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EXTRACEREBRAL HEMORRHAGE

Acute epidural hematomas are often associated with skull fractures and lacerations of the
dural vessels, most often meningeal arteries and veins but occasionally a dural sinus. Two-thirds
of epidural hematomas are in the temporo-parietal region and they usually have a biconvex or
lentiform configuration. Epidurals are limited by the firmer attachment of the dura at the suture
margins, but they may cross the midline, especially with superior sagittal sinus lacerations, and
they also can bridge the supra- and infratentorial compartments with tears along the torcula and
transverse sinuses.

Subdural hematomas, both acute and chronic, are most often caused by bleeding from torn
bridging dural veins. Subdural hematomas are less frequently associated with skull fractures, but
more frequently associated with parenchymal brain damage. The subdural space is a more freely
communicating space and the hematomas form a crescentic shaped layer over the brain surface.
Subdural hematomas readily cross suture lines but do not cross the midline. Instead, they extend
along the dura of the falx into the interhemispheric fissure and onto the tentorium, which
epidurals cannot do. Both epidural and subdural hemorrhages occur within the confined space of
the bony calvarium and compress the adjacent brain, often requiring emergency evacuation.

Chronic subdural hematomas are usually related to a slower venous bleed without
accompanying cerebral parenchymal injury. A thick,vascular dural membrane forms that can be a
source for repeated episodes of hemorrhage. These collections are more often biconvex, rather
than the crescentic shape of acute subdural hematomas. The injury leading to a chronic subdural
can be relatively minor and may have occurred weeks before presentation. Patients often present
with disturbances of mentation and consciousness rather than focal or lateralizing signs. An
iatrogenic cause is overshunting or too rapid decompression of chronic hydrocephalus.

Multiple studies have demonstrated improved visualization of extra-axial hemorrhage with


MR compared to CT, largely related to the high conspicuity of hyperintense subacute
hemorrhage (methemoglobin) on T1-weighted images and the multiplanar capabilities of MR.
Coronal images are very helpful for identifying subtemporal collections and hemorrhage
adjacent to the tentorium cerebelli. Chronic subdural hematomas are often isointense with gray
matter on T1-weighted images, probably due to dilution and partial resorption or breakdown of
free methemoglobin. High T1 signal within what otherwise appears to be a chronic subdural
hematoma suggests rebleeding. Hemosiderin is rarely seen in subdural hematomas without
repeated episodes of bleeding, due to either low macrophage activity or removal of hemosiderin
that has formed. The presence of membranous strands coursing through an extra-axial collection
is additional evidence for a chronic subdural hematoma. The thick subdural membranes will also
enhance following contrast infusion.

SHEAR INJURIES

Severe head injuries are often associated with rotational forces that produce shear stresses on
the brain parenchyma. The brain itself has very little rigidity and is extremely incompressible.
Brain volume can be decreased only by exerting great pressure. On the other hand, the brain is
soft and malleable. Relatively little effort is required to distort the shape of the brain. The
parenchyma is of relatively uniform density, except for differences between the CSF of the
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ventricles and surrounding brain tissue. Slight differences in density also exist between gray and
white matter.

When the skull is rapidly rotated, it carries along the superficial brain parenchyma but the
deeper structures lag behind, causing axial stretching, separation and disruption of nerve fiber
tracts. Shear stresses are most marked at junctions between tissues of differing densities. As a
result, shear injuries commonly occur at gray/white matter junctions, but they are also found in
the deeper white matter of the corpus callosum, centrum semiovale, brain stem (mostly the
midbrain and rostral pons) and cerebellum. Lesions in the basal ganglionic regions are usually
found along the borders between the ganglia and the internal or external capsules, in other words,
the deep gray-white matter junctions of the cerebral hemispheres. The thalamic and basal ganglia
injuries are hemorrhagic in slightly more than 50% of cases. On the other hand, shear injuries of
the corpus callosum and centrum semiovale are more often nonhemorrhagic. Attempts to
correlate CT findings with acute and chronic sequelae of closed head trauma have been
discouraging, largely related to the insensitivity of CT to many cerebral injuries. Chiefly among
these, poorly seen by CT and well seen by MR, are the diffuse axonal injuries or white matter
shear injuries. These injuries constitute the most frequent findings on MR in head trauma,
comprising as high as 40% of all lesions. Shear injuries are most often multiple, ovoid and
parallel to white matter fiber bundles. They are hyperintense on T2 and hypointense of T1-
weighted scans, unless hemorrhagic components are present, in which case more complex
patterns are observed. During transition phases of hematoma evolution, combinations of
methemoglobin, hemosiderin rings and peripheral edema can result in layers of differing signal
intensity and a target-like appearance. The axial plane is the primary plane of imaging for both
cortical contusions and shear injuries, but supplemental coronal views are helpful to assess
injuries to the body of the corpus callosum and the inferior frontal and temporal lobes. Fast scan
techniques or gradient-echo images have lower resolution but are useful in uncooperative
patients. Contrast enhancement has little role in the evaluation of brain contusions.

