin within the hematoma will cause a signal void due to susceptibility effect, and “blooming” (appears to be larger than its true size) will be noted on gradient-echo sequence.

Figure 1-5 Calcified subdural hematomas. A, Colpocephaly configuration of lateral ventricles. B, Bone window/level settings more clearly show the calcified subdurals in this adult patient shunted as a child for congenital hydrocephalus.

Subdural hygroma is another type of collection and is commonly thought to be synonymous with chronic subdural hemorrhage. The actual definition of a hygroma is an accumulation of fluid due to a tear in the arachnoid membrane, usually by some type of trauma or from rapid ventricular decompression with associated accumulation of CSF within the subdural space. Many still use this term interchangeably with chronic subdural hematoma. CT demonstrates a fluid collection isodense to CSF in the subdural space. MR can be useful in differentiating CSF from chronic hematoma based on the imaging characteristics of the fluid on all sequences. Occasionally hygromas are difficult to differentiate from the prominence of the extra-axial CSF space associated with cerebral atrophy. Position of the cortical veins can be a helpful clue. In atrophy, the cortical veins are visible traversing the subarachnoid space, whereas with a hygroma they are displaced inward along with the arachnoid membrane by the fluid in the subdural space.

Subarachnoid Hemorrhage

Subarachnoid hemorrhage (SAH) fills the space between the pia and the arachnoid membrane, outlining the sulci and basilar cisterns. This can be due to a variety of causes, including trauma, ruptured aneurysm, hypertension, arteriovenous malformation, occult spinal vascular malformation, and hemorrhagic transformation of ischemic infarction. SAH is often associated with overlying traumatic subdural hematoma. Subarachnoid hemorrhages generally do not cause mass effect or edema. On CT, hyperdensity is seen within the sulci and/or basilar cisterns (Figs. 1-6 and 1-7).

Figure 1-6 Subarachnoid hemorrhage from ruptured aneurysm. A, Noncontrast CT shows ill-defined hyperdense subarachnoid hemorrhage in left Sylvian cistern (black arrow) and rim calcification in the wall of the aneurysm (white arrow). B, Volume-rendered image from CT angiography shows large aneurysm projecting above lesser sphenoid wing. C, Reconstruction from 3D rotational digital subtraction angiogram shows carotid-ophthalmic aneurysm to best advantage.

Figure 1-7 Subarachnoid hemorrhage and complications. A, Three CT images show diffuse hyperdense subarachnoid hemorrhage filling basal cisterns and cerebral sulci bilaterally. Diffuse loss of gray–white differentiation and effacement of sulci and cisterns probably preclude the need for further workup. B, Volume-rendered image from CT angiography demonstrates lack of intracranial flow consistent with expected elevation of intracranial pressure.

Although MR imaging may be as sensitive for the detection of acute intraparenchymal and subarachnoid hemorrhage, CT generally remains the modality of choice (and imaging gold standard). Sensitivity of CT for detection of SAH compared with CSF analysis can vary from up to 98% to 100% within 12 hours to approximately 85% to 90% after 24 hours of symptom onset. Other factors affecting sensitivity are hemoglobin concentration, size, and location of the hemorrhage. CT is widely available, rapid, and relatively inexpensive. In several small studies, MR has demonstrated sensitivity equivalent to CT for detection of acute parenchymal hemorrhage and SAH. In some cases of “CT-negative” (subacute) hemorrhage, MR has shown greater sensitivity. However, results may be confounded by artifacts from CSF pulsations, elevated protein (meningitis), or oxygen concentration (high fraction of inspired oxygen) in CSF on FLAIR images and presence of blood products from previous microhemorrhages on gradient-echo images.

Intraventricular Hemorrhage

Intraventricular hemorrhage (IVH) is typically caused by trauma in the adult population. It can result from extension of parenchymal hemorrhage into the ventricles or redistribution of subarachnoid hemorrhage. Primary intraventricular hemorrhage is uncommon and usually caused by a ruptured aneurysm, intraventricular tumor, vascular malformation, or coagulopathy (Fig. 1-8). Large IVHs are quite conspicuous on CT or MR. They may occupy a majority of the ventricle(s) and may result in hydrocephalus and increased intracranial pressure. Small amounts of IVH may be difficult to detect; one must check carefully for layering hemorrhage within the atria and occipital horns of the lateral ventricles. Normal choroid plexus calcifications in the atria of lateral ventricles, the fourth ventricle, and extending through the foramina of Luschka should not be mistaken for acute IVH.

Figure 1-8 Intraventricular hemorrhage. A, FLAIR MR image shows hyperintense hemorrhage isolated to frontal horn of right lateral ventricle. B, Image from right internal carotid artery digital subtraction angiogram in late arterial phase shows nidus (arrow) and early draining vein (arrowhead)diagnostic of an arteriovenous malformation.

Another less common type of extracerebral intracranial hemorrhage that may present acutely is pituitary hemorrhage. It is usually associated with pituitary apoplexy due to pituitary necrosis that may become hemorrhagic. Presenting symptoms may include headache, visual loss, ophthalmoplegia, nausea, and vomiting. Other causes of pituitary hemorrhage include tumors (macroadenoma, germinoma) and, less commonly, trauma.

Contusion

Parenchymal contusions result from blunt trauma and can occur in the cortex or white matter. Their locations are typically at the site of greatest impact of brain on bone, including the anterior/inferior frontal lobes and the lobes. They can be considered coup (occurring at the site of impact) or contrecoup (opposite the site of impact) types. On CT, a contusion typically appears as an area of hyperdensity with a surrounding rim of hypodense edema. It can initially appear as a focal area of subtle hypodensity and may blossom on follow-up exam at 12 to 24 hours with development of an obvious central area of hyperdensity and a larger surrounding zone of hypodense edema (Fig. 1-9). On MR, signal characteristics reflect the hemorrhagic and edematous components. Over time, the density and signal characteristics of the hemorrhage will evolve in a fashion similar to a spontaneous hemorrhage. Parenchymal hemorrhage due to penetrating trauma, such as from gunshot wound or impalement, will follow the same general pattern of evolution.

Figure 1-9 Blossoming contusion. A, CT shows thin left frontoparietal subdural hematoma tracking along anterior falx and mild sulcal effacement. B, Follow-up CT after 24 hours shows hyperdense parenchymal hemorrhage and surrounding edema in left frontal lobe and stable subdural hematoma. Notice mass effect on left lateral ventricle.

Diffuse Axonal Injury

Diffuse axonal injury (DAI) is another type of traumatic brain injury that may present with parenchymal hemorrhages and is distinct from parenchymal contusion. DAI is an injury to the axons caused by acceleration/deceleration injury with a rotational component (usually from motor vehicle collision or other blunt trauma to the head). There may be complete transection of axons with injury to the associated capillaries, or partial disruption of the axons. The lesions of DAI typically occur at the inter-faces of gray and white matter in the cerebral hemispheres, the body and splenium of the corpus callosum, midbrain, and upper pons. Lesions may also be seen in the basal ganglia. Patients sustaining DAI typically lose consciousness at the moment of impact. DAI may be suspected when the clinical exam is worse than expected based on the findings on initial CT scan. Usually, the greater the number of lesions, the worse the prognosis. Individuals who recover usually demonstrate lingering effects such as headaches and cognitive deficits. Initial CT scans in more than half of patients with DAI may be negative. CT findings include hypodense foci due to edema in areas of incomplete axonal disruption and hyperdense foci due to petechial hemorrhage where there is complete transection of the axons and associated capillaries (Fig. 1-10). MR is more sensitive than CT for detection of DAI. Approximately 30% of those negative by CT will demonstrate abnormal findings on MR. These findings include FLAIR and T2 hyperintensities (edema) and gradient-echo hypointensities (hemorrhages) (Fig. 1-11). Lesions may appear hyperintense on diffusion-weighted images. It is estimated that more than 80% of the lesions of DAI are nonhemorrhagic. Generally, if imaging is repeated within 3 to 5 days, more lesions will become apparent as the process evolves. A staging system for DAI based on locations of lesions on histopathology may be applied to MR findings. Stage 1 is based on subcortical lesions in the frontal and temporal lobes. Stage 2 will also show lesions in the corpus callosum and lobar white matter, and stage 3 will have lesions in the midbrain and pons. Diffusion tensor imaging, particularly helpful in evaluation of white matter tracts, has been shown to be more sensitive than conventional MR for detection of diffuse axonal injury and correlates more closely with clinical outcomes.

Figure 1-10 Shear hemorrhages of diffuse axonal injury. Noncontrast CT shows three small hemorrhages in the left superior frontal gyrus following blunt head trauma.

Figure 1-11 Diffuse axona linjury.A, FLAIR hyperintensities in posterior limb of internal capsule (arrow) and subcortical white matter (arrowhead). B, Gradient-echo hypointensities in subcortical white matter indicative of hemorrhages (arrows) were not evident on other sequences. Note IVH in occipital horns of lateral ventricles.

Subfalcine Herniation

Subfalcine herniation is due to displacement and impingement of the cingulate gyrus underneath the falx. It is usually caused by mass effect on the frontal lobe and is associated with ipsilateral lateral ventricle compression and obstruction of the foramen of Monro with dilatation of the contralateral ventricle (“trapped ventricle”). The degree of midline shift (not synonymous with subfalcine herniation) can be estimated by drawing a line between the anterior and posterior attachments of the falx and measuring the shift of the septum pellucidum relative to this line (see Fig. 1-3). Anterior cerebral artery territory infarct(s) may result from this type of herniation.

Transtentorial Herniation

Transtentorial herniations include two major types, which are the descending transtentorial herniation (DTH) and the ascending transtentorial herniation (ATH). An early DTH is known as uncal herniation, in which the uncus is displaced medially and occupies the ipsilateral suprasellar cistern. A later-stage DTH is caused by continued mass effect with displacement of the medial temporal lobe through the incisura, which completely occupies the suprasellar cistern (along with the uncus) and causes enlargement of the ipsilateral and effacement of the contralateral ambient cisterns. This phenomenon occurs because, as there is marked shifting of brain in the supratentorial compartment, there is also shift of the brainstem in the same direction. There is also compression of the ipsilateral cerebral peduncle. Occasionally, when there is marked mass effect, there can be compression of the contralateral cerebral peduncle against the tentorium, or “Kernohan’s notch,” which leads to ipsilateral motor weakness (this phenomenon may be a false localizing sign). Other imaging findings include a “trapped” temporal horn of the lateral ventricle contralateral to the side of the mass and Duret hemorrhages—hemorrhages of the midbrain and pons caused by stretching and tearing of the arterial perforators. In cases of bilateral mass effect, there can be displacement of both temporal lobes and midbrain through the incisura leading to effacement of the basilar cisterns bilaterally. Complications of this type of herniation include compression of the posterior cerebral artery and penetrating basal arteries with associated infarcts in these vascular distributions (see Fig. 1-2). In addition, there can be compression of the oculomotor nerve (CN III) with an associated palsy. ATH is less common and is caused by superior displacement of the cerebellum and brainstem through the incisura. It is usually due to mass effect in the posterior fossa (as from hemorrhage, tumor, or infarct), and on imaging there is compression on the posterolateral midbrain bilaterally with associated effacement of the ambient and quadrigeminal plate cisterns. There is usually hydrocephalus due to obstruction at the level of the cerebral aqueduct of Sylvius.

Figure 1-2 Epidural hematoma and complications. A, “Swirl” sign in this large epidural hematoma suggests continued bleeding. B, Pontine (Duret) hemorrhage (arrow) and effacement of basal cisterns as a result of downward herniation. C, Uncal herniation (arrow shows margin of left temporal lobe) and resultant left posterior cerebral artery territory infarct. The brainstem is distorted left and also abnormally hypodense. D,Infarcts in bilateral anterior, left middle, and left posterior cerebral artery territories as a result of herniations.

Tonsillar Herniation

Tonsillar herniation is caused by downward displacement of the cerebellar tonsils through the foramen magnum into the spinal canal (generally by more than 5 mm). On imaging, there is a peglike configuration to the tonsils with obliteration of the CSF space in the foramen magnum (Fig. 1-12). Complications include obstructive hydrocephalus from compression of the fourth ventricle. Mild tonsillar ectopia, Chiari I malformations, and sagging tonsils due to intracranial hypotension should not be mistaken for acute tonsillar herniation, but should be considered seriously when downward mass effect is expected based on brain edema, mass, or hemorrhage.

Figure 1-12 Tonsillar herniation. A, Sagittal T1 image shows pegged appearance of the cerebellar tonsils extending through the foramen magnum, simulating a Chiari I malformation. (This was a dramatic change from a previous exam.) B, Postgadolinium T1 image shows cerebellar leptomeningeal enhancement due to cryptococcal meningoencephalitis in this patient with AIDS.

Extracranial Herniation

An extracranial herniation is the displacement of brain parenchyma through a cranial and dural defect that is usually caused by trauma or craniectomy (usually performed to prevent downward herniation from acute cerebral edema). Complications may include infarct of the herniated brain tissue.

Transalar Herniation

Transalar herniation is uncommon and, by itself, does not cause symptoms. It is usually associated with subfalcine and transtentorial herniations. This type of herniation is caused by displacement of the temporal lobe anteriorly or frontal lobe posteriorly across the sphenoid wing. Look for anterior or posterior displacement of the middle cerebral artery to identify this type of herniation.

In the setting of severe head trauma, many of these different types of injuries may coexist. The mechanism of injury should correspond with the degree of injury. In cases when the reported mechanism is mild, nonaccidental trauma (“Trauma X,” “shaken-baby syndrome”) should be considered. Infants, children, those with mental or physical disabilities, and the elderly are particularly at risk. Skull fractures, SAH, SDH, contusions, shear injuries, infarcts, vertebral compression fractures, and retinal hemorrhages constitute the usual neuroradiologic spectrum of abnormalities. Injuries of different ages, metaphyseal and rib fractures, and visceral injuries are other common findings in child abuse.

