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.

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