IMAGING OF STROKE AND CEREBRAL ISCHEMIA

CAUSES OF STROKE

The five major causes of cerebral infarction are vascular thrombosis, cerebral embolism,
hypotension, hypertensive hemorrhage, and anoxia/hypoxia. Thrombotic strokes may occur
abruptly but the clinical picture often shows gradual worsening over the first few hours. Primary
causes of arterial thrombosis include atherosclerosis, hypercoagulable states, arteritis, and
dissection. Secondary compromise of vascular structures can result from traumatic injury,
intracranial mass effect, neoplastic encasement, meningeal processes, and vasospasm.

Embolic strokes characteristically have a very abrupt onset. After a number of hours, there
may be sudden improvement in symptoms as the embolus lyses and travels more distally. The
source of the embolus is usually either the heart (patients with atrial fibrillation or previous
myocardial infarction) or ulcerated plaques at the carotid bifurcation in the neck.

Hypotension can be cardiac in origin or result from blood volume loss or septic shock.
Hypertension can cause a primary intracerebral hemorrhage, or the elevated arterial pressure can
overwhelm the brain's autoregulatory mechanism, resulting in breakthrough of the blood-brain
barrier and brain edema. The latter phenomenon of hypertensive encephalopathy is a potential
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complication of eclampsia, but is usually transient and reversible. Anoxia/hypoxia events are
usually related to respiratory compromise from severe lung disease, perinatal problems, near
drowning, high altitude, carbon monoxide inhalation, or CNS mediated effects.

CT AND MR IMAGING

Acute Infarcts

CT and MR scans in patients with asymptomatic bruits or TIA's are usually negative, unless
they disclose abnormalities related to previous events. In patients with stroke, the earliest sign
may be abnormal vascular density/signal. Acute thrombus or embolus is hyperdense on CT.
Acute clot may be difficult to detect on MR, but the occluded artery should be apparent by the
absence of a normal flow void. The absent flow void is easiest to see in the larger arteries at the
base of the brain on T2-weighted images. It is not possible to conclusively distinguish a complete
occlusion from a critical stenosis with markedly reduced flow. Subacute clot is hyperintense and
is easiest to visualize in the basilar and middle cerebral arteries on T1-weighted images. One
must be careful not to mistake in-flow enhancement with intraluminal clot. This phenomenon is
most often observed in the end slices of a multislice set in arteries with slow flow entering the
imaging volume.

Another valuable sign of acute stroke is arterial enhancement. With slow arterial flow, the
spin-echo is able to capture the intravascular signal, and the T1 shortening effect of the
gadolinium renders the arteries hyperintense on T1-weighted images. Arterial enhancement is
more apparent in the smaller distal branches. It will be present in up to 45% of patients during
the first week.

The first parenchymal changes observed on CT and MR reflect the cytotoxic edema affecting
primarily the gray matter. It is important to remember that the CT scan may be negative for the
first 24-36 hours. Massive infarctions may be visible as early as 6 hours. The MR scan is usually
positive within three to four hours following a stroke. One of the earlier signs on CT is loss of
the normal gray-white contrast as the edematous cortex becomes isodense to the underlying
white matter. A similar phenomenon is not observed on MR because the increased water in the
gray matter renders the cortex higher signal on T2-weighted images and lower signal on T1-
weighted images, thereby increasing gray-white contrast. It is often easier to appreciate the
increased cortical signal on proton density-weighted images. The cortical swelling is more
apparent on T1-weighted scans. Cortical edema produces effacement of the sulci on both CT and
MR.

After 6-8 hours the accompanying vasogenic edema highlights the areas of brain infarction.
These fluid shifts are more profound and are responsible for effacement of the ventricles and
midline shifts. The mass effect increases over the first few days and becomes maximal at about
five days.