Hemorrhagic Stroke: Spontaneous Parenchymal Hemorrhage

Approximately 10% to 15% of strokes present with an acute parenchymal hemorrhage. The most common cause is hypertension (Fig. 1-13). Coagulopathies, hematologic disorders including hypercoagulable states, amyloid angiopathy, drugs, vascular malformations and aneurysms, vasculitides, and tumors round out the usual list of etiologies. Hemorrhages resulting from illicit drug use and vascular malformations are commonly found in young adults (Fig. 1-14). Sickle cell disease and venous infarcts may also present with parenchymal hemorrhage. A ruptured intracranial aneurysm may occasionally cause a parenchymal hemorrhage in association with subarachnoid hemorrhage. Hypertensive hemorrhages most commonly occur in the basal ganglia and thalami but may also primarily arise within the cerebral hemispheres, brainstem, or cerebellum. Cerebral amyloid angiopathy (CAA) is another common cause of intracranial hemorrhages in patients over 65 years of age. CAA can be found in patients with mild cognitive impairment, dementia of Alzheimer type, and Down syndrome with extracellular deposition of beta amyloid occurring in the cortex and subcortical white matter. CAA can be hereditary (autosomal dominant, Dutch type), sporadic (presence of Apoε4 allele), or acquired (as from hemodialysis). The lobar hemorrhages of CAA typically occur in the frontal and parietal regions. MR is sensitive for the detection of hemosiderin deposition resulting from multiple microhemorrhages over the course of time appearing as small hypointense foci on gradient-echo sequences.

Figure 1-13 Spontaneous parenchymal hemorrhage secondary to uncontrolled hypertension. Noncontrast CT in a patient with uncontrolled hypertension shows a large hyperdense parenchymal hemorrhage arising in the basal ganglia with intraventricular extension. Note the ventriculostomy catheter in the right lateral ventricle.

Figure 1-14 Parenchymal hemorrhage due to illicit drug use—Ecstasy (3,4 methylenedioxymethamphetamine). A, CT shows hyperdense acute hemorrhage with minimal surrounding hypodense edema. B, T1-weighted image shows iso- to mild hyperintensity with hypointense edema. FLAIR (C) and fat-suppressed T2 gradient and spin echo (D) show hypointensity with surrounding hyperintense edema. E, Gradient echo shows peripheral rim of signal loss and blooming. In summary, signal changes on T1-weighted image and T2-weighted image are consistent with deoxyhemoglobin although the gradient echo suggests only a rim of deoxyhemoglobin.

Imaging of Acute Ischemic Stroke

Computed Tomography

The role of imaging in acute stroke diagnosis and management continues to evolve. Since the mid-1970s, unenhanced CT has been the first-line modality to determine the etiology of acute neurologic deficits. CT can offer the chance to detect an ischemic infarct, generally in the middle cerebral artery territory, within 3 hours in up to one third of cases based on findings of subtle parenchymal hypodensity, loss of gray–white matter differentiation (including loss of the insular ribbon or margins of basal ganglia; Fig. 1-15), and effacement of sulci. A hyperdense vessel sign may indicate the presence of an acute thrombus and support the diagnosis. The sensitivity for detection of acute stroke has been shown to increase with the use of an “acute stroke” window and level settings (see Fig. 1-15). A very narrow window width of 8 Hounsfield units (HU) and a level of 32 HU (compared with 80 and 20 HU, respectively) may increase the sensitivity of CT to approximately 70% without a loss of specificity. CT is currently used to screen patients who may be considered for treatment with intravenous recombinant tissue plasminogen activator (rt-PA) within 3 hours of onset based on guidelines from the National Institute of Neurologic Disorders and Stroke (NINDS) rt-PA trial. Beyond 3 hours, the risk of intracranial hemorrhage due to intravenous thrombolysis was shown to outweigh potential benefits. An association between larger stroke volumes (greater than one third of the middle cerebral artery territory) and reperfusion hemorrhage was initially reported. This criterion for the use of 100 mL estimated infarct volume has been commonly applied in stroke trials. The Alberta Stroke Program early CT score (ASPECTS), a 10-point topographic scoring system, was later developed to try to more easily quantify initial stroke volumes. This score has been shown to correlate with the initial National Institutes of Health stroke score (NIHSS).

Figure 1-15 Hyperacute infarct. A, Noncontrast CT with window/level of 80/40 shows subtle decrease in density of the right insular cortex. B, Insular “ribbon” sign is more conspicuous with stroke window/level of 40/40 (arrows). C, Infarct is much more conspicuous on diffusion-weighted image. D,Time-of-flight MR angiography shows attenuation of right middle cerebral artery distal branches.

Magnetic Resonance: Diffusion-weighted Imaging

MR, with diffusion-weighted imaging (DWI), which became widely available in routine clinical practice in the late 1990s, offers significantly greater sensitivity and specificity for the detection of acute stroke (greater than 90% compared with approximately 60% for CT). To put it very simply, energy depletion will trigger a cascade that will alter the internal cellular milieu and result in development of cytotoxic edema. The restriction of water molecule diffusion appears as hyperintensity on diffusion-weighted images. The diffusion “experiment” can be performed with a variety of rapid imaging techniques, such as echo planar imaging, and can acquire images of the entire brain in half a minute. This minimizes the effects of patient motion, especially important when the clinical presentation includes alteration of mental status. The apparent diffusion coefficient value is a quantitative measure that may be calculated from the diffusion-weighted images. Since diffusion-weighted images rely on both diffusion and T2 effects, it is wise to confirm that the apparent diffusion coefficient values are indeed reduced before diagnosing an acute infarct. This will reduce the number of false positives due to “T2 shine-through” effect from old infarcts (gliosis) or other T2 hyperintense processes such as vasogenic edema.

Acute ischemic infarcts may appear as hyperintense regions on DWI (see Fig. 1-15), and this can occur as quickly as 30 minutes after onset. Up to 100% sensitivity has been demonstrated in clinical studies. However, in routine practice, small lesions in the brainstem may not be perceived initially, only to be detected on a follow-up exam prompted by persistent symptoms. It is also possible that a region of ischemia (prior to completed infarction) may go undetected on an initial imaging study, resulting in a false negative result. False positives on DWI can be due to processes that mimic stroke and also cause diffusion restriction, such as certain neoplasms, multifocal metastatic disease, and abscesses. Presence or absence of associated findings on conventional MR sequences—such as loss of gray–white matter differentiation on T1WI, and hyperintense edema on FLAIR and T2WI—may help with diagnosis, although these signs may be inconspicuous for 6 to 12 hours after stroke onset. Blooming on gradient-echo sequences due to intravascular thrombus and loss of expected vascular flow voids are other useful clues.

Lacunar infarcts are generally less than 1 cm in diameter and presumed to be due to occlusion of small perforating branches due to embolic, atheromatous, or thrombotic lesions. They occur most commonly in the basal ganglia, internal and external capsules, immediate periventricular white matter (corona radiata), and, less frequently, the centrum semiovale. Occlusion of basilar artery perforators will result in lacunes in the brainstem. Diffusion imaging offers the ability to identify very small, acute infarcts even in the background of chronic white matter disease and remote lacunes (Fig. 1-16). While MR is still considered a relatively expensive technique, it has the potential to reduce the number of unnecessary hospital admissions for recurrent small vessel infarcts in many patients. It may also help to select the most appropriate pathway for patients with central embolic sources of infarcts based on detection of infarcts in different vascular territories.

Figure 1-16 Acute lacunar infarct. A, CT shows multifocal hypodensities. B, FLAIR image shows corresponding hyperintensities due to chronic small vessel disease. C, Diffusion-weighted image shows the acute infarct in the left lentiform nucleus/posterior limb of internal capsule in a patient with acute onset of right-sided weakness. Apparent diffusion coefficient map (not shown) confirmed restricted diffusion. Other periventricular white matter mild hyperintensities are the result of “T2 shine-through.”

MR is also valuable in the setting of neonatal hypoxic ischemic encephalopathy. Cranial ultrasonography and CT may be used to evaluate germinal matrix hemorrhages, periventricular leukomalacia, and hydrocephalus. Diffusion-weighted MR is most sensitive for evaluating the different patterns of injury. In preterm infants subjected to mild hypotension, the periventricular regions are most often affected. With more severe hypotension, the basal ganglia, brainstem, and cerebellum may be involved. In full-term infants with mild hypotension, infarcts in the border zones between anterior and middle cerebral arteries or between middle and posterior cerebral arteries may result. Severe hypotension may result in infarcts of basal ganglia, hippocampi, corticospinal tracts, and sensorimotor cortex.

Diffusion-weighted hyperintensity generally begins to decline after a few days, with the process of apparent diffusion coefficient (ADC) pseudonormalization usually taking place over the next few weeks. Final ADC values will vary based on degree of gliosis or cavitation of the infarct. It should be noted that infarction development depends on the magnitude and duration of ischemia and the metabolic demands of the affected tissue. While diffusion restriction due to ischemia almost always results in infarction, rare cases of spontaneous reversible diffusion abnormalities have been reported, as well as those occurring in the setting of thrombolytic therapy.

Computed Tomography: Perfusion Imaging

The advent and wide availability of helical and, more recently, of multidetector CT (MDCT) scanners has led to the use of CT angiography (CTA) and CT perfusion (CTP) imaging in the workup of suspected acute ischemic stroke. The ability to acquire a large 3D volume of data rapidly during bolus contrast administration combined with submillimeter spatial resolution results in CT angiographic images that in many instances approach the diagnostic quality of more invasive digital subtraction angiograms. Large detector arrays and cine or shuttle modes of scanner operation allow for generous coverage of the brain during perfusion studies. Detector arrays from 4 to 64 rows wide are available now and newer models with 256 and more are in development. Analogous to PWI, CT perfusion is based on measurement of tissue density as a function of time during a first pass of intravenous contrast and commonly uses deconvolution analysis. In contrast to PWI, as a result of the proportionate increase in tissue attenuation due to iodine concentration, quantitative (rather than relative) estimation of CBV (and therefore CBF) can be obtained by CTP.

CTP applied in the setting of acute stroke has been validated with clinical outcomes and follow-up imaging and also by comparison with diffusion-weighted imaging. Wintermark and colleagues have proposed that regions with CBV less than 2.5 mL/100 g be considered the “core infarct” and regions with CBF reduction of more than 34% be defined as the penumbra. These values are based on correspondence with initial DWI abnormality and final infarct size. Schaefer and colleagues have proposed other absolute values and the use of normalized CBV and CBF ratios to help distinguish ischemic tissue likely to infarct from that likely to survive following intra-arterial recanalization therapy. Perfusion maps can be visually compared to determine if a penumbra is present but may underestimate or overestimate the extent of tissue at risk (Fig. 1-17). Software packages are available that can automatically segment the processed perfusion maps into core infarct, penumbra, and normal regions based on thresholding techniques.

Figure 1-17 Perfusion CT—large mismatch. A, Noncontrast CT shows decreased density of left caudate head and putamen. B, CBF and mean transit time abnormalities are much larger than core infarct (CBV abnormality). (Color functional maps are more easily interpreted on a color monitor.) C, CT follow-up 1 week after conservative management shows that the final infarct volume closely matches the initial CBV abnormality. D, Initial CT angiogram showed abrupt occlusion of left middle cerebral artery stem (arrow) but with filling of distal branches due to robust leptomeningeal collateral circulation.

The ongoing MR RESCUE (MR and recanalization of stroke clots using embolectomy) trial is employing a similar, automated analysis of PWI data to determine eligibility for inclusion. Patients presenting with intracranial arterial occlusions within 8 hours of symptom onset and having a suitable penumbra are randomized to embolectomy with the Merci Retriever device (Fig. 1-18).

Figure 1-18 Mechanical thrombectomy. A, Acute right middle cerebral artery occlusion. B, Merci retriever deployed distal to thrombus. C, Recanalization of right middle cerebral artery following clot retrieval.

Data from the recently completed DIAS 2 trial, a phase III study that used either DWI/PWI/MRA or CT/CTP/CTA as eligibility criteria, are still being analyzed. However, initial reports suggest that the results were not as favorable as those of previous trials. It is hoped that analysis of outcomes with respect to imaging features may help to identify a subset of patients who might achieve therapeutic benefits with a reduced risk of symptomatic hemorrhage.

Hemorrhagic Transformation

Hemorrhagic transformation of an ischemic infarct, thought to result from reperfusion injury, can be a dreaded complication of therapy or may happen spontaneously within hours or after a period of several weeks (Fig. 1-19). If a large hematoma is present at the time of initial imaging, it may not be possible to distinguish a primary parenchymal hemorrhage from hemorrhagic transformation. The blood products generally cause substantial artifacts on DWI. However, if the hemorrhage is confined within a larger zone of restricted diffusion, the etiology may be clear. Petechial hemorrhage occurs very commonly within an ischemic infarct, is best detected by gradient-echo imaging, and does not usually lead to increased morbidity.

Figure 1-19 Hemorrhagic transformation of ischemic infarct. Noncontrast CT 24 hours postictus shows hyperdense hemorrhage within a large left middle cerebral artery territory infarct.

Cortical Laminar Necrosis

A pattern of gyriform T1 hyperintensity developing a week or two after an ischemic infarct may be attributed to cortical laminar necrosis (Fig. 1-20). It seems that gray matter is more vulnerable to ischemic necrosis than white matter (especially the third layer of the six cortical layers), and, although the signal changes may lead one to diagnose hemorrhage or calcification, in one histologic study neither was detected. The exact cause of the T1 shortening is uncertain, but it may be due to high concentrations of proteins and macromolecules.

Figure 1-20 Cortical laminar necrosis. T1-weighted image shows gyriform hyperintensity in a perisylvian distribution 1 week after middle cerebral artery infarct.

