Edema

Cerebral edema is an abnormal accumulation of water within brain tissue that can be localized or diffuse. Three types of edema have been described:

Except for location, the CT and MRI appearance of all types of edema is similar. Increased water content appears dark on CT because of hypodensity. It also appears dark on T1-weighted imaging (T1WI) but bright on T2-weighted imaging (T2WI) sequences, including fluid-attenuated inversion recovery (FLAIR) studies in which CSF in the ventricles, cisterns, and arachnoid spaces is made to appear dark. Vasogenic edema within the white matter extends along fiber tracts, creating “fingers” that extend toward the cortical gray matter (Figure 40-1). This pattern has a nonvascular distribution and is associated with mass effect. Cytotoxic edema can involve gray and white matter, follows a vascular distribution when associated with ischemic injury, and produces less mass effect for its size (Figure 40-2). DWI can distinguish between the increased diffusivity of vasogenic edema and the resticted diffusivity of cytotoxic edema. Interstitial edema may be limited to a narrow rim that abuts the ventricular wall and fades gradually into the surrounding white matter and is best seen on MRI, particularly with FLAIR sequences.²⁰ Engorgement caused by increased arterial or venous CBV, often localized when associated with an arteriovenous dural fistula, can mimic edema on routine imaging studies but is apparent on cerebral perfusion studies.²¹

Figure 40-1 Vasogenic edema in glioblastoma.

Non-contrast-enhanced axial CT scan (A), axial T1-weighted MRI scan (B), and axial T2-weighted MRI scan (C) all demonstrate an area of edema (E). Edema extends along white matter fibers (dots), with normal gray matter interposed. Axial T1-weighted MRI scan following contrast enhancement (D) demonstrates the enhancing tumor nidus (arrow), distinct from surrounding edema. Subfalcine herniation is also demonstrated on these images by displacement of the falx (curved arrows).

Figure 40-2 Cytotoxic edema and acute infarct.

Axial non-contrast-enhanced CT scan demonstrates an area of decreased density (asterisk) involving the left middle cerebral artery territory. Gray and white matter structures are involved, and there is little mass effect.

Hemorrhage

Intracranial hemorrhage may be parenchymal or extraaxial (epidural, subdural, or subarachnoid) in location. Parenchymal hemorrhage can be traumatic in origin but in adults is more likely nontraumatic, associated with an underlying lesion such as a tumor or vascular malformation, a vasculopathy such as vasculitis or cerebral amyloid angiopathy, or a systemic disease such as hypertension. Extraaxial hemorrhages are most often due to trauma, but subarachnoid hemorrhage also is commonly seen with aneurysm rupture.

The imaging appearance of hemorrhage depends on the stage of clot formation and lysis, location, and the degree to which it is mixed with other fluids. On CT, hemorrhage may be isodense to brain parenchyma and difficult to visualize in the hyperacute stage, but it typically becomes hyperdense within several hours (Figure 40-3, A) before again becoming isodense over days to weeks and then hypodense over several weeks (Table 40-1). Acute hematomas may continue to appear isodense in the acute stage in anemic patients with a hemoglobin (Hb) below 8 to 10 g/dL or in patients with a coagulopathy who fail to produce clot retraction.^22,23 The final CT appearance of resolved hemorrhage may show no residual abnormality or demonstrate a focus of low attenuation or calcification.

Figure 40-3 Hemorrhage.

Axial CT image (A) demonstrates a large area of acute hemorrhage (H) in right temporal lobe. T1-weighted (B) and T2-weighted (C) MRI scans demonstrate the hemorrhage in various stages of breakdown. Center of lesion is dark on T1- and T2-weighted images, indicating oxyhemoglobin (1). Intermediate zone is bright on T1-weighted image and gray on T2-weighted image, indicating intracellular methemoglobin (2). Outer rim is bright on both T1-and T2-weighted images, indicating extracellular methemoglobin (3).