Cerebral Venous Infarction and Sinus Thrombosis

An uncommon (annual incidence estimates of less than 1 case per 100,000 population) but important cause of hemorrhage is cerebral venous thrombosis (Fig. 1-21). This may affect cortical veins and other portions of the superficial and deep venous drainage systems. Hypercoagulable states due to pregnancy and the postpartum period, or from oral contraceptive use, dehydration, regional infections, and trauma, are relatively common causes. Common presenting symptoms include headache, seizure, and focal neurologic deficits. Fluctuating symptoms and intracranial hypertension are common as well. Bilateral parenchymal hemorrhages or infarcts that do not obey usual arterial territorial borders can be clues to diagnosis. A working knowledge of the normal anatomy of the major venous structures and the common variants is necessary to avoid diagnostic pitfalls, especially false positives. On unenhanced CT, normal venous structures may appear denser than usual due to dehydration or elevated hematocrit, whereas thrombosis should appear hyperdense relative to arteries. A filling defect or occlusion may be detected on contrast-enhanced CT. CT venography can be performed with thin-section, volumetric technique allowing for creation of 2D and 3D reconstructions. Normal and thrombosed venous sinuses take on many different appearances on MR depending on scan parameters, flow velocity, and turbulence. Unexpected hyperintensity, loss of usual flow voids, and blooming on gradient-echo sequence are clues that flow-sensitive MR venography (MRV) should be performed. Time-of-flight MRV may be less sensitive than phase contrast technique due to shine-through of methemoglobin in a thrombosed sinus simulating flow in the vessel. Contrast-enhanced MRV may be more sensitive, although enhancement of chronic thrombus can be misleading. Associated findings of edema, hemorrhage, or ischemic infarct may help toward arriving at the correct diagnosis, but brain swelling without signal changes has been reported in up to approximately 40% of patients. Cavernous sinus thrombosis is discussed in relation to complex sinus and orbit infections in the section on head and neck imaging. Prompt diagnosis of cerebral thrombosis is critical, as many of the parenchymal changes may be reversible. Systemic anticoagulation and local catheter-based thrombolytic, mechanical, or rheolytic clot dissolution are treatment considerations. Intracranial hypertension and collateral formation leading to dural arteriovenous malformations are possible long-term sequelae.

Figure 1-21 Venous sinus thrombosis. A, T1-weighted image shows loss of usual flow voids in superior sagittal and straight sinuses (arrows). B, Two-dimensional phase contrast MR venography shows corresponding lack of flow-related signal. C, Three-dimensional phase contrast MR venography 1 week after systemic anticoagulation shows recanalization.

Spontaneous Cervical Dissection

Spontaneous cervical arterial dissection used to be considered a rarity, but since the 1980s, largely due to improvements in imaging, there has been an increase in awareness of this cause of stroke. It is now estimated that up to 25% of strokes in young and middle-aged adults occur on this basis. Community-based studies have found annual incidence of internal carotid artery dissection at 3 per 100,000 per year and of vertebral artery dissection at 1.5 per 100,000 per year. History of a trivial precipitating event, such as minor movement of the neck, is commonly reported. Chiropractic manipulation of the cervical spine has become recognized as a potential cause of dissection, but estimates of the rate of occurrence vary widely. Many different kinds of triggering events associated with hyperextension or rotation of the neck—including sport and recreational activities, ceiling painting, coughing, sneezing, and vomiting—have been reported. A higher incidence in the autumn suggests inflammation or an excess amount of sneezing and coughing related to upper respiratory tract infections as predisposing factors. The effect of genetics has not yet been completely determined, but approximately half of patients show mild ultrastructural connective tissue alterations similar to Ehlers-Danlos syndrome. Traditional vascular risk factors have not been systematically studied, but atherosclerosis is generally not found in patients with spontaneous dissections. Migraine has been suggested as an independent risk factor.

Traumatic Cervicocerebral Injuries

The evaluation of vascular injuries of the neck and head has undergone a dramatic transformation due to the capabilities of helical and now multidetector CT angiography. Since 2000, favorable results from the use of CTA in the setting of penetrating trauma have supported its clinical application on a routine basis. High sensitivity and specificity for the detection of vascular injuries has been reported in a number of studies. It has essentially replaced DSA, still the gold standard, as the initial screening modality of choice for penetrating neck injuries at many institutions. In many cases it has been used as a complementary technique to surgical exploration of the neck, but, more recently, a normal CTA may avert the need for exploration. CTA has been applied to the setting of blunt trauma with similar results and has resulted in a decrease in the number of DSA exams performed. Abnormalities that may be detected include stenosis, occlusion, dissection, pseudoaneurysm formation, and contrast extravasation from vessel rupture. Vascular evaluation is generally limited to the common carotid, internal carotid, and vertebral and proximal branches of the external carotid arteries. With currently available equipment, submillimeter, subsecond imaging is possible, and even minor abnormalities of the distal external carotid branches are now being diagnosed prospectively. Nondiagnostic exams may occur as a result of technical deficiencies such as extravascular contrast infiltration from intravenous catheter problems, patient motion, and so on. Using a contrast test bolus or bolus tracking techniques helps to reduce the number of poor-quality scans due to arrhythmias or compromised cardiac output. Since intravenous contrast bolus may be impeded by transient compression of the left brachiocephalic vein due to pulsations of the great vessels, a right-sided antecubital injection site is preferred. Streak artifacts from dental fillings and hardware and beam-hardening effects also take their toll on image quality. Positive findings on CTA help guide therapeutic decisions toward medical, surgical, or endovascular intervention; however, well-defined pathways do not yet exist for most vascular injuries. It is the clinical expectation that by prompt diagnosis and implementation of antithrombotic or other vascular treatments, the incidence of stroke will be reduced. As more subtle injuries will be detected with advances in CT technology, outcomes research will be necessary to help determine the most appropriate therapy. It is well known that a certain (small) percentage of patients will present with delayed formation and rupture of a post-traumatic pseudoaneurysm, yet recommendations for and timing of follow-up examination remain rather dubious (Fig. 1-24).

Figure 1-24 Arterial dissection secondary to blunt trauma. A, Volume-rendered image from CT angiogram shows comminuted mandibular fracture (arrows). Internal jugular vein obscures internal carotid artery. B, 180-degree rotation and application of an anterior cutting plane reveal tapered contour of the internal carotid artery (arrows) due to dissection. C, Multiplanar reconstruction from follow-up CT angiogram 1 week later shows development of a small pseudoaneurysm (arrow) with residual, mild, distal stenosis.

Dissection of the internal carotid and vertebral arteries may be the direct result of blunt trauma with a reported incidence of less than 1% in some series. As might be expected, the risk of vascular injury in the setting of spine fracture is substantially higher. Another mechanism of carotid injury is intraoral trauma, such as from a fall with a pencil in the mouth or from iatrogenic causes. Basilar skull fracture, especially involving the carotid canal, is also included in this category in most studies of traumatic dissection. The indications for CTA continue to broaden. Due to the potential for devastating neurologic consequences of cerebrovascular injuries, some have suggested a liberalized screening approach—including not only patients with symptoms referable to vascular injury, but also asymptomatic patients undergoing CT for head and cervical spine trauma. In such a study reported by Biffl and colleagues in 2006, 5.4% of patients had blunt cerebrovascular injuries. In a recent 2-year retrospective review of patients at our center (unpublished data), 8% of 106 patients with fractures of the cervical spine and skull base (involving foramen transversarium or near the carotid canal) had vascular injuries detected by CTA. Of 161 trauma patients without fractures who also underwent CTA, 2% had vascular injuries detected. Therefore, presence of a fracture yielded an odds ratio for vascular injury of approximately 4 to 1 in this population. False positive and false negative results are generally considered few in number, with the expectation that they will continue to decline as technology advances and experience with the technique increases.

Some authors propose mandatory imaging for the following reasons: (1) arterial bleeding from the mouth, nose, ears, or wound; (2) expanding cervical hematoma; (3) bruit in patients over 50 years of age; (4) acute infarct; (5) unexplained neurologic defect or TIA; (6) Horner syndrome, neck or head pain. In one angiographic study of asymptomatic patients with skull base fractures, up to 60% had abnormal angiograms. Other studies have reported significantly lower rates of serious injury. One recent series found a 4% incidence of traumatic carotid-cavernous fistula in patients with skull base fractures. While prompt diagnosis and treatment of carotid-cavernous fistula are desirable, diagnosis at the time of admission is not as critical as it is for dissection with its inherent risk of stroke.

Whether performed for screening or based on symptoms, the workup and treatment of dissection continue to evolve. As with other vascular disorders, catheter angiography was once the only method available and is still used for confirmation if other studies are equivocal. The most common finding is a smoothly or mildly irregular tapered mid-cervical narrowing. Dissections that result in occlusion may show a “rat tail” or “flame-shaped” lumen; this may help distinguish other causes such as thromboembolism or atherosclerotic disease from dissection (Fig. 1-25). Saccular or fusiform aneurysmal dilatation (pseudoaneurysm) may also be identified. Presence of an intimal flap or a false or double lumen is unusual in the cervicocerebral vessels. In the internal carotid, the dissection is typically found a few centimeters beyond the carotid bifurcation or a few centimeters below the skull base. The most common sites of vertebral artery dissection are at the entry into the C6 foramen transversarium and at the C1-C2 level.

Figure 1-25 Acute dissection. Digital subtraction angiogram shows sharply tapered occlusion of the internal carotid artery due to spontaneous dissection.

Ultrasound assessment of cervical internal carotid and vertebral artery dissections is possible, but there are many pitfalls. In addition to the findings that may be demonstrated by angiography, a thickened, hyperechoic vessel wall may be detected. This technique may be better for exclusion of dissection based on high negative predictive value.

The combination of MR and MRA is considered by many to be the preferred technique. MRA should be able to demonstrate the morphologic features of the vessel in a fashion similar to DSA. In addition, MR images may demonstrate an eccentrically located narrowed lumen, a crescentic or circumferential intramural hematoma, and an increase in the external artery diameter. Fat-suppressed T1-weighted images are recommended to improve sensitivity for detection of the intramural hematoma (Fig. 1-26). However, in the acute setting, the clot should not be expected to appear hyperintense, as it may take a few days for conversion to methemoglobin to take place. The reported sensitivity and specificity for detection of carotid dissection are very high, approximately 95% and 99%, respectively. Sensitivity is lower for vertebral dissection (approximately 60%) due to the smaller size of the native vessel and relatively high incidence of hypoplasia. One must remember that lack of flow-related signal due to slow flow in a vessel may simulate occlusion. These noninvasive techniques are very useful for follow-up of dissection due to the lack of ionizing radiation or need for contrast injection.

Figure 1-26 Internal carotid artery dissection—CT and MR angiograms. A, CT angiogram source image shows narrowed upper cervical right internal carotid artery lumen with increase in external caliber of vessel (arrow). B, Fat-suppressed T1WI shows corresponding narrowed flow void with hyperintense eccentric intramural hematoma (arrow). C, Time-of-flight MR angiogram shows narrowed segment of right internal carotid artery (arrow).

CT angiography shares many of the advantages of MRA and provides higher spatial resolution. Another specific sign reported by CTA is the “target” sign, composed of a thickened wall and a narrowed eccentric lumen surrounded by a thin rim of contrast enhancement. CTA is certainly the fastest way to screen patients in the emergency setting, often done immediately after imaging of the head and cervical spine.

CT angiography has also become the initial method for evaluation of stable patients with penetrating trauma to the neck, face, and head based on availability, efficiency, and similar profiles of sensitivity and specificity as in blunt trauma. The high sensitivity of CT for the detection of small amounts of contrast extravasation or air in the soft tissues helps to localize subtle injuries to major vessels that might otherwise go unnoticed. An understanding of the expected trajectory of bullets or knives based on skin entry and exit wounds may increase the likelihood of injury detection. Detection of dissection, transection, pseudoaneurysm, and arteriovenous fistula formation can help guide treatment—medical versus open surgical versus endovascular. Post-traumatic vasospasm may lead to a false positive diagnosis of dissection or transection, appearing normal on immediate follow-up angiography. Retained bullets and shrapnel often cause substantial artifacts that limit the diagnostic value of CTA. Digital subtraction angiography can usually overcome this limitation through the use of multiple oblique projections.

Spontaneous Intracranial Dissection

Intracranial arteries lack an external elastic lamina and have thinner media and adventitia compared with extracranial vessels. Therefore, intracranial dissections may behave differently. If the dissection occurs between the intima and media, then luminal stenosis or occlusion may lead to ischemia or infarct similar to the extracranial setting. If the dissection plane is between the media and adventitia, then (dissecting) pseudoaneurysm formation is likely. Due to the thin media and adventitia, rupture and subarachnoid hemorrhage may occur. SAH is reported in approximately 20% of intracranial internal carotid dissections and more than 50% of intracranial vertebral dissections. The supraclinoid segment of the internal carotid and the segment the vertebral near the posterior inferior cerebellar artery (V4) are the most common sites of intracranial dissection. The cause of intracranial dissection remains unknown, with some related to trauma or underlying connective tissue disorders (such as fibromuscular dysplasia, Marfan’s, and Ehlers-Danlos types). It may not be possible to differentiate traumatic stenosis or occlusion from atherosclerosis or thromboembolism by any imaging technique. The only truly diagnostic findings of dissection are presence of a dissecting pseudoaneurysm and a double lumen.

Treatment options vary depending on stenosis versus pseudoaneurysm configuration and presence of infarct or subarachnoid hemorrhage. Endovascular intervention with stent placement may be considered when medical therapy for stenosis has failed. Aneurysm coiling, proximal occlusion, and trapping of an abnormal segment are other possible techniques.

Hydrocephalus

Disturbance of the usual pattern of CSF flow or production/absorption may result in dilatation of the ventricular system. Hydrocephalus may occur acutely or may be of chronic duration, and the distinction between the two forms may not be entirely clear based on imaging alone. Hypodensities/T2 hyperintensities in the periventricular white matter of the frontal and periatrial regions may be a sign of transependymal flow of CSF and may be seen with acute hydrocephalus. Chronically compensated hydrocephalus is less likely to demonstrate this finding. Terminology can be confusing: obstruction at the level of foramen of Monro, cerebral aqueduct of Sylvius, or foramina of Magendie and Luschka is considered noncommunicating hydrocephalus, whereas obstruction at the level of the arachnoid granulations is considered communicating hydrocephalus. One should always remember the value of prior exams, since long-standing, compensated hydrocephalus is generally not a cause for alarm even if encountered in the emergency setting. Ventricular obstruction may develop as a result of SAH, IVH, intraventricular mass, aqueductal stenosis, and any lesion that may cause extrinsic mass effect. Analysis should include evaluation of basal cisterns and search for possible complications that may result from herniation. Ideally, treatment of hydrocephalus will prevent such complications. Recurrence of symptoms due to ventricular shunt malfunction is a common problem that may result from catheter/tubing obstruction (intrinsic or in the peritoneal cavity), disconnection, or migration (Fig. 1-27).

Figure 1-27 Hydrocephalus—shunt malfunction. Severe hydrocephalus. Portions of bilateral ventriculoperitoneal shunts are visible. Abdominal CT (not shown) demonstrated a pseudocyst as a cause for malfunction.

Classification is complicated further by normal pressure hydrocephalus; the etiology of this disorder in which intracranial pressure is not elevated is unknown. In the setting of ventriculomegaly out of proportion to sulcal prominence, the presence of the classic triad of dementia, abnormal gait, and urinary incontinence can help to make this diagnosis. However, by the time the classic symptoms are evident, treatment may be ineffective. The fourth ventricle may be relatively spared and signs of transependymal flow of CSF may be present in normal pressure hydrocephalus.

A related disorder is pseudotumor cerebri (idiopathic intracranial hypertension), which may be due to poor CSF absorption such as from venous sinus thrombosis. Incidence is highest in obese females of child-bearing age and may present with headache and visual loss due to papilledema. Although intracranial pressure may be severely elevated in this disorder, the ventricular system is generally small. Progressive visual loss may be an indication for emergent, fluoroscopic-guided, therapeutic lumbar puncture.

Colpocephaly is the term applied to enlarged occipital horns of lateral ventricles that are due to a developmental structural abnormality of the brain and that may sometimes be mistaken for acute hydrocephalus. Other congenital abnormalities such as agenesis of corpus callosum will also present with abnormal ventricular configuration and should be recognized as an expected part of the constellation of findings. Benign external hydrocephalus is the term applied to the pattern of mild ventriculomegaly and generous subarachnoid spaces in neonates and infants. It is associated with macrocephaly and usually resolves spontaneously by 1 to 2 years of age.

Infections

Meningitis

Suspected meningitis is a very common cause for imaging, not necessarily for diagnosis, but as a precaution prior to performance of a lumbar puncture. In adults with suspected meningitis, clinical features can be used to identify those who are unlikely to have abnormal findings on CT of the head. However, many practitioners still rely on CT prior to lumbar puncture in order to exclude unsuspected mass effect and lesions that might result in rapid increases in intracranial pressure; this is especially true for patients who are immunocompromised or older than 60 years. The majority of exams are normal, but detection of findings such as brain edema possibly leading to herniation, hydrocephalus, or other complication will alter management. On FLAIR images, sulci may appear hyperintense due to proteinaceous exudates; however, SAH or high concentration of inspired oxygen may also cause the same appearance. In the vast majority of cases, meningitis is aseptic (generally of viral origin, commonly enteroviruses) and is self-limited. Bacterial meningitis is more likely to result in severe disease, and in some cases the source of meningitis may evident on imaging, such as a sinus or ear infection. On intravenous contrast-enhanced CT and MR exams, diffuse enhancement within the sulci (leptomeningeal) may be detected. Imaging is also indicated for those patients who do not respond to antibiotic treatment in hope of detecting a drainable source such as subdural empyema or parenchymal abscess. Gadolinium-enhanced MR is generally preferred to CT due to its relatively higher soft tissue contrast. Neonatal meningitis due to Citrobacter species is another indication for imaging since brain abscess develops in 80% to 90% of cases. Meningoencephalitis (encephalomeningitis) is the term applied to brain parenchymal infection in association with meningitis. Other complications of meningitis include infarcts, venous thrombosis, subdural empyema or hygroma, and obstructive or communicating hydrocephalus (Fig. 1-28). Subdural empyema and epidural abscess are illustrated in the section on head and neck imaging.

Figure 1-28 Meningitis caused by group B streptococcus in a 4-year-old. A, Postgadolinium T1 image shows mild diffuse leptomeningeal enhancement and abnormal enhancement of the bilateral CN III (black arrows). B, MR angiogram shows bilateral internal carotid artery terminus and anterior cerebral artery and middle cerebral artery origin stenoses (white arrows). C, Diffusion-weighted image shows resultant infarcts.

Many other infectious agents may cause meningitis, including Lyme disease (Borrelia) and, especially in the immunocompromised setting, HIV, toxoplasmosis, cryptococcosis, tuberculosis, syphilis, cytomegalovirus, and a variety of fungi (see Fig. 1-12).

Diffuse thickened enhancement of the dura is a sign of pachymeningitis. This can be due to carcinomatous, granulomatous, and noninfectious causes including idiopathic intracranial hypotension (Fig. 1-29). Tuberculosis has a predilection for causing basal meningitis with resultant stroke due to involvement of arteries at the base of the brain.

Figure 1-29 Pachymeningitis. Postgadolinium T1-weighted image shows diffuse, pachymeningeal, thickened enhancement due to neurosarcoidosis.

Brain Parenchymal Infection

The term encephalitis refers to inflammation of the brain and is usually applied in the setting of viral infection. Cerebritis is often used interchangeably; however, it should be reserved for the cerebrum with cerebellitis added when necessary. Usually the findings are nonspecific, with simultaneous involvement of various structures. A certain pattern may suggest a particular organism, such as the classic findings of T2 hyperintensity, restricted diffusion, and minimal enhancement within the temporal lobe(s) and limbic system due to herpes simplex type 1 infection (Fig. 1-30). Nonspecific patchy T2 hyperintensities, variable diffusion, and enhancement characteristics may lead to a differential diagnosis including ischemia, infiltrating neoplasm, status epilepticus, and toxic/metabolic causes. Rather than identify the exact agent, imaging findings may be able to suggest infection and exclude other possibilities.

Figure 1-30 Herpes encephalitis. Diffusion-weighted (A) and FLAIR (B) images show corresponding hyperintensities in left temporal lobe and insula as a result of herpes simplex virus type I infection. Note the motion artifact so commonly encountered in patients evaluated for a change in mental status.

Abscess

Abscess is a focal parenchymal infection due to bacteria, fungi, or parasites. The imaging characteristics reflect the phase of the infection as it evolves from early cerebritis to late cerebritis, then to early and finally late encapsulated stages. If diagnosed early, it often appears as a low-density (on CT), T2 hyperintense region with faint enhancement and a mild amount of surrounding edema. Once in the capsule stage, a typical fluid collection with a thin rim of enhancement and larger amount of edema becomes evident (Fig. 1-31). Over time (with treatment), the lesion may decrease in size and develop a thicker rim of enhancement and surrounding edema will wane. The rim is typically T2 hypointense and thinner along the deep margin. This may predispose cerebral lesions to rupture into the ventricular system, leading to ventriculitis and a dramatic clinical decline. A bacterial abscess typically shows diffusion-weighted hyperintensity; this may help to distinguish a bacterial abscess from a necrotic tumor. Lesions in the differential diagnosis other than neoplasm might include demyelination, subacute infarct, and subacute hematoma. In the setting of immune suppression, fungal abscess should be considered. In the setting of AIDS, the differential for single or multiple ring-enhancing lesions includes toxoplasmosis versus lymphoma (Fig. 1-32). Also prevalent in the AIDS population is M. tuberculosis and Cryptococcus, which can present as either meningitis or focal parenchymal lesions. To further complicate matters, another classic presentation of cryptococcosis is that of nonenhancing, gelatinous pseudocysts that distend the perivascular spaces.

Figure 1-31 Pyogenic abscess. A, T2 image shows hyperintense fluid collection in the right frontal lobe with a hypointense rim and extensive surrounding edema. B, Corresponding hyperintensity on diffusion-weighted image. C, Postgadolinium T1-weighted image shows a relatively thin rim along the deeper portion of the abscess adjacent to the lateral ventricle.

Figure 1-32 Toxoplasmosis. A, FLAIR image shows isointense lesions in right basal ganglia and left parietal lobe with surrounding edema. B, Postgadolinium T1-weighted image shows faint rim enhancement of right basal ganglia lesion. C, Postgadolinium T1-weighted image shows typical “target” sign in left frontal lobe lesion.

Single or multiple abscesses may develop from septic emboli due to endocarditis. Initially, these appear similar to other cardioembolic infarcts but in time develop relatively more surrounding edema and enhancement due to the inflammatory response (Fig. 1-33). If cardiac valve replacement is considered, screening for mycotic aneurysms may be requested prior to surgery.

Figure 1-33 Septic emboli. Diffusion (left), FLAIR (middle), and postgadolinium T1-weighted image (right) show multiple small lesions with edema and faint rim enhancement.

Neurocysticercosis is the intracranial infection by the pork tapeworm, Taenia solium, which is endemic in many parts of the world. It is the leading cause of seizures worldwide and has a unique life cycle and imaging After ingestion of contaminated food or water, larvae migrate from the gastrointestinal tract to the brain and skeletal muscle. Once intracranial, the larvae develop into cysticerci, and these cysts may be located in the subarachnoid spaces, brain parenchyma, or ventricular system. The cysts then progress through four stages with distinct imaging features based on the lesion and the host response. In the vesicular stage, the lesions appear as thin-walled, fluid-filled cysts, possibly with mild rim enhancement, but without surrounding edema. Lesions are generally small (less than 1 cm), and often an eccentric scolex of a few millimeters can be detected. In the colloidal vesicular stage, in which the larva starts degenerating, a thicker rim of enhancement and surrounding edema develops. It is in this stage that the appearance is similar to any other brain abscess. Next is the granular nodular stage in which the cyst involutes, the wall thickens, the lesion begins to calcify, and edema decreases. In the final nodular calcified stage, only a small calcification persists and edema resolves completely. Since lesions may progress at different rates, it is not uncommon to find more than one type of lesion. Identification of cysts in different compartments, presence of a scolex, variable amounts of edema, and small calcifications in the same patient offer great sensitivity and specificity. It is not often that the can show such confidence in diagnosis, and therefore neurocysticercosis deserves special recognition (Fig. 1-34). One might not expect this to be common in the United States; however, due to travel and immigration, it presents fairly commonly in patients presenting to our ED with new or recurrent seizures.

Figure 1-34 Neurocysticercosis. A, CT (left), FLAIR (middle), and post-gadolinium T1-weighted image (right) demonstrate cyst with scolex, thin rim of enhancement, and surrounding edema in the vesicular stage. B, FLAIR (left) and postgadolinium T1-weighted image (right) showing signal loss related to calcification, small amount of edema, and rim enhancement in the granular nodular stage.

Tumors

As with infection, it is not possible to review all of the myriad entities in this category. Within the scope of this chapter it is possible to provide only a limited framework and describe some of the more common lesions.

Metastases account for approximately half of all intracranial neoplasms in adults. They may present as multiple small enhancing lesions at the gray–white junction or as a single large lesion with extensive surrounding edema. Lesions are usually found in the cerebral hemispheres, and may be solid, cystic, calcified, or hemorrhagic, and approximately 50% will present as a solitary lesion. The most common primary tumors are lung, breast, and melanoma. Calcification may imply a tumor of mucinous origin (gastrointestinal tract), and hemorrhage may indicate hypervascular primaries such as choriocarcinoma or renal or thyroid primaries in addition to the other most common culprits. The World Health Organization classification of primary central nervous system neoplasms is generally based on either cell type of origin or other location (e.g., sellar). Knowledge of this classification system is important for accurate communication among clinicians from different subspecialties, especially pathology, neuro-oncology, and neurosurgery. In addition, the radiologist should be familiar with the typical imaging characteristics, locations, and demographics of the common lesions in each category. As in any field, expertise requires effort and experience. Although it may be very satisfying to correctly identify the tumor histology (or at least narrow the differential diagnosis to a select few), the major goal in the emergency setting is to recognize subtle lesions, bring attention to those that may soon result in significant complications, and provide reassurance when intervention is not indicated. Perhaps the first step in this process should be to try to determine whether a mass is intra-axial or extra-axial. While not always clear, this distinction helps to guide the differential diagnosis toward the proper category. Location of the lesion, supratentorial versus infratentorial; relation to the skull base and cisterns (anterior or middle fossa, sellar/parasellar, pineal region, cerebellopontine angle cistern, intraventricular, etc.); and multiplicity are also important details. Demographics and clinical presentation may be equally important. One must also be aware that the differential for many primary neoplasms includes metastasis, as well as infection, infarct, demyelination, inflammatory conditions, and congenital/developmental anomalies. Although space limitations preclude even the most basic description of each of the intracranial tumors, a few examples are presented to illustrate common imaging features to be recognized during workup of patients in the emergency setting (Figs. 1-35 to 1-39).

Figure 1-35 Hemangioblastoma. A, CT shows fluid density mass in the cerebellum and surrounding edema resulting in compression of the fourth ventricle. B, On FLAIR image the signal is relatively hyperintense to CSF suggesting protein content. C, Postgadolinium T1-weighted image shows small enhancing mural nodule within the cystic mass. Note dilated lateral ventricles due to obstructive hydrocephalus.

Figure 1-36 Craniopharyngioma. A, Coronal reformat of noncontrast CT shows a large cystic sellar/suprasellar mass with peripheral calcifications. B, Volume-rendered image shows the cystic components of the lesion as a semitransparent surface. It is more easily appreciated on a color monitor. By varying the transparency of the mass, the remodeled sella is easily demonstrated. This 5-year-old girl was sent by her ophthalmologist for urgent CT due to worsening visual acuity.

Figure 1-37 Central neurocytoma.Noncontrast CT (left), FLAIR (middle), and postgadolinium T1-weighted image (right)show a large, enhancing intraventricular mass related to the septum pellucidum causing hydrocephalus. This 22-year-old female presented to the emergency department with worsening headaches.

Figure 1-38 Glioblastoma multiforme (astrocytoma WHO Grade IV/IV). A, On noncontrast CT the mass cannot be clearly separated from the edema. B, Postgadolinium T1-weighted image shows an irregular rim of enhancement of this mass that crosses the midline via the corpus callosum. This 50-year-old male presented with altered mental status.