On MRI, the evolving appearance of a hemorrhage is largely explained by Hb having different paramagnetic properties as it is deoxygenated and metabolized. In the hyperacute to acute stages, diamagnetic oxyhemoglobin is predominant and appears slightly hypo- to isointense on T1WI and iso- to hyperintense on T2WI. As Hb becomes deoxygenated, it becomes paramagnetic and very hypointense on T2WI. In the subacute stage, Hb breakdown to methemoglobin begins peripherally and advances toward the center of the clot. Intracellular methemoglobin appears hyperintense on T1WI and hypointense on T2WI. As red blood cells lyse and release methemoglobin into the extracellular space, its signal becomes hyperintense on T1WI and T2WI. In the chronic stage, beginning within 2 weeks and lasting for years, methemoglobin undergoes phagocytic degradation to hemosiderin, which appears hypointense on T1WI and T2WI.⁷ The evolution of a hematoma is influenced by many factors, and there may be simultaneous overlap of two or more of these stages (see Figure 40-3, B and C). The widespread use of the gradient-recalled echo (GRE) sequence, and the increasing use of susceptibility-weighted imaging (SWI) sequences, has greatly increased the sensitivity of MRI for extravasated blood.²⁴

Most intraparenchymal hematomas are associated with a surrounding area of vasogenic edema and evolve somewhat more quickly (owing to higher tissue thromboplastin concentration and lower oxygen tension) than extraaxial blood collections. Intraparenchymal hematomas expand significantly, usually within 3 hours from onset, in about one-third of patients,²⁵ and contrast extravasation into the hematoma on CT is predictive of expansion.²⁶ Vasogenic edema surrounding an intraparenchymal hematoma can also expand over several days, causing a significant increase in mass effect.

Mass Effect, Shift, and Herniation

Cerebral lesions may lead to brain herniation, either as a direct result of lesion growth, as with tumor growth or hematoma expansion, or secondary to intralesional cytotoxic edema, perilesional vasogenic edema, or obstructive hydrocephalus.²⁷ Two relatively fixed dural partitions are present within the skull and create compartments across which the brain may herniate. The falx cerebri separates the cerebral hemispheres, and the tentorium cerebelli separates the cerebral hemispheres from the posterior fossa structures. Herniation is described in terms of location.

Subfalcine herniation occurs when the medial surface of a hemisphere, usually the cingulate or supracingulate gyrus, is compressed against and displaced beneath the falx. With CT or MRI, early signs may appear as compression or distortion of the lateral ventricles (see Figure 40-1). Later stages are recognized by deviation of the falx, identification of the hemispheric structures that are crossing the midline, and ischemia from compression of the anterior cerebral artery.

Transalar herniation occurs when a mass displaces brain tissue across the ridge of the greater sphenoid wing. Ascending transalar herniation refers to a large temporal lobe mass displacing brain above the sphenoid ridge and into the anterior cranial fossa. Descending transalar herniation refers to a large frontal lobe mass displacing brain below the sphenoid ridge and into the middle cranial fossa. Imaging studies may identify displacement of the sylvian portion of the middle cerebral artery (MCA), which may lead to ischemia and infarction within the MCA territory.

Masses arising on either side of the tentorium can result in transtentorial herniation. Descending transtentorial herniation involves a supratentorial mass pushing the medial temporal lobe through the incisura. On CT or MRI, the herniated brain pushes against and rotates the brainstem. This produces widening of the ipsilateral brainstem cistern and effacement of the contralateral cistern (Figure 40-4). Associated findings may include dilatation of the contralateral temporal horn secondary to ventricular trapping. Ascending transtentorial herniation is caused by an infratentorial mass displacing the pons, vermis, and adjacent portions of the cerebellar hemispheres upward through the incisura. On CT and MRI, the brainstem cisterns are symmetrically effaced as the cerebellar vermis bulges up through the incisura. This is often associated with acute hydrocephalus caused by compression of the cerebral aqueduct.

Figure 40-4 Right descending transtentorial herniation in patient with large right parietal subdural hematoma.

Axial non-contrast-enhanced CT scan of head at level of midbrain shows that ipsilateral subarachnoid cistern is widened (arrow), and contralateral subarachnoid cistern is obliterated because of brainstem rotation. Left temporal horn is also dilated (asterisk), indicating trapping of left lateral ventricle.

Tonsillar herniation occurs when the cerebellar tonsils are pushed through the foramen magnum. This results in medullary compression and dysfunction of vital respiratory and cardiac control centers. Sagittal MRI is the preferred modality for demonstrating tonsillar herniation and the secondary effects on the brainstem.

Traumatic Brain Injury

Noncontrast head CT continues to be the primary modality for the initial evaluation of patients with traumatic brain injury (TBI).²⁸ Its advantages include fast examination time, wide availability, fracture detection, lack of contraindications, and high accuracy. Although MRI is more sensitive in detecting intracranial injuries, it is limited by longer examination times, need for sedation in uncooperative patients, and difficulties with monitoring potentially hemodynamically unstable patients. Once patients have been stabilized, MRI becomes the modality of choice for fully elucidating the nature and extent of the injury and for informing prognosis.²⁹

Injury to brain parenchyma may result in contusion, axonal (shear) injury, or hematoma. Contusions are caused by the direct impact of parenchyma against bone and are most common along the gyral surface of the frontal and temporal lobes. Larger contusions may contain petechial hemorrhage and appear as ill-defined heterogeneous lesions with little or no mass effect. Edema and mass effect may increase in the first 48 hours after TBI, making these lesions more evident on imaging studies.

Shear injuries are secondary to rotational forces that produce tears in axonal fibers and are most common within the white matter (subcortical white matter, corpus callosum, internal capsule, and brainstem). Except for location, the imaging characteristics of nonhemorrhagic contusions and shear injuries are similar. Initial studies may be normal or demonstrate small foci of edema. Shear injuries may be apparent on MRI, particularly with the use of (1) susceptibility-weighted imaging (SWI), which is exquisitely sensitive to the microhemorrhages associated with moderate shear injuries; (2) DWI, which may show cytotoxic edema from more severe shear injuries; and (3) MRS, which may show elevations of choline (Cho) and myoinositol (mI) and decreases in N-acetylaspartate (NAA) proportional to injury severity.

Damage to the brain coverings may lead to hemorrhage into the epidural, subdural, and subarachnoid (and, by extension, intraventricular) spaces. On CT, intraventricular and subarachnoid hemorrhage is identified by replacement of the normal low-density CSF by high-density blood. When subtle, subarachnoid hemorrhage can be mistaken for generalized edema, with loss of the basal cisterns. Subdural hematomas typically appear as crescentic mixed or hyperdense collections that cross suture lines but not dural attachments (Figure 40-5, A). Epidural hematomas typically appear as biconvex hyperdense collections that cross dural attachments but not suture lines (see Figure 40-5, B). With rapid accumulation of blood, unretracted semiliquid clot may be present. In this situation, CT demonstrates hypodense areas within the hyperdense hematoma, the so-called swirl sign.³⁰ Distinction between epidural and subdural hematomas is important, because epidural hematomas often have an arterial source, expand rapidly, and require emergent drainage to avoid herniation.³¹

Figure 40-5 Subdural and epidural hematoma.

A, Axial CT scan of head demonstrates a mixed-density subdural hematoma along right frontoparietal lobes. Mixed-density appearance is most likely due to presence of unretracted semiliquid clot. B, Axial CT scan of head demonstrates a left biconvex hyperdense collection that is classic for epidural hematoma. A fracture (arrow) can also be identified.

Abusive head trauma (AHT) is a significant cause of neurodevelopmental morbidity and mortality in children younger than 2 years old.³² Mechanisms that have been proposed include blunt trauma, axonal shearing from shaking, and secondary ischemic injury from strangulation, arterial dissection, suffocation, or brainstem injury leading to respiratory arrest. Intracranial injuries commonly encountered include skull fracture, subdural hematoma, subarachnoid hemorrhage, and shear injuries. Subdural hematoma is regarded as one of the most characteristic CNS lesions encountered in the “shaken baby” syndrome. In fact, subdural hematomas in young children are more often associated with AHT than with accidental trauma.³² The CT appearance of AHT in children is similar to that in adults. However, subdural hematoma is more common along the posterior interhemispheric fissure and appears as increased attenuation along the falx. Other common locations include the anterior interhemispheric, tentorial, and parieto-occipital regions. MRI can determine the age of the blood products and provide an estimate of when the hemorrhage occurred, as discussed earlier. Coexistence of blood products of different ages (Figure 40-6) is suggestive of recurrent bleeding and repeated abuse but must be interpreted with great caution.⁷

Figure 40-6 Abusive head trauma.

Axial T1- (A) and T2-weighted (B) MRI scans of an infant reveal bilateral subdural blood collections of different ages. Right collection shows blood in the late subacute phase (2–4 weeks old), and left shows blood in the chronic phase (>1 month). This finding is almost proof positive of repeated abuse.