Figure 1-39 Metastatic lung carcinoma. Noncontrast axial CT, FLAIR, T2, T1, and sagittal and coronal postgadolinium T1-weighted images. This single lesion is hyperdense, FLAIR/T2 isointense, T1 mildly hyperintense, and homogeneously enhancing. There is a moderate amount of edema relative to the size of the lesion.

Disorders of White Matter

No review of nontraumatic emergencies could be complete without mention of the following set of loosely related disorders. The common bond may be that they do not fall into the infectious or neoplastic categories. Some are quite common and the others are becoming more frequently diagnosed due to the relatively classic imaging features and recognized clinical associations.

Multiple Sclerosis

Patients presenting with a clinically isolated syndrome (first episode of neurologic dysfunction) often undergo imaging in the emergency setting mainly to exclude infarction or other process. White matter lesions detected by CT or MR may raise the suspicion of a demyelinating disorder. The diagnosis of multiple sclerosis (MS) can be complex, requiring dissemination of lesions in time and space and exclusion of other causes such as Lyme disease, vasculitis, neurosarcoidosis, lupus, and others. The Revisions to the McDonald Diagnostic Criteria for MS imaging are a standardized set of diagnostic guidelines that are applied clinically and to clinical trials; these are based on number, location, and enhancement of lesions. Classically, hypodense/T2 hyperintense lesions are located in a periventricular distribution, in the corpus callosum (callosal-septal interface), and also the brainstem, cerebellum, and spinal cord. Transient disruption of the blood-brain barrier will lead to solid or rim enhancement of active plaques (Fig. 1-40). Active demyelination may appear hyperintense on DWI. Magnetization transfer and MR spectroscopy techniques may demonstrate abnormalities even in normal-appearing white matter. Genetic and environmental factors and female to male ratios of almost 2 to 1 (adults) and greater than 5 to 1 (children) have been found. As the name implies, the unusual tumefactive variety simulates a neoplasm, often leading to biopsy. Another autoimmune-mediated disorder that is generally monophasic is acute disseminated encephalomyelitis (ADEM) and may be indistinguishable from MS on initial imaging (Fig. 1-41). Another presumably autoimmune disorder that mimics MS and ADEM is Susac syndrome. This rare syndrome has a clinical triad of encephalopathy, branch retinal artery occlusions, and hearing loss.

Figure 1-40 Multiple sclerosis—optic neuritis. A, FLAIR image shows a few white matter hyperintensities. B, One enhancing lesion (arrow) is detected on postgadolinium T1-weighted image. C, Coronal STIR image shows asymmetric hyperintensity of the right optic nerve (arrow). D, Asymmetric enhancement of the right optic nerve (arrow) is shown on postgadolinium, fat-suppressed T1-weighted image.

Figure 1-41 Acute disseminated encephalomyelitis. A, FLAIR image shows nonspecific periventricular and subcortical white matter hyperintensities. Diffusion-weighted image (B) and apparent diffusion coefficient map (C) show central areas of restricted diffusion and surrounding vasogenic edema (“T2 shine-through”). This acute demyelinating process mimics acute stroke. The distribution of the lesions is not typical of an acute infarct.

Progressive Multifocal Leukoencephalopathy

In the immunocompromised host (especially due to AIDS), nonenhancing T2 hyperintensities (often confluent) in the parietal and occipital lobes should raise suspicion of progressive multifocal leukoencephalopathy (Fig. 1-42). This demyelinating process due to infection with the JC virus was originally thought to affect only white matter, but cases with both gray and white matter lesions and variable enhancement have been reported. The progressive nature of the disorder is also less certain due to current, highly active, antiretroviral regimens.

Figure 1-42 Progressive multifocal leukoencephalopathy. FLAIR images show asymmetric white matter hyperintensities involving predominantly the left external capsule and periventricular and subcortical white matter. No enhancement or mass effect was present. This patient with AIDS presented with a rapid decline in mental status.

Posterior Reversible Encephalopathy Syndrome

Posterior reversible encephalopathy (and seizure) syndrome (PRES) has a number of common causes such as (pre)eclampsia, hypertensive crisis, lupus and other causes of nephropathy, and drug toxicity (including immunosuppressants and erythropoietin). In the workup of new seizures, the classic features of T2 hyperintensity in a rather symmetric distribution within the occipital, parietal, and posterior frontal lobes should bring this diagnosis to mind (Fig. 1-43). Although white matter is primarily affected, gray matter structures in the basal ganglia, brainstem, and cerebellum may also be involved. Diffusion imaging is most helpful to differentiate this process from acute infarction. Small amounts of hemorrhage (and infarcts) may occur within the background of vasogenic edema resulting from abnormal vascular autoregulation. Differentiation from acute or subacute stroke is important in directing the search toward an offending agent rather than initiating the stroke clinical pathway.

Figure 1-43 Posterior reversible encephalopathy syndrome. FLAIR images demonstrate slightly asymmetric hyperintensities primarily involving the cerebellum, thalami, and posterior frontal, parietal, and occipital lobes. Note involvement of both gray and white matter structures. This patient presented with new-onset seizures. Signal abnormalities resolved completely within 1 month.

Toxic Encephalopathy

Whether due to accidental or intentional exposure/ingestion, a variety of well-known toxins may cause encephalopathy. Symmetric bilateral hypodensities/T2 in the globus pallidus are the hallmark of hypoxic damage due to carbon monoxide poisoning; hemispheric white matter may also be involved. Methanol toxicity typically affects the putamen and can be hemorrhagic. In addition to cerebellar degeneration, chronic alcoholism may lead to the development of Wernicke encephalopathy. It can also be the result of thiamine deficiency and a variety of other, less common, systemic conditions, presenting with lesions of the hypothalamus, mammillary bodies, dorsal medial thalamus, and periaqueductal gray matter. Ischemic and hemorrhagic complications related to illicit drug use have already been discussed. Toxic encephalopathy may also result from drug abuse. The pattern of white matter abnormality that results from inhalation of heroin vapor (known as “chasing the dragon”) can be quite dramatic (Fig. 1-44). Encephalopathy may also be iatrogenic and related to chemotherapy (e.g., methotrexate) or radiation therapy, and generally affets the periventricular white matter in a diffuse fashion.

Figure 1-44 Toxic encephalopathy. A, FLAIR image shows symmetric, confluent, primarily white matter hyperintensities. B, Postgadolinium T1-weighted image shows minimal enhancement. The key to the diagnosis is the association with inhalation of heroin vapor—“chasing the dragon.”

Another potentially iatrogenic disorder may result from the rapid correction of hyponatremia, leading to the classic central pontine or extrapontine varieties of demyelination (myelinolysis).

Skull Fractures

The workup of head trauma used to include skull radiographs, but those days are gone. The use of CT has become the standard of care for rapid assessment of the skull and intracranial contents. In the early days of CT, it was estimated that more than half of skull fractures were not detected, since they were oriented almost parallel to the imaging plane and therefore volume averaged with adjacent normal bone. With recent decreases in section thickness and multidetector-row technique, this limitation has effectively been overcome (Fig. 1-45). Careful review of millimeter or submillimeter thickness sections and 3D volume-rendered images and familiarity with normal sutural anatomy and variants may be necessary to accurately detect fractures. The radiologic evaluation should start with the scalp, as soft tissue swelling and scalp hematoma are very helpful indicators of possible underlying fracture. Skull fractures may be linear or comminuted and either type may be depressed. Diastasis is the term applied to separation of linear fracture fragments or sutures. Diastatic fractures occur more commonly in children. If the arachnoid membrane gets trapped within a diastatic fracture, a “growing fracture” (leptomeningeal cyst) may develop over time. Bullet wounds may leave behind a wake of comminuted bone and metallic fragments and burst fractures at the point of exit. Identification of a fracture should lead to the dedicated search for other important findings, such as intracranial hemorrhage. Fractures through the skull base may lead to other complications such as vascular or cranial nerve injuries or CSF leak. Intracranial air should prompt the search for fracture through an aerated paranasal sinus or pneumatized portion of the temporal bone, as antibiotic therapy may be indicated for prophylaxis against meningitis. One should not be alarmed by all bubbles of air, since reflux into the cavernous and other dural sinuses often occurs following insertion of intravenous catheters and injections of saline, medications, or contrast material with lax technique. The presence of fluid within the sphenoid sinuses, middle ear cavities, or mastoid air cells should also prompt a search for fractures through these regions. Temporal bone fractures may result in damage to the facial nerve, ossicles, and otic capsule. Screening for potential vascular injury in the setting of fracture of the central skull base may be accomplished with CTA. This was discussed in the section on cerebrovascular emergencies. (see also Fig. 1-54).

Figure 1-45 Skull fracture. A, Nondisplaced skull fracture is occult on routine 5-mm-thick section due to volume averaging. Fracture is most conspicuous on 0.625-mm section although with an increase in noise. B, Volume-rendered image shows fracture is nearly parallel to axial imaging plane.

Maxillofacial Fractures

MDCT has also revolutionized the workup of facial fractures. Once within the realm of plain film radiography, now these injuries are almost exclusively evaluated with CT. The general principles of fracture detection are often taken for granted but deserve quick mention. An unexpected linear lucency, disappearance or displacement of a normal structure, and a double density from abnormal overlap of adjacent structures are classic radiographic findings of facial fractures. A cortical defect, separation of a suture, and presence of subcutaneous, orbital, or periorbital air are findings that apply equally to radiographic and CT examinations. Likewise, soft tissue swelling and fluid levels in the paranasal sinuses are equally important clues to recognize, although these are less specific and occur without fractures. Whereas several CT scans used to be necessary to evaluate the brain and face (including both thin-section axial and direct coronal scans), now complete evaluation of the head and facial skeleton can be performed with a single exposure. As an example, our 64-detector scanner offers the prospective creation of routine 5-mm-thick contiguous sections processed with a soft tissue algorithm to evaluate the brain and 0.625- or 1.25-mm-thick contiguous sections processed with a bone algorithm for evaluation of the face and skull. The thinner sections are routinely reformatted in coronal and sagittal planes, and, if desired, 3D volume-rendered images may be created at the CT console or other workstation. Depending on clinical exam findings, imaging of the head may begin at the level of the dental occlusal plane or include the chin and continue to the vertex. This method improves detection and characterization of facial fractures and reduces the amount of additional radiation exposure and scan time. Comprehension of the fracture may be improved by illustrating its relationship to normal anatomic landmarks. This helps the radiologist to apply the most appropriate terminology or classification and the surgeon to determine the need for operative reduction and fixation, usually with titanium plates and screws. Sometimes an implant is necessary to repair a large defect, as for the orbital floor. The reader is encouraged to consult review articles or texts (see Suggested Readings) for descriptions of commonly used medical devices.

The facial skeleton can be considered as composed of several vertical and horizontal buttresses of thickened bone that support the functions of the face, eyes, mouth, and airway. The buttresses are linked to each other and act as attachments of the face to the calvarium and skull base. The individual components of this system and the sutures are important anatomical landmarks for the radiologist and the surgeon but are beyond the scope and space limitations of this chapter. A brief overview of common facial fractures and associated injuries follows.

Orbital Blow-out Fractures

Isolated trauma to the orbit, a common cause of ED visits, plays a role in many cases of head trauma. Nontraumatic orbital emergencies are discussed later in this chapter. Fractures and injuries to the orbital soft tissues come in many different varieties. A blow to the eye causes an increase in intraorbital pressure, which is transmitted to the thin walls of the orbit. Blow-out fractures may involve the orbital floor, the medial wall, or both; the orbital rim should not be involved (Fig. 1-46). Even though the medial wall (lamina papyracea) is thinner, the network of ethmoid sinus septations acts as a support, and therefore isolated orbital floor fractures are more common. In up to about half of floor fractures, medial wall fractures will also occur. Orbital emphysema and herniation of orbital contents are possible associated findings. Coronal images are very useful to assess the degree of displacement of fracture fragments. Sagittal reformatted images help to define the anteroposterior extent of orbital floor fractures. Fragment size and displacement help to determine conservative versus operative management. Numbness of the upper cheek due to injury to the infraorbital nerve and diplopia may be presenting symptoms. Persistent diplopia and enophthalmos are possible long-term complications. Fractures that affect the orbital apex may be surgical emergencies. A bone fragment or hematoma can compress the optic nerve leading to acute decrease in visual acuity. An afferent papillary defect should also prompt careful review of this region with bone and soft tissue algorithms and display settings. While extraocular muscle entrapment is a clinical diagnosis, certain imaging features may offer guidance to the surgeon. If the inferior rectus muscle is displaced and does not retain its normal flattened shape on coronal images, then the fascial sling of the globe may be disrupted. Herniation of the muscle into the maxillary sinus can occur in the absence of a visible defect in the floor, implying that a “trap-door” fragment has sprung back into place, and prompt repair will clearly be necessary. Hematomas within the orbital soft tissues may occur in association with fractures, including retrobulbar and subperiosteal locations.

Figure 1-46 Orbital blowout fractures. A, Axial CT shows displaced fracture of medial wall of the left orbit (lamina papyracea). B, Direct coronal CT image shows displaced left orbital floor fracture with an air–fluid level in the maxillary sinus. (This is of historical value, as most coronal images are now obtained by reformation.) Inferior rectus muscle is swollen (arrow). This patient was hit in the eye with a baseball.

Although orbital decompression results from the blowout mechanism, up to 25% have an associated ocular injury. Imaging findings can signal the need for ophthalmologic exam that may be overlooked in the setting of multitrauma. A ruptured globe, caused by either blunt or penetrating trauma, is small, often with a flattened contour. Hemorrhage within the eye appears relatively hyperdense and can occur in several different compartments, including subretinal, subchoroidal, and subhyaloid. The distinction between these can often be made based on shape and limits of the hemorrhage but is best made by physical exam. Dislocation of the lens, whether partial or complete, is not usually a subtle finding but can be easily overlooked if not included in the usual search pattern. Rupture of the capsule of the lens results in lens edema, appearing as a decrease in attenuation of this usually high density (proteinaceous) structure. Intraorbital and intraocular foreign bodies may be detected by CT; however, certain materials, such as wood, are better detected by ultrasound or MR. Calcifications of the trochlear apparatus, the sclera, and optic drusen are common and should not be misinterpreted as foreign bodies. The shrunken, calcified globe (phthisis bulbi) resulting from past trauma or infection should not be mistaken for an acute injury. Likewise, intraocular silicone oil or gas, and scleral buckles (both high- and low-density silicone) for treatment of retinal detachments and other devices, should also be properly recognized and not become causes of concern.