Vascular Lesions

Ischemia, Hypoxia, and Infarct

Although CT demonstrates only about half of infarcts within the first 48 hours, it remains the imaging modality of choice in the acute evaluation of patients with transient or persistent focal neurologic deficits that may be associated with cerebral ischemia, because rapid exclusion of a hemorrhagic etiology is critical in determining whether a patient can be treated with thrombolytic agents.³³ CT can in some cases confirm the thromboembolic etiology of an ischemic stroke by showing subtle cerebral edema in a vascular distribution or by showing hyperdense clot within a thrombosed artery. It can also be immediately helpful in demonstrating mass lesions such as tumors, infections, and vascular lesions that can produce symptoms that mimic stroke and may require emergent surgical treatment.⁵ Small lacunar infarcts and infratentorial strokes are more difficult to visualize by CT.³⁴

The CT appearance of an ischemic injury evolves over time. In the hyperacute stage (first 24 hours), the CT scan may be normal or demonstrate a subtle decrease in density and loss of gray-white differentiation (Figure 40-7). An artery obstructed by thromboembolism may appear hyperdense. During the acute stage (within the first week), the infarct becomes more pronounced owing to the mass effect and decreased density related to cytotoxic edema (see Figure 40-2). The infarct is better defined, involves gray and white matter, and corresponds to a known vascular territory. During the subacute stage (1–3 weeks), the edema and mass effect begin to resolve. Chronic infarcts demonstrate parenchymal replacement, with well-defined, sharply marginated zones of cystic encephalomalacia and gliosis. The infarct behaves like a contracting rather than an expanding mass.

Figure 40-7 Acute infarct.

Axial non-contrast-enhanced CT images obtained at level of temporal lobe (A) and through level of basal ganglia (B) demonstrate area of low density involving gray and white matter of right hemisphere. There is loss of gray-white matter differentiation, especially noticeable in region of basal ganglia (asterisk, B). Compare right and left sides. High density is identified within right middle cerebral artery (arrow, A), representing clot. Axial non-contrast-enhanced CT scan obtained 48 hours later (C) demonstrates marked edema involving territories of right, middle, and posterior cerebral arteries. Note sparing of right anterior cerebral artery territory (asterisk, C).

The MRI appearance of an ischemic infarct also evolves in a predictable fashion (Figure 40-8). Nonhemorrhagic infarcts begin with subtle increased signal intensity on T2WI and minimal changes on T1WI. Subtle findings include stagnation of blood flow (arterial enhancement) and swelling of the involved gyri. DWI (Figure 40-9) can show cytotoxic edema within minutes of the onset of a stroke, and the intensity of the abnormal signal is typically maximal at 3 to 5 days and then gradually fades over another 1 to 2 weeks. Because DWI shows directionally restricted water movement as a bright signal but also shows bright signal in areas that are bright on T2WI (T2 shine through), the presence of cytotoxic edema is best evaluated by the apparent diffusion coefficient (ADC) map, in which brain regions with fully restricted water diffusion appear darker than surrounding brain.

Figure 40-8 Infarct.

Axial T1-weighted (A) and T2-weighted (B) MRI scans of patient being evaluated for stroke. Initial CT scan (not shown) was normal. MRI demonstrates an area of cytotoxic edema involving distal left middle cerebral artery territory. Edema is hypointense to brain on T1-weighted image and hyperintense to brain on T2-weighted image. Left internal carotid artery angiogram (C) demonstrates occluded branch of left middle cerebral artery (arrow). Within the proper time frame, intraarterial thrombolysis would be a method of management for this patient.

Figure 40-9 Hyperacute infarct.

Axial T1-weighted image before (A) and after (B) contrast administration reveal subtle low intensity and arterial enhancement (arrow) in right insular cortex. Fluid-attenuated inversion recovery (FLAIR) sequence (C) helps define area of involvement. Diffusion-weighted sequence (D) shows infarct to best advantage. Acute phase is confirmed by low signal on apparent diffusion coefficient map (E).

CT and MRI perfusion techniques can demonstrate diminished blood perfusion within minutes of an insult. When MRI perfusion studies are coupled with diffusion images, a penumbra can be identified as a zone of decreased perfusion surrounding an area of absent perfusion (Figure 40-10). Only the central area shows the diffusion restriction. The penumbra represents viable tissue at risk for infarction, which may still be salvageable.⁹

Figure 40-10 Perfusion deficit.

MRI perfusion study shows hypoperfusion in right posterior inferior cerebellar artery territory. Normal left side measured 270.6, and abnormal right side measured 130.8.

Imaging protocols that use a number of MRI sequences for acute evaluation of a suspected stroke may provide the ideal combination of information about regional anatomy (standard MRI), presence of blood (GRE or SWI), extent of infarction (DWI), vascular anatomy (MRA), blood flow (PWI), and metabolic alterations (MRS) (see Figure 40-10). The feasibility of using such protocols continues to be studied.³⁵

Hypertensive encephalopathy is a syndrome that occurs in patients with elevated blood pressure of any cause. Severe preeclampsia and eclampsia of pregnancy are the most common causes, and CNS involvement is common. MRI findings include symmetric vasogenic edema in the subcortical white matter, primarily in the occipital and parietal lobes but occasionally extending into the frontal lobes. Radiologically similar lesions, referred to as posterior reversible encephalopathy syndrome (PRES), have been seen in association with a number of other conditions, including thrombotic thrombocytopenic purpura, sepsis, glomerulonephritis, and exposure to the immunosuppressants, cyclosporine and tacrolimus. The association with hypertension led to the presumption that edema was secondary to hyperemia and blood-brain barrier breakdown, but nearly half of patients with PRES lack a history of even moderate hypertension, and most perfusion studies have shown decreased perfusion in the areas of edema, rather than hyperemia, and the typical watershed distribution of the lesions is consistent with hypoperfusion contributing somewhat to the pathophysiology.³⁶ In 15% to 25% of cases, cytotoxic edema and hemorrhage are also seen, and these patients are less likely to show the typical reversibility of the associated clinical symptoms.³⁷ Brief episodes of severe hypotension, hypoxia, and hypoglycemia will typically result in infarction within a similar watershed distribution, whereas more prolonged episodes will cause progressively more severe injuries to the basal ganglia, thalami, hippocampi, cerebellum, and brainstem.³⁸

Venous infarction can occur in isolation and is associated with thrombosis of a dural sinus or large draining vein. In contrast to arterial infarctions, venous infarctions are typically hemorrhagic and primarily affect the white matter. Pregnancy, dehydration, sepsis, and other acquired hypercoagulable states are common risk factors. CT can demonstrate the hemorrhagic infarct as well as the high-density clot in the venous sinus. MRI is very sensitive in detecting the hemorrhage and edema as well as the thrombosis of the venous sinus. Magnetic resonance venography can also be helpful in identifying the occlusion.

Imaging of newborns and children with cerebrovascular disease must take into account the imaging changes that occur with development. In general, the brain of a term infant has its greatest myelination and metabolic activity in the brainstem, basal ganglia, cerebellum, and perirolandic cortex. Global hypoxic-ischemic injuries in term neonates are most commonly seen in these areas, particularly in the specific regions with the highest expression of excitatory NMDA receptors, including the putamina, ventrolateral thalamic nuclei, lateral geniculate bodies, dorsal brainstem nuclei, hippocampi, and perirolandic cortex.³⁹ Because of the greater propensity for the injured cells of neonates to undergo apoptosis, the full extent of an ischemic injury may not be apparent on MRI for at least 72 hours. During a child’s first year, as cerebral myelination proceeds from inferior to superior and posterior to anterior, the patterns of injury seen from vascular insults become more similar to those seen in older children and adults, with selective vulnerability seen in the striatum, lateral geniculate bodies, hippocampi, and frontal and parieto-occipital cortex, with sparing in moderate injuries of the thalami and perirolandic cortex.³⁸ The relative sparing of the cerebellum, even with severe global hypoxic-ischemic injury of the cerebral hemispheres, can result in a “cerebellar reversal” sign on CT (Figure 40-11) in which the supratentorial structures all appear hypodense in comparison to the cerebellum.⁴⁰

Figure 40-11 Global anoxic injury.

Axial CT scan of a child following cardiac arrest. There is diffuse low density in cerebral hemispheres and compression of ventricles and sulci, reflecting increased water accumulation (edema) and resultant mass effect. Basal ganglia and thalami appear bright, showing the “reversal” sign of global anoxia.

In the preterm brain, early imaging findings after an anoxic event include germinal matrix hemorrhage, periventricular venous infarction, and periventricular leukomalacia. The germinal matrix is a rich vascular stroma in the subependymal caudothalamic groove that is very vulnerable to hemorrhage. When an insult occurs, the germinal matrix bursts, and blood leaks into the ventricles or parenchyma. Ultrasonography is used to stage the degree of hemorrhage. Venous infarctions are similar to those discussed earlier but occur in the periventricular region. These focal hemorrhages are readily seen with MRI and are frequently seen with CT. Periventricular leukomalacia represents areas of coagulation necrosis of the white matter, leading to reduction of the central white matter. CT and MRI demonstrate loss of white matter in the parietal and occipital regions, and enlargement of the ventricles, with ragged borders (Figure 40-12). Cystic areas may be present, and the sulci may extend almost to the ventricles.³⁸

Figure 40-12 Periventricular leukomalacia.