Orbital roof fracture is an uncommon injury that may extend to the frontal or ethmoid sinuses. It is best appreciated with coronal and sagittal reformatted images. With a “blow-in” type of fracture, as from pressure phenomenon due to a gunshot wound to the head, progressive herniation of the frontal lobe into the orbit may result from cerebral edema. Blowout fracture of the orbital roof is rarely seen.

Nasal Fractures

Nasal fractures commonly occur in isolation but are often associated with other fractures of the midface. They account for approximately half of all facial fractures. Radiographs may occasionally be requested for isolated nasal trauma, and therefore one should be aware that fractures are usually oriented perpendicular to the nasal bridge and will cross the normal nasomaxillary suture and groove for the nasociliary nerve. These can be of cosmetic importance or may result in airway obstruction. Attention must be paid to the nasal septum since treatment of a septal hematoma might be necessary to avoid possible complications of ischemic necrosis, saddle deformity, and abscess formation.

As the name implies, naso-orbitoethmoid fractures are more complex and involve the nasal bones as well as the central upper midface. Impaction of the nose and disruption of the medial canthal regions, medial orbital walls, and ethmoid sinuses will result in widening of the intercanthal distance and the need for repair. Involvement of the nasofrontal duct or nasolacrimal canal may lead to significant morbidity and may also require surgical attention in order to reduce the chance of frontal sinus mucocele development.

Zygomaticomaxillary Complex Fractures

The zygoma has four sutural attachments, two to the skull and two to the maxilla. The zygoma is the second most commonly fractured facial bone. Isolated arch fractures account for a minority of zygomatic fractures and can be easily demonstrated with the traditional submentovertex view (“bucket handle”) radiograph. More commonly, 3D volume-rendered images from an MDCT dataset are used to arrive at the same impression. This injury may require repair for cosmetic reasons, or because impaction of fracture fragments against the coronoid process of the mandible or temporalis muscle may result in trismus.

The more common injury to the zygoma involves the three major attachments (zygomaticomaxillary, zygomaticofrontal, and zygomaticosphenoid) and therefore has acquired the term tripod fracture. The preferred term may be zygomaticomaxillary complex (ZMC) fracture as it is more aptly considered a quadripod fracture due to involvement of the posteriorly located zygomaticotemporal attachment. Specific components include the infraorbital rim, orbital floor, and lateral wall, as well as the attachments to the skull base (sphenoid and temporal bones). Impaction and rotation of a large fracture fragment will result in significant deformity of the cheek and orbit (Fig. 1-47). Fractures of the pterygoid plates or greater wing of the sphenoid may sometimes be seen with severe ZMC fractures.

Figure 1-47 Zygomaticomaxillary complex fracture. Composite images show fractures of the left maxillary sinus anterior wall (white arrow) and posterolateral wall (double arrows), orbital floor (arrowhead), and infraorbital rim (double arrowheads). Volume-rendered images demonstrate diastasis of zygomaticofrontal suture (black arrow) and degree of impaction of the malar eminence.

Le Fort Fractures

The Le Fort classification of midface fractures applies to separations of the maxilla from the skull base. The three-tier classification was developed by Le Fort in 1901 based on cadaveric experiments. These fractures rarely occur in their pure forms and while originally described as being bilateral, common usage allows for unilateral and combined bilateral types. The Le Fort I type is a fracture involving the maxillary antra, crossing midline above the hard palate. If unilateral, a sagittally oriented fracture of the palate will be present. Fractures of the pterygoid plates may occur, although some consider this a requirement by definition. With this injury, the hard palate will be allowed to separate from the rest of the face, and this will often be diagnosed by physical exam. In Le Fort II type, fractures involve both maxillary antra and inferior orbital rims crossing at the nasion (either at the nasofrontal junction or frontal process of the maxilla). The maxilla will be separated from the rest of the face. In Le Fort III type, also termed craniofacial dissociation, the inferior orbital rims are intact but the lateral orbital walls and zygomatic arches are fractured. This allows separation of the face from the rest of the skull. Variations and combinations of Le Fort and ZMC fractures are common (Fig. 1-48).

Figure 1-48 Le Fort fractures. Volume-rendered image from an unrestrained driver involved in a rollover motor vehicle collision shows multiple displaced fractures. Components: dots Le Fort I; triangles, unilateral Le Fort II; asterisks, unilateral Le Fort III; squares may be considered the zygomaticomaxillary complex. Arrow, fracture of mandibular symphysis.

Smash Fractures

The term facial smash is a general term applied to severely comminuted fractures of the facial bones that generally occur in association with fractures of the calvarium. Intracranial hemorrhage and traumatic brain injury occur commonly with these types of fractures. The frontal type commonly involves the anterior and posterior walls of the frontal sinus (Fig. 1-49). The naso-orbitoethmoid complex can be considered in this category. Central skull base types include fractures of the sphenoid bone. Vascular injuries related to skull base fractures are discussed in the sections on temporal bone fractures and cerebrovascular emergencies.

Figure 1-49 Smash fracture. A, Volume-rendered image shows complexity of comminuted frontal smash fracture that involves frontal sinuses and both orbits. B, FLAIR image months later shows residual signal abnormality involving gyrus rectus of both frontal lobes due to prior contusions.

Mandibular Trauma

Fractures of the mandible are common and are classified by location—alveolar, symphyseal, parasymphyseal, body, angle, ramus, subcondylar (neck), or condylar. The mandible may be considered a ring structure, but with some flexibility due to the temporomandibular joints. Therefore, one, two, or more fractures may occur depending on the magnitude and direction of the applied force.

Bilateral temporomandibular joint dislocation without fracture is an uncommon injury resulting from a blow to the symphysis. The mandibular condyles should normally be seated symmetrically in the glenoid fossae. On occasion, the condyles may be anteriorly displaced, simply a reflection of normal open mouth position at the time of image acquisition. However, in a true dislocation, the glenoid fossae are empty, with condyles positioned to the glenoid tubercles, and the jaw locked in the open position.

If the styloid process is disrupted in the setting of mandibular fracture, air may be seen in the infratemporal fossa, possibly related to oral or Eustachian tube laceration. Mandibular fractures may be associated with hematomas within the masticator space.

Airway compromise may result from bilateral parasymphyseal fractures since the symphysis becomes a free fragment, allowing the tongue to obstruct the oral cavity. Fractures across the mandibular canal may cause injury to the inferior alveolar nerve (branch of mandibular division of the trigeminal nerve) and result in paresthesia of the chin. Fractures affecting the teeth are considered open and require antibiotic prophylaxis. Fractured or avulsed teeth can pose a risk for aspiration, particularly in the unresponsive patient. A dedicated search for radiopaque foreign bodies in the airway on all other imaging studies is therefore necessary. Muscular forces may act favorably or unfavorably, resulting in nondisplaced or displaced fractures, respectively. Displacement may occur in either the vertical or horizontal direction. Reduction with maxillomandibular fixation or open reduction and internal fixation may be required to restore occlusion and allow proper masticatory function, speech, and facial contour. As with other facial fractures, multiplanar reconstruction and 3D volume-rendered images are helpful in comprehending the injury, especially the orientation of fracture fragments and relationships to the coronoid processes and condyles, as well as aid in surgical planning (Figs. 1-50 and 1-51).

Figure 1-50 Mandibular fractures. A, Axial and reformatted coronal CT images show bilateral mandibular subcondylar fractures (arrows) and fracture of right ramus (arrowheads). B, Volume-rendered images provide a clear overview of the fractures.

Figure 1-51 Mandible fracture. Axial, reformatted coronal and sagittal images show a comminuted displaced fracture of the mandible with involvement of the alveolar ridge. Volume-rendered image clearly demonstrates the relationship of the mobile teeth. (Volume-rendered image with dental shading is more realistic on a color monitor.)

Temporal Bone Fractures

Temporal bone fracture should always be suspected when opacification of the mastoid air cells and/or middle ear compartments is present in the trauma setting. Slice thickness of 1 mm or less may be necessary to clearly identify and fully characterize the fracture. Temporal bone fracture usually occurs secondary to blunt head injury and is classically characterized as either longitudinally or transversely oriented relative to the long axis of the petrous bone. The other components of the temporal bone, namely, the mastoid, styloid, squamous, and tympanic, can be involved as well. Temporomandibular joint dislocation and styloid process fracture are discussed with mandibular fractures in the section on facial trauma. In practice, however, fractures through this region tend to be complex, and more typically than not demonstrate both longitudinal and transverse fracture characteristics (Fig. 1-52). In these cases, it is more important to characterize whether or not the otic capsule (the bony housing of the inner ear structures including cochlea and semicircular canals) and internal auditory canal are involved.

Figure 1-52 Complex temporal bone fracture. Longitudinal (arrow)and transverse (arrowhead) components are shown. Ossicles and otic capsule were not disrupted in this case.

Longitudinal fractures parallel the long axis of the petrous bone and are more common than transverse temporal bone fractures (Fig. 1-53). Fracture components can secondarily involve the external auditory canal, tympanic cavity, and squamosal portions of the temporal bone. Blood and fracture fragments in the external auditory canal and tympanic cavity and ossicular disruption can account for the common clinical presentation of conductive hearing loss. Longitudinally oriented fracture tend to extend anteriorly toward the Eustachian tube and middle cranial fossa avoiding the bony labyrinth (anterior subtype). The glenoid fossa can be involved, and disruption of the middle meningeal artery can result in concomitant epidural hematoma. Less often the fracture plane may extend posteriorly behind the bony labyrinth to involve the jugular foramen and posterior fossa (posterior subtype). In these instances, careful attention should be paid to evaluate for involvement of the foramen lacerum and the sphenoid bone, which puts the traversing internal carotid artery at risk for traumatic injury. If the fracture plane is demonstrated to approximate the carotid canal, or if fractures extend into the carotid canal, CT angiography or conventional angiography can be performed to evaluate for possible internal carotid artery injury at the skull base (Fig. 1-54).

Figure 1-53 Longitudinal temporal bone fracture. Fracture (arrowhead) extends along orientation of petrous bone. Note partial opacification of mastoid air cells.

Figure 1-54 Skull base fractures—vascular injury. A, This patient sustained bilateral temporal bone fractures after a motor vehicle collision. On the right, nondisplaced transverse temporal bone fracture, lateral subtype (black arrowhead), and associated air in the vestibule of the semicircular canals (white arrowhead) were identified. Nondisplaced fracture through the left temporal bone perpendicular to the carotid canal (black arrow) was also identified. Incidental note made of foramen of Vesalius (white arrow), normal anatomy seen in up to 80% of patients. B, Given concern of fracture plane extending to carotid canal, CT angiogram was performed, and demonstrated intimal flap within the petrous portion of the right internal carotid artery (arrow). There was also suspicion of left petrous internal carotid artery dissection on multiple contiguous images. C, Noncontrast head CT 6 days post-trauma demonstrates diffuse loss of the gray–white differentiation and sulcal and ventricular effacement consistent with bilateral hemispheric infarcts.

Injury to the facial nerve is not uncommon in the setting of longitudinal fracture, although most literature emphasizes facial nerve injury with transverse fractures. Careful search for fractures along the entire course of the facial nerve from the internal auditory canal to the stylomastoid foramen is necessary. Focal swelling or hematoma developing within an otherwise intact facial nerve may manifest clinically as partial facial weakness in a delayed rather than immediate fashion. This is associated with better long-term prognosis for facial nerve function since the nerve is not disrupted.

Transversely oriented fractures are perpendicular to the long axis of the petrous bone and can be further classified into medial and lateral subtypes, depending on the position of the fracture plane relative to the arcuate eminence. The medial subtype transgresses at or medial to the lateral-most aspect of the internal auditory canal, while the lateral subtype transgresses the bony labyrinth. As with longitudinal fractures, careful attention must be paid to the relationship of the fracture plane with the carotid canal, as injury to the internal carotid artery can be seen in this setting. Both transverse subtypes can be associated with acute and permanent sensorineural hearing loss, secondary to acute transection of the vestibulocochlear nerve. Facial nerve paralysis, if present, is also immediate and complete, due to transection of the facial nerve.

Given the complex anatomy of the temporal bone, normal sutures and channels can often be mistaken for fracture planes. Normal petro-occipital, temporo-occipital, and occipitomastoid sutures can demonstrate irregular, coarse margins, raising concern for possible fracture (Fig. 1-55). Diastasis of sutures (equivalent to a fracture) can be seen without apparent fracture. Intrinsic sutures to the temporal bone itself, including tympanosquamous, tympanomastoid, and petrotympanic sutures, also can be confused with acute fractures (Fig. 1-56). Small channels in the middle and inner ear such as the cochlear and vestibular aqueducts, singular canal, and subarcuate fossa can also convey an appearance similar to fracture planes. An understanding of normal temporal bone anatomy is essential to avoid these errors. Symmetry, lack of opacification of mastoid air cells and middle ear compartments, absence of overlying soft tissue swelling, and the clinical context can also provide reassurance that no fracture is present.

Figure 1-55 Normal occipitomastoid suture. Note jagged but well-corticated margins along suture plane.

Figure 1-56 Normal tympanosquamous suture. Suture is present at the anterior bony wall of the external auditory canal.