Axial fluid-attenuated inversion recovery (FLAIR) image obtained on a child with spastic diplegia and a history of prematurity and hypoxic episodes. Multifocal white matter hyperintensities, reduced white matter volume, irregular ventricular contours, and cystic changes are typical findings of periventricular leukomalacia.

Congenital Aneurysm and Subarachnoid Hemorrhage

Evaluation of a patient with suspected subarachnoid hemorrhage should begin with a noncontrast head CT (Figure 40-13). If subarachnoid blood is confirmed by CT or lumbar puncture, a conventional angiographic study is done to assess the patient for the presence of cerebral aneurysms (see Figure 40-13). MRA and CTA may be helpful in the evaluation of patients suspected of having unruptured aneurysms but are insufficiently sensitive to exclude an aneurysmal source of bleeding.⁴¹ In addition, when one or more aneurysms are present, conventional angiography provides the superior anatomic detail needed for planning endovascular occlusion or surgical treatment.

Figure 40-13 Subarachnoid hemorrhage and aneurysm.

A, Axial non-contrast-enhanced CT scan of head reveals high density (blood) replacing normal low density of CSF within suprasellar cistern and subarachnoid spaces. This indicates subarachnoid hemorrhage. Also note dilated temporal horns (arrows), indicating acute hydrocephalus. B, Right internal carotid artery angiogram demonstrates presence of congenital anterior communicating artery aneurysm (arrow), as well as vasospasm (curved arrows).

From 10% to 30% of patients with aneurysmal subarachnoid hemorrhage will develop morbidity from a delayed ischemic neurologic deficit from vasospasm, but many such patients are obtunded or sedated and are clinically difficult to assess for new deficits. A combination of imaging modalities may be best for identifying patients with vasospasm and ischemia.⁴² Angiographic studies show vasospasm in most patients and do not clearly differentiate between patients with symptomatic and asymptomatic narrowing. TCD is commonly used to identify vessels with increased blood flow velocity from narrowing, but comparison between TCD and xenon CT has shown that increased velocity is commonly associated with increased rather than decreased flow.⁴³ Transluminal balloon angioplasty and intraarterial papaverine infusion improve outcomes for patients with symptomatic vasospasm, and several other interventional techniques are under investigation.^44,45

Vascular Malformations

Four types of vascular malformations are described: (1) arteriovenous malformation (AVM), (2) capillary telangiectasia, (3) cavernous angioma, and (4) developmental venous anomaly (DVA) or venous angioma.

AVMs are the most common type. The vessels of an unruptured AVM may be apparent on CT as tubular structures that become hyperdense with contrast administration. On MRI, the abnormal vessels may appear hypointense due to blood flow. Conventional angiography is preferred for the evaluation of suspected AVMs to differentiate them from arteriovenous fistulas, identify associated aneurysms, and provide a detailed assessment of the number, size, and location of feeding arteries and draining veins (Figure 40-14).⁴⁶ The interventional radiologist may be able to embolize some or all of the arterial feeders, making surgery either less complex or unneccesary.⁴⁷

Figure 40-14 Arteriovenous malformation.

A, Axial non-contrast-enhanced CT scan of head reveals a vague area of hyperdensity in posterior left parietal region. B, Contrast-enhanced CT scan demonstrates serpiginous enhancement of this lesion (arrow). C, Internal carotid artery angiogram demonstrates arteriovenous malformation being fed by middle cerebral artery.

Capillary telangiectasia and cavernous angioma are best evaluated by MRI, because angiography is typically normal and CT is insensitive. The MRI signal characteristics vary based on the presence or absence of associated hemorrhage.

DVAs are composed of a large draining vein surrounded by a caput medusae of small feeding veins. The veins are typically inapparent on non-contrast-enhanced CT but enhance with contrast and can be seen on conventional MRI as flow voids. DVAs are rarely symptomatic other than when associated with a cavernous angioma or AVM, and conventional angiography is recommended only when an apparently simple DVA is associated with hemorrhage or edema that cannot be explained by thrombosis of the draining vein.⁴⁸

Neoplasms

Neoplasms are typically grouped according to location. Knowledge of the imaging characteristics of specific tumors, age and gender of the patient, clinical presentation, and lesion location can narrow the differential diagnosis further and often provides a specific diagnosis. On CT, low-grade gliomas may appear as subtle nonenhancing masses, but higher-grade gliomas often demonstrate heterogeneous enhancement, with large areas of necrosis and vasogenic edema (see Figure 40-1). Metastatic lesions may be low-density and enhancing masses, as seen with lung or breast carcinoma, or they may have high density secondary to hemorrhagic components, as seen with melanomas and thyroid or renal cell carcinomas (Figure 40-15). Cystic tumors such as cystic astrocytomas may be composed of large cysts with the density of CSF (Figure 40-16). Epidermoid and dermoid tumors frequently contain areas of fat density that appear hypodense to CSF.

Figure 40-15 Intracranial metastatic disease.

Axial contrast-enhanced CT scan of head reveals multiple enhancing nodules throughout gray and white matter structures, consistent with metastatic disease.

Figure 40-16 Recurrent high-grade astrocytoma.

Study performed after radiation therapy (not shown) showed increased edema and mass effect; differential diagnosis included recurrent tumor and radiation necrosis. A, Axial MRI scan shows volume of tissue (box) selected for spectroscopy. B, Proton spectroscopy reveals increase in choline peak (arrow), decrease in N-acetyl aspartate peak (curved arrow), and appearance of a lactate peak (open arrow). This appearance is consistent with recurrent tumor, which was verified with repeat surgery and biopsy.

MRI has high sensitivity but low specificity in the evaluation of neoplasms, because most tumors appear similar. Tumors are typically of low intensity on T1WI and high intensity on T2WI (see Figure 40-1), although there are a few exceptions. Advanced imaging techniques have many applications in the study of brain tumors.¹⁵ DWI and MRS are helpful in presurgical grading, selection of optimal biopsy sites, determining the extent of subtle dissemination, and monitoring the response to therapy.⁴⁹ DTI and fMRI have proven useful in visualizing the relation between eloquent cortex and critical white matter tracts around tumors, which can aid in defining and minimizing risk of morbidity from resection.⁵⁰ MRS and DWI can help in distinguishing delayed treatment effects like postradiation ischemic necrosis from tumor recurrence, which can both show contrast-enhancing hyperintensity on conventional T2WI.¹⁰ PET studies show CBF, glucose consumption, and oxygen metabolism to be increased in recurrent tumor and decreased in necrosis.⁵¹

Infection and Inflammation

Spinal Cord Injury

The sequence of performing the various imaging studies to evaluate spine injury remains controversial and is usually based on their availability at the particular trauma center. Initial evaluation usually involves a series of plain x-rays, which are able to identify most unstable injuries. Lateral and anteroposterior studies are sufficient for most thoracic and lumbar injuries, although oblique views are sometimes added for clarification; lateral, oblique, and odontoid views are typically ordered for cervical injuries. However, some vertebral fractures and misalignments are missed on these screening studies (Figure 40-19, A). CT with axial, coronal, and sagittal reconstructions should be considered whenever fractures are seen or suspected because of the severity of trauma or if the patient’s examination is unreliable owing to altered mental status or a distracting injury.⁶²

Figure 40-19 Post-traumatic vertebral body compression fracture.

A, Lateral plain film of thoracolumbar junction reveals a compression fracture involving L1 vertebral body (asterisk). Decreased height of vertebral body and inferior anterior corner fracture are well seen. Retropulsed body can also be seen when outline of adjacent vertebral bodies (lines) are compared. Axial (B) and sagittal reconstructed (C) CT scans of same patient add substantial detail to degree of canal narrowing secondary to retropulsed fragment. Left laminar fracture (arrow, B) is also seen—not apparent on the plain film. D, Sagittal T2-weighted MRI demonstrates compression fracture of L1 and retropulsed posterior body, as well as contusion and swelling of conus (arrows) as a direct result of compression fracture.

MRI is recommended when the patient has neurologic deficits, an unstable injury by prior imaging, or symptoms of an unstable injury despite a normal CT. MRI will rarely identify spinal injuries that require surgical stabilization in patients with no apparent neurologic deficits and a normal CT,⁶³ but most studies suggest that spinal MRI is unnecessary even in obtunded and comatose trauma patients.⁶⁴ MRI is the only imaging modality that can directly visualize intrinsic spinal cord and soft-tissue injuries. It can identify and distinguish between hemorrhagic (hematoma) and edematous (contusion) cord injuries. Cord hematoma has a poor prognosis and indicates a complete lesion, whereas localized edema has a better prognosis for functional recovery. Traumatic disc herniations can be readily identified. A disc herniation with cord compression can change management from nonsurgical to surgical or change a posterior stabilization approach to a combined anterior and posterior approach. MRI is also useful in detecting ligamentous injury by showing edematous changes or discontinuity in the ligaments. Although these findings are usually secondary, detection of isolated ligamentous injury may identify patients at risk for delayed instability. Epidural hematomas and the extent to which they compress the cord are also identified with MRI. Finally, although fractures are difficult to detect with MRI, the effect of bony fragment displacement and alignment abnormalities on the cord or nerve roots is elegantly seen with this modality (see Figure 40-19, D).