In addition to varied severity of facial weakness and conductive and sensorineural hearing loss, complex temporal bone fractures can have long-term complications. Squamous epithelial proliferation along fracture planes can result in cholesteatoma without concurrent mastoid disease. CSF leak can result from disruption of the epitympanic roof; this frank communication of the intracranial CSF space and middle ear can present as otorrhea if the tympanic membrane is disrupted or rhinorrhea if the tympanic membrane is intact. While otorrhea and rhinorrhea may resolve in the early post-traumatic setting, persistent leakage needs to be surgically managed due to increased risk of meningitis. Cephalocele is also possible, if the bony defect is large enough. Post-traumatic perilymphatic fistula between the inner and middle ear can occur with disruption of the oval or round windows, or fractures through the otic capsule, and may present with hearing loss and vertiginous symptoms. Perilymphatic fistulas are difficult to demonstrate radiographically, but can be suspected based on clinical manifestations.

Airway and Pharyngeal Injuries

Acute trauma to the airway and pharynx occurs typically in the setting of penetrating trauma (stab wounds and gunshot wounds) or can be iatrogenic (traumatic intubation). Injury to the aerodigestive tract should be suspected in the setting of unexplained gas in the soft tissues adjacent to the airway or pharynx. It is important to keep in mind that lack of associated soft tissue gas does not exclude injury to these structures. Soft tissue gas adjacent to the aerodigestive tract could be secondary to superior tracking of pneumomediastinum and pneumothorax from a penetrating chest wound or could be related to the tract of the penetrating object itself. Tracheal diverticula are often seen at the thoracic inlet level on the right; this is a common normal variant. Presence of air along the aerodigestive tract can be idiopathic or related to asthmatic pneumomediastinum. Correlation with clinical presentation is necessary to avoid unnecessary imaging studies.

If injury is suspected, endoscopic evaluation with direct visual inspection is essential. A single contrast radiographic swallow study with water-soluble contrast may be helpful in the initial evaluation of hypopharyngeal injury; however, in a patient with potential concomitant airway injury or poor airway control, it may not be safe to do such an examination given the risk of aspiration and possible complication of chemical pneumonitis.

Injuries to the airway may be accompanied by injury to the larynx and vocal cords. Presence of laryngeal hematoma and vocal cord injury should be suspected if there is asymmetry in these regions when comparing right and left (Fig. 1-57). Patients with such injury typically present with hoarseness soon after the acute event. Again, if such injury is suspected, direct visualization by endoscopy is indicated. It should be remembered that patient phonation or phase of respiration can result in apposition of the vocal cords, creating an appearance of airway obstruction. Lack of associated soft tissue swelling and clinical correlation can help in minimizing the false positive diagnosis of laryngeal injury in these cases.

Figure 1-57 Laryngeal fracture. Extensive subcutaneous and deep space emphysema was due to extension of pneumothoraces in this patient after a motor vehicle collision. However, due to soft tissue density in the right supraglottic larynx, laryngeal hematoma was suspected. This was confirmed on endoscopy.

Peritonsillar Abscess

Pharyngitis is typically a clinical diagnosis, but imaging may be performed if there is clinical suspicion of complications. Imaging findings of tonsillar or peritonsillar soft tissue asymmetric enlargement with adjacent fat stranding may signal inflammation. Peritonsillar abscess is often seen in pediatric and immunocompromised patients. It is a peripherally enhancing fluid collection formed in the potential space between the fibrous capsule of the tonsil and pharyngeal constrictor muscles. The patient typically presents with dysphagia, odynophagia, ear pain, and trismus after improvement of acute symptoms of tonsillitis. Infection extending beyond the pharyngeal constrictor muscles into the parapharyngeal space may cause mycotic aneurysms and thrombophlebitis. A discrete abscess identified by imaging may require immediate incision and drainage. Associated reactive lymphadenopathy is usually present.

Retropharyngeal Infection

Spread of pharyngeal infection to the medial or lateral (Rouvière) retropharyngeal nodes may lead to cellulitis or development of suppurative adenitis (enlarged, rim-enhancing node). Associated edema of the retropharyngeal soft tissues is quite common, noted by expansion and diffusely increased density of the retropharyngeal fat. Extracapsular spread of nodal infection may result in a true retropharyngeal abscess typically identified as a rim-enhancing bow-tie-shaped fluid collection. Retropharyngeal space infections may quickly spread into the mediastinum (Fig. 1-58), which is a serious complication with high mortality and morbidity. Immediate surgical drainage of a retropharyngeal abscess may be indicated. Imaging plays an important role in determining the indication and access route for surgical drainage. Vascular complications of infection include spasm, arteritis and mycotic aneurysm of the internal carotid artery, and thrombophlebitis of the internal jugular vein (Lemierre syndrome). The latter condition was more common in the preantibiotic era, with rare cases still encountered in the present day. On postcontrast CT or MR imaging, a filling defect in the internal jugular vein with enhancement of the vessel wall can be demonstrated. Early diagnosis is critical, as the untreated thrombus can propagate systemically, resulting in septicemia and pulmonary emboli/infarcts.

Figure 1-58 Retropharyngeal abscess. A, Abscess (arrow) is demonstrated within the lateral retropharyngeal node (of Rouvière) in a young patient presenting with painful swallowing. Note associated smaller caliber of the cervical left internal carotid artery secondary to vasospasm (arrowhead), common in pediatric patients with intranodal abscess. B, Sagittal reformat demonstrates associated retropharyngeal fluid extending to the C5 level. Lack of peripheral enhancement suggested that this fluid was reactive, rather than a discrete abscess. Because the patient’s condition did not improve with intravenous antibiotics, incision and drainage was required.

In the setting of peritonsillar and retropharyngeal infections, careful examination of the airway is vital. Prophylactic intubation should be considered if the airway is significantly compromised.

Prevertebral Infection/Inflammation

Prevertebral collections in the neck typically occur in the setting of discitis and osteomyelitis of the cervical spine (Fig. 1-59). An associated prevertebral abscess can progress in size to potentially compromise the airway. In these cases, urgent intubation and surgical drainage may have to be considered. Retropharyngeal inflammation is often seen secondary to prevertebral space infection. Diagnosing the primary site of infection is important for appropriate patient management.

Figure 1-59 Discitis/osteomyelitis secondary to intravenous drug use. A, Sagittal fat-suppressed T2-weighted image shows abnormally hyperintense signal in the C5-C6 disc and adjacent vertebral bodies and a large associated prevertebral process (arrow). B, Postgadolinium axial T1-weighted image shows enhancement of prevertebral phlegmon (arrowhead) and circumferential epidural extension (arrow) resulting in spinal cord compression.

Salivary Gland Disorders

Inflammation of the submandibular or parotid glands demonstrated by glandular enlargement and surrounding fat stranding could be related to distal obstruction in Wharton’s or Stensen’s ducts, respectively, often due to obstructing calculus. Of the salivary glands, the submandibular gland is most prone to sialolithiasis, due in part to stasis from the descending then ascending course of its duct and the relatively more alkaline nature of its glandular secretions. Bacterial and viral infections can also result in salivary gland inflammation. Bacterial inflammation is most commonly seen in debilitated patients or neonates, caused by localized Staphylococcus aureus infection, and is typically unilateral. Viral inflammation occurs in children, tends to be related to systemic infection, most commonly mumps, and is usually bilateral. The inflamed gland is enlarged, hyperenhancing, with stranding of adjacent fat reflecting cellulitis, or may contain a discrete abscess (Fig. 1-60). Enlarged heterogeneous parotid glands with solid and cystic changes may reflect lymphoepithelial lesions seen in the setting of HIV disease. Similar lesions can be seen in Sjögren syndrome and other autoimmune disorders. In the chronic phase of this condition, atrophy of the parotid gland with parenchymal calcifications can be seen.

Figure 1-60 Salivary gland inflammation. A, In this patient with acute right facial swelling, computed tomography coronal reformat demonstrates an enlarged, hyperenhancing right parotid gland (arrow) with stranding of the subcutaneous fat. B, Axial image with bone window/level settings confirms a sialolith (arrow) within the gland.

Thyroid-related Disorders

When inflamed, the thyroid gland can appear diffusely enlarged, or relatively hypoenhancing, and may demonstrate an associated fluid collection. Suppurative thyroiditis is rare due to its iodine content. In such cases, pyriform sinus fistula, or third or fourth branchial pouch anomaly, should be considered as an underlying etiology. Most involve the left lobe of the thyroid. Such patients require a barium swallow after completion of antibiotic therapy to identify the fistulous tract.

Thyroglossal duct cyst is a remnant of the thyroglossal duct and can be found in a midline or paramidline location between the foramen cecum at the base of the tongue and the thyroid bed. The cyst is classically embedded within the strap muscles, which helps distinguish this lesion from other midline neck masses such as dermoid and epidermoid. While these cysts are found most commonly at the level of the hyoid bone, they can also be suprahyoid or infrahyoid in location. If the cystic lesion exhibits peripheral rim enhancement, superinfection should be suspected in the appropriate clinical setting. The cyst is usually lined by respiratory or squamous epithelium and may occasionally contain thyroid tissue; this carries the potential for development of malignancy, most commonly papillary carcinoma. For this reason, any enhancing soft tissue within a thyroglossal duct cyst should be reported, and surgical excision should be strongly considered.

Branchial Cleft Cysts

Branchial cleft cysts are congenital epithelial-lined cystic lesions in the neck originating anywhere from the level of the mandible (first branchial cleft) to the supraclavicular region (fourth branchial cleft). These can become superinfected and present as an acutely enlarging neck mass. The second branchial cleft cyst is most common, present in the submandibular region, anteromedial to the sternocleidomastoid muscle and anterolateral to the carotid vessels (Fig. 1-61). An infected branchial cleft cyst will demonstrate peripheral rim enhancement. Necrotic infectious and metastatic lymphadenopathy may present similarly and should be considered in the differential diagnosis, particularly in adult patients.

Figure 1-61 Second branchial cleft cyst. This second branchial cleft cyst is in the classic location, that is, the submandibular region, anteromedial to the sternocleidomastoid muscle and anterolateral to the carotid vessels.

Superficial Abscesses

Multiple bilateral superficial neck abscesses can be seen in intravenous drug abusers or “skin poppers.” Broken needles may occasionally be found. Following routine operations on the neck, fluid collections may develop in the superficial or deep soft tissues. In these cases, careful evaluation of adjacent vascular structures is warranted to assess for potential injury (pseudoaneurysm, dissection, thrombosis, or occlusion) or extension of inflammation (Fig. 1-62).

Figure 1-62 Neck abscess. A, In this patient who developed an infected graft soon after carotid endarterectomy, post-contrast axial CT image demonstrates organized fluid collection (arrowhead) adjacent to abnormal enhancing inflammatory tissue surrounding the carotid bifurcation on the right (arrow). B, Slightly inferiorly, a fistulous tract between the collection and the inflammatory tissue is identified (arrow). C, Coronal reformat demonstrates that the inflammatory tissue encasing the carotid bifurcation extends superiorly along the internal carotid artery, causing focal critical stenosis.

Lymphadenopathy

Cervical lymphadenopathy can present clinically as diffuse neck swelling, and may be related to an inflammatory process or underlying neoplasm. The presence of necrosis within normal-sized or enlarged cervical lymph nodes can be due to intranodal abscess formation but should raise suspicion for metastatic disease, especially from squamous cell carcinoma. If metastatic, the primary tumor typically arises from the base of the tongue, tonsils, nasopharynx, and pyriform sinus, or from papillary thyroid cancer. This form of thyroid cancer often affects relatively young women. Certainly, necrotic adenopathy can be seen in the setting of infection such as tuberculosis and atypical mycobacterial infections such as Mycobacterium avium-intracellulare complex, particularly in immunocompromised patients. Large conglomerations of necrotic lymph nodes can be seen in these settings. Careful evaluation of the lung apices for an inflammatory process is necessary, as this can support the diagnosis of tuberculous adenitis. Imaging can play an important role in raising the possibility of tuberculosis in unsuspected patients. In such a case, the referring service should be notified immediately, since isolation may be required. Interestingly, calcifications related to tuberculosis are not typically found in the cervical lymph nodes.

Croup

In the pediatric patient population, laryngotracheobronchitis, or “croup,” presents clinically with a characteristic cough. The condition usually occurs in children younger than 3 years of age, and is thought to be most often caused by parainfluenza virus, although other respiratory viruses and Mycoplasma have also been implicated. Croup is the most common pediatric infection causing stridor, accounting for approximately 15% of clinic and ED visits for pediatric respiratory infections. The cough is a consequence of subglottic edema and manifests classically on plain radiographs with symmetric, subglottic narrowing, the so-called “steeple” sign (Fig. 1-63). Coronal CT reformats can now replicate this appearance, although cross-sectional imaging is typically not necessary for this particular indication.

Figure 1-63 Croup. In this patient who presented acutely with barking cough, frontal radiograph of the neck demonstrates the classic “steeple” sign (arrow) representing concentric subglottic edema.

Epiglottitis

Epiglottitis is now less commonly seen in the pediatric emergency room setting, due to childhood immunization against the offending agent, H. influenzae. However, epiglottitis can occur at any age, and there has been a recent increase in incidence in the adult population, which is often underappreciated. Patients who have not been immunized can present with acute airway compromise and may require urgent intubation. On lateral radiograph, the classic “thumb” (or “thumbprint”) sign is produced by the thickened, inflamed epiglottis (Fig. 1-64). The clinical picture and radiographic imaging are usually so characteristic that cross-sectional imaging is generally unnecessary. CT imaging can provide greater diagnostic detail and can demonstrate the inflamed epiglottis along with symmetrically thickened and inflamed aryepiglottic and pharyngoepiglottic folds. However, management should be based on clinical and radiographic findings, and obtaining a CT examination might delay proper treatment.

Figure 1-64 Epiglottitis. In this young child who presented with difficulty breathing, lateral neck radiograph demonstrates classic “thumb(print)” sign (arrow) of the inflamed epiglottis.

Angioedema

Although not due to infection, angioedema is included in this section on airway disorders. It can be hereditary or acquired and may be idiopathic, manifesting as acute narrowing of the airway, possibly resulting in airway compromise. Angioedema due to allergic reactions is often associated with urticaria. While clinical diagnosis should be straightforward, CT imaging can be useful for further evaluation. Imaging can show diffuse mucosal and submucosal swelling involving the hypopharynx and larynx, with infiltration of the subcutaneous fat and deep tissue planes of the neck.

Sinus and Orbital Infections

Uncomplicated acute sinusitis is typically clinically diagnosed and managed. On imaging, findings of acute sinusitis are not very specific. An air–fluid level within a sinus can suggest acute sinusitis; however, lack of this finding does not mean a patient does not have acute sinusitis. Occasionally, hyperdense opacification in the paranasal sinuses can be seen; the hyperdensity can reflect hemorrhage related to trauma, trapped proteinaceous debris, or fungal infection. Fungal infection is an important diagnostic consideration, since steroids probably should be incorporated into the treatment regimen if the cause is related to allergic disease (Fig. 1-65).

Figure 1-65 Sinusitis. A, Mucosal thickening in the left maxillary sinus is accompanied by an air–fluid level due to acute sinusitis in this patient presenting with sinus pressure, pain, and headache. B, In a different patient, coronal reformat in soft tissue window/level settings demonstrates hyperdense material in most of the paranasal sinuses due to allergic fungal sinusitis.

When more advanced sinus disease is of concern, imaging plays a more definitive role. Complicated sinus disease should be clinically suspected if the patient presents with visual changes, altered mental status, or seizures. Initial imaging for workup of complicated sinusitis can begin with CT. At our institution, axial images through the facial bones are routinely acquired at 1.25-mm intervals with coronal and sagittal reformats using bone and soft tissue algorithms. If there is concern for intracranial or orbital extension of infection, contrast-enhanced CT using similar imaging parameters can provide additional critical information. If there is clinical concern for intracranial extension, the entire brain should be imaged. Since complicated sinus infection usually warrants close follow-up imaging, MR is the preferred imaging modality to minimize radiation exposure, especially in the pediatric setting. Typical brain MR protocol includes sagittal T1, axial FLAIR, fat-suppressed T2, gradient echo, and diffusion-weighted images, followed by multiplanar postcontrast T1 images of the brain. If orbital extension is of clinical concern, high spatial resolution T2 images with and without fat suppression through the orbits, and axial and coronal pre- and postcontrast T1-weighted images, can provide excellent diagnostic detail.

CT is particularly useful in establishing the integrity of paranasal sinus walls and can effectively demonstrate areas of bony dehiscence. Intracranial or orbital spread of infection can occur directly through areas of bony dehiscence or indirectly by perivascular extension, most commonly secondary to frontal or ethmoid sinus disease. Perivascular spread more commonly occurs in the pediatric setting. Intracranial extension is usually seen in the setting of frontal sinus infection, with involvement of the anterior cranial fossa and frontal lobes (Fig. 1-66). Imaging can demonstrate associated dural enhancement, epidural or subdural collections, and meningoencephalitis with abscess formation. There may be concomitant swelling of the soft tissues of the forehead, known as Pott’s puffy tumor (Fig.1-67). This does not imply neoplastic involvement, but rather describes osteomyelitis with extracranial soft tissue abscess formation. The presence of pachymeningeal enhancement does not necessarily imply that brain parenchyma is involved, and may only reflect dural reaction. Epidural and subdural collections can be demonstrated on either CT or MR as extra-axial fluid, possibly compressing the subjacent brain parenchyma. Subdural collections can cross sutures and generally maintain a crescentic shape, whereas epidural collections are restricted by sutures and may have a lentiform (biconvex) shape. While a reactive subdural effusion may be associated with smooth pachymeningeal enhancement, an infected subdural or epidural collection can demonstrate restricted diffusion and thickened, more irregular dural enhancement on MR. Leptomeningeal involvement is demonstrated as curvilinear enhancement extending into sulci. This may be accompanied by FLAIR hyperintensity in a corresponding distribution, which is a sensitive but nonspecific finding. Parenchymal involvement can be demonstrated by FLAIR hyperintensity and enhancement. Frank abscess formation can be demonstrated by CT or MR as a peripherally enhancing fluid collection. Restricted diffusion in the collection can support this impression.

Figure 1-66 Sinusitis—subdural empyema and infarct. A, Axial T2-weighted image shows proteinaceous material within the frontal sinuses. B, Post-gadolinium coronal T1-weighted image demonstrates associated subdural abscess and leptomeningeal enhancement.

Figure 1-67 Sinusitis—Pott’s puffy tumor and epidural abscess. A, Axial CT image shows opacification of the frontal sinuses and overlying soft tissue swelling. A tract from the anterior table of the frontal sinus (arrow)and adjacent fluid collection (arrowhead)are shown. B, Axial T2-weighted image demonstrates abnormal hyperintensity of marrow in the frontal bone (arrowheads) and overlying soft tissue swelling, including small scalp fluid collection (arrow). C,Postgadolinium sagittal T1-weighted image shows epidural abscess (arrow) and fluid-filled paranasal sinuses with inflamed mucosa (arrowhead).

While posterior ethmoid disease can also lead to intracranial involvement, more commonly, untreated ethmoid sinusitis can extend into the medial aspect of the orbit (Fig. 1-68). Infection can spread in a subperiosteal fashion along the medial wall of the orbit, appearing as an elliptical shaped phlegmon or fluid collection. This may cause displacement of extraocular muscles. Without treatment, the phlegmon or abscess can then break through the periosteum and extend directly into the orbit and into the extraocular muscles. Depending on the size of the inflammatory process, there can be displacement of extraocular muscles and the globe, along with distortion, stretching, and compression of the optic nerve. Such findings constitute an ophthalmologic emergency, as prolonged mass effect on the optic nerve can result in permanent blindness.

Figure 1-68 Sinusitis—complications. A, Axial CT in a young patient with mild acute proptosis demonstrates opacification of the right ethmoid air cells with abnormal soft tissue in the medial aspect of the right orbit (arrowhead), displacing the medial rectus muscle. Normally, this space should contain orbital fat, but in this case, there has been perivascular extension of inflammation into the orbit; note that the lamina papyracea is intact. B, Coronal T1-weighted image demonstrates extensive collection extending from the sinuses (arrowhead) into the orbit (arrow), displacing extraocular muscles and optic nerve inferiorly. C, Postgadolinium coronal T1-weighted image shows that much of the abnormal soft tissue in the orbit (arrow) is due to subperiosteal abscess (arrowhead).

Other possible critical complications of orbital infection include extension of infection and involvement of contents of the orbital apex (cranial nerve II), superior orbital fissure (cranial nerves III, IV, V1, VI, and superior orbital vein), and inferior orbital fissure (V2, infraorbital nerve). Idiopathic inflammation involving the cavernous sinus, known as Tolosa-Hunt syndrome, can manifest clinically as palsies of the cranial nerves that traverse the cavernous sinus, namely, III, IV, V1, V2, and VI.

Venous sinus thrombosis can result from ethmoid or sphenoid sinus or orbital infection, and careful attention to the cavernous sinuses on postcontrast images is necessary. Facial soft tissue, dental, and ear infections are other possible causes. Direct signs of septic cavernous sinus thrombosis, also termed cavernous sinus thrombophlebitis (CST), include an enlarged sinus with a convex border, and a single large or multiple irregular filling defect(s). Normal neural structures and intracavernous fat deposits should not be mistaken as true filling defects. Indirect signs include dilation of the superior ophthalmic vein, exophthalmos, soft tissue edema, thrombi in the superior ophthalmic vein, superior and inferior petrosal, or sigmoid sinuses, and decrease in caliber of the internal carotid artery. Thin-section, contrast-enhanced CT with coronal reformats may be equivalent to MR for the detection of these findings. However, once venous sinus thrombosis is suspected, MR imaging of the brain may confirm the diagnosis and evaluate for possible complications of meningitis, subdural empyema, cerebritis, and even pituitary necrosis. Postcontrast T1 coronal and axial images are generally sufficient to make the diagnosis. Contrast-enhanced MR venography may also offer support in diagnosis. (Phase contrast MR venography is generally limited for this evaluation. Contrast-enhanced CT [CT venography] and MR with thin slices are generally more helpful to diagnose CST.) Prior to the antibiotic era, CST was almost always fatal. In the modern era, mortality in the range of to 30% may still be expected. In addition to antibiotics, early institution of anticoagulant therapy may reduce mortality. Morbidity may result from cranial nerve dysfunction including blindness, pituitary insufficiency, and hemiparesis.

Ear Infections

Much like uncomplicated paranasal sinus disease, external and middle ear infections can be diagnosed and followed clinically. Acute and chronic otomastoiditis can occasionally be picked up on imaging and should be reported since these conditions may be clinically unsuspected (Fig. 1-69). If there is clinical concern for a more complicated infectious process, CT and MR can be very useful adjuncts in diagnosis. CT imaging of the temporal bone includes the entire auditory system. At our institution it is performed with overlapping 0.625-mm-thick sections with coronal and sagittal reformats in bone and soft tissue algorithms. If there is clinical concern for intracranial involvement, contrast-enhanced CT using the same imaging parameters can provide additional diagnostic detail. MR imaging can be particularly useful in the setting of cranial nerve involvement. Our technique includes high spatial resolution T2, and pre- and postcontrast axial and coronal images from the level of the orbits to the base of the brain, in addition to routine brain imaging.

Figure 1-69 Mastoiditis. A, Opacification of mastoid air cells without bony changes in a patient with symptoms of acute mastoiditis. B, Opacification of the middle ear with sclerotic changes of the mastoid bone in a patient with a history of chronic otomastoiditis.

Malignant otitis externa is typically seen in diabetic and immunocompromised patients, and is a rare but serious complication of external ear infection. The inflammation can quickly progress to involve the entire ear, external auditory canal, and middle and inner ear structures. Evaluation of the stylomastoid foramen for extension of inflammation with fat stranding is important, particularly in patients with facial nerve symptoms. Associated osteomyelitis is seen as a locally aggressive destructive process of the temporal bone. Urgent treatment is indicated usually with surgical débridement, as intracranial extension of infection can develop rapidly. Cranial nerve involvement from untreated middle ear infection can occur secondarily by spread of inflammation into the cavernous sinus, typically involving cranial nerve V within Meckel’s cave and cranial nerve VI within the cavernous sinus (Gradenigo syndrome) (Fig. 1-70). Additional cranial nerve involvement can quickly ensue. Intracranial extension can result from dehiscence of the temporal bone, with direct spread into the middle cranial fossa. As with complicated paranasal sinus infection, extension into the middle cranial fossa can result in epidural abscess, subdural empyema, meningoencephalitis, or brain abscess. Transverse sinus, sigmoid sinus, and jugular vein thrombosis are other possible complications (Fig. 1-71).

Figure 1-70 Gradenigo syndrome. A, In this patient with mastoiditis and facial pain, axial fat-suppressed T2-weighted image demonstrates bright signal in the right mastoid air cells. Axial (B) and coronal (C) postgadolinium T1-weighted images demonstrate abnormal enhancement within Meckel’s cave on the right side. This patient complained of new facial pain in the setting of chronic mastoid disease.

Figure 1-71 Mastoiditis—septic thrombophlebitis. A, Initial noncontrast CT in patient with headache demonstrates chronic right otomastoiditis. B, Based on suspicious findings on the noncontrast exam, a contrast-enhanced CT study was performed, demonstrating filling defect within the right transverse sinus. C, T2-weighted image shows hyperintense subperiosteal abscess (arrow). There is also T2 hyperintense signal in the expanded sigmoid sinus (arrowhead) rather than the expected flow void. D, Maximal intensity projection reformat from three-dimensional phase contrast MR venography demonstrates lack of flow-related signal in the right transverse and sigmoid sinuses and right internal jugular vein, consistent with venous sinus thrombosis.

Complicated Dental Disease

Periapical lucencies around individually infected teeth are often incidentally detected on routine CT images of the mandible and maxilla performed for other reasons. Occasionally, the infection can progress to the medullary bone, eventually breaking through the overlying buccal or lingual cortex. In these cases, this sinus tract acts as a conduit for spread of infection into the adjacent soft tissues (Fig. 1-72). With time, an abscess can develop, and the patient may present to the emergency room with pain, swelling, and elevated white blood cell count. Fluid collections in the face should therefore be carefully evaluated for a possible dental source, since the soft tissue infection will not be cured by drainage alone. Rapid progression of infection into other spaces, including the orbit and intracranial compartment, is a serious and potentially complication. Ludwig’s angina is characterized by extensive facial swelling and hardened cellulitis centered in the submandibular space, classically bilaterally, related to periodontal disease (Fig. 1-73).

Figure 1-72 Perimandibular abscess. A, In this patient with right facial pain and swelling, contrast-enhanced CT demonstrates a fluid collection (arrow) and subcutaneous stranding along the buccal surface of the right mandible. B, Within the mandible at the same level is a periapical lucency related to a molar tooth with a defect consistent with a sinus tract.

Figure 1-73 Ludwig’s angina. This patient presented with massive neck swelling and on imaging the inflammation extended from the upper face to the axilla. Extensive emphysema throughout the neck was of concern for necrotizing fasciitis. On surgical exploration, the source of inflammation was suspected to be dental disease, but the dentition was so poor and inflammation so extensive that the causative tooth could not be determined. Cultures from the neck grew mixed flora, including fusobacterium, commonly found in oral flora.

In the case of a suspected dental-related facial abscess, maxillofacial CT with thin (1.25 mm) axial sections and coronal and sagittal reformats in bone and soft tissue algorithms should be performed. Intravenous contrast-enhanced exam increases the sensitivity for detection of abscess based on peripheral rim enhancement. CT is particularly useful in identifying areas of cortical disruption of the mandible or maxilla, whereas MR may identify the fluid collection but could easily miss the source of the infection, namely, the affected tooth, due to artifacts inherent to MR imaging.

Summary: Head and Neck

There is a wide variety of pathology that may present as emergencies in the head and neck region. While many conditions can be diagnosed and managed clinically, imaging plays an important role in the diagnosis and management when more complicated disease and acute traumatic injuries are encountered. A clear understanding of the history and physical findings based on communication between radiologist and referring clinician will guide selection of the most appropriate imaging modality and protocol. As with all other parts of the body, a working knowledge of the anatomy and variants as well as the disorders specific to the region is necessary to provide excellent patient care.