Spinal Infection

Infections involving the spine may involve the vertebral bodies (spondylitis), intervertebral discs (discitis), epidural and subdural spaces, or the spinal cord (myelitis, pyogenic cord abscess). In the management of spinal infections, delayed treatment can lead to increased morbidity and mortality, making early diagnosis critical. MRI is the primary imaging modality in all types of spinal infection because of its higher sensitivity and ability to detect changes earlier than plain films and CT.⁶⁵

In spondylitis, involvement is seen in at least one entire spinal segment composed of two consecutive vertebrae and the intervening disc. Characteristic MRI findings include narrowing of the disc space, contrast enhancement, hypointensity on T1WI in the vertebral bodies, and hyperintensity on T2WI in the vertebral bodies and disc (Figure 40-20). These findings may not be present early, however, and can be mimicked by noninfectious processes. Skip lesions and associated large paraspinal abscesses are very suggestive of mycobacterial infection. Nuclear medicine studies such as FDG PET may be particularly useful in evaluating patients suspected of having chronic spondylitis or infected surgical hardware.⁶⁶ Although MRI is sensitive in defining areas of myelitis, the findings are nonspecific and resemble those of other noninfectious and demyelinating disorders. Typically, focal or diffuse areas of hyperintensity are seen on T2WI with variable contrast enhancement.⁶⁷

Figure 40-20 Discitis with epidural abscess.

Sagittal postcontrast T1-weighted (A) and T2-weighted (B) MRI scans demonstrate features of discitis and adjacent osteomyelitis. Vertebral bodies and disc space are of low signal intensity on T1-weighted image and of bright signal intensity on T2-weighted image (straight arrows). Epidural abscess surrounding and compressing cord is also identified (curved arrow).

Neoplasm

Neoplasms involving the spinal axis typically present with progressive symptoms of myelopathy or cord compression. MRI is the primary modality for the evaluation of any suspected spinal tumor. It can demonstrate the location, extent, and nature of most tumors, regardless of the compartment of origin. Primary tumors of the bony elements and direct extension from paraspinal neoplasms are also easily identified with MRI.⁶⁸

The spinal column is among the most common sites of tumor metastasis, third only to the lungs and liver. The most common primary tumor sites responsible for spinal metastasis are breast, prostate, thyroid, lung, and kidney. Plain radiographs can suggest the presence of spinal metastasis, with a blurred outline or generally moth-eaten appearance of a vertebral body suggesting diffuse cortical destruction. Focal bone loss that involves the posterior wall of the vertebral body is fairly indicative of neoplasia. Vertebral collapse is more likely to be due to neoplasia than degenerative disease when there is unilateral bone destruction, irregular or angular distortion of the vertebral endplates, involvement of the upper thoracic spine, a soft-tissue mass, or pedicle destruction.⁶⁹ CT is more sensitive than plain radiography for many of these features, and MRI is yet more sensitive, particularly for epidural and paraspinous soft-tissue involvement and cord compression. The bone marrow of vertebral bodies with neoplastic infiltration appears hypointense on T1WI and hyperintense on T2WI (Figure 40-21). The bone marrow of vertebral fractures with benign fractures has normal imaging characteristics (Figure 40-22).

Figure 40-21 Metastatic disease.

Sagittal T1-weighted (A) and T2-weighted (B) MRI scans of spine show metastatic lesions (arrows) as low intensity on T1-weighted image, replacing normal bright marrow. High signal within uninvolved vertebral bodies represents postradiation changes. Hypointense lesions on T2-weighted image (in contrast to more typical hyperintensity) reflect posttreatment appearance. Multiple compression fractures are identified within upper thoracic spine, with collapse, retropulsed fragments, and cord compression. Edematous changes within cord secondary to compression (asterisk) are also identified.

Figure 40-22 Benign compression fracture.

Sagittal T1-weighted (A) and T2-weighted (B) MRI scans demonstrate compression fracture of L5. Compare signal characteristics of remaining bony elements and pedicles with signal of normal bony structures.