Subacute and Chronic Infarcts

The subacute stage begins during the second week with capillary proliferation in the area of
infarcted brain tissue. This neovascularity is devoid of any blood-brain barrier and intravascular
contrast freely diffuses into the interstitial spaces. The serpiginous character of the gyral
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enhancement is quite distinctive of cerebral infarction. A focal cerebritis or encephalitis can
mimic this pattern, but usually the clinical picture sets apart these entities. Following contrast
infusion, infarcts will typically enhanced between 2 and 8 weeks, but the enhancement can
persist for up to three months.

As an infarct evolves, it becomes progressively lower in density on CT (higher in signal on


T2-weighted images) and more well defined over the next few weeks, eventually approaching
the density of CSF. As the mass effect resolves and the infarcted tissue is resorbed, the adjacent
sulci and ventricle will enlarge. The end result is a chronic infarct with focal areas of cystic
encephalomalacia and some surrounding parenchymal change due to gliosis.

Vascular Patterns

Since most infarcts result from occlusion of vessels, the CT or MR pattern of abnormality
should follow one of the major vascular territories, such as the anterior cerebral, middle cerebral
or posterior cerebral arteries. Infarcts can usually be distinguished from inflammatory and
neoplastic disease because unlike the white matter pattern of edema found with tumors and
abscesses, infarcts involve the cortex as well and, therefore, the abnormal density or signal
intensity should extend peripherally to involve the cortex. As mentioned above, the enhancement
pattern of infarcts is also fairly characteristic, having a gyral pattern of enhancement along the
cortex. If a stroke is due to systemic hypotension or hypoxia, the area of infarction is commonly
found in watershed areas between the major vascular territories.

Lacunar infarction results from occlusion of the small penetrating arteries at the base of the
brain, including the lenticulostriate and thalamoperforating arteries. They are smaller infarcts
(less than 1 cm) and are found in the basal ganglia, thalamus and brainstem. MR is far more
sensitive than CT for detecting small lacunar infarcts, particularly in the brainstem where CT
scans are often degraded by artifacts from the bone at the skull base.

Hemorrhagic Stroke

The four major causes of hemorrhagic stroke are hypertension, hemorrhagic infarction,
hypocoagulable state, and amyloid angiopathy. The criteria for hypertensive hemorrhage
include a hypertensive patient, 60 years of age or older, and a basal ganglia or thalamic location
of the hemorrhage. A CT scan is the procedure of choice for evaluating these patients.
Arteriography is necessary only if one of these criteria is missing. Hypertensive hemorrhages are
often large and devastating. Since they are deep hemorrhages and near ventricular surfaces,
ventricular rupture is common. One-half of hypertensive hemorrhages occur in the putamen; the
thalamus in 25%; pons and brainstem, 10%; cerebellum, 10%, and cerebral hemispheres, 5%.

In stroke patients, despite the fact that the CT is often negative for the first 24-48 hours, it is
often obtained on the day of admission to exclude an intracerebral hemorrhage before the patient
is placed on anticoagulant therapy. Hemorrhage into an infarct can occur during the first week,
usually between the third and fifth days. Hemorrhagic infarction is a hallmark of embolic
infarction. This occurs after the embolus breaks up, resulting in reperfusion of the infarcted area.
As mentioned above, hemorrhage is also common with venous infarction.
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IMAGING OF CEREBRAL HEMORRHAGE & AV


MALFORMATIONS

INTRACEREBRAL HEMORRHAGE

CT Features

Together, hypertension, aneurysm, and vascular malformations account for 80% of


intracerebral hemorrhages. All cerebral hematomas, whatever the cause, have a similar resolution
pattern on CT. The rate of resolution depends on the size of the hematoma, usually within one to
six weeks, and they resorb from the outside toward the center. Perihematoma low density appears
in 24-48 hours. Rim enhancement appears in one week and persists for six weeks. The end result
of a hematoma is decreased parenchymal density, focal atrophy and local ventricular dilatation.

MR Appearance

Intracerebral hematomas have a very dynamic appearance on MR, changing in signal


intensity over time. Acute blood, in the form the oxyhemogloblin, is isointense with the brain
parenchyma. Within a few hours, the oxyhemoglobin is converted to deoxyhemoglobin within
the hematoma. Deoxyhemoglobin has a predominant effect of shortening T2, resulting in low
signal on T2-weighted images. After three to four days, the deoxyhemoglobin is progressively
converted to methemoglobin, which is a paramagnetic substance. Although methemoglobin
shortens both T1 and T2, the predominant effect is T1 shortening. As a result, at this stage,
hematomas are high signal in both T1-and T2-weighted images. Over the next few months, the
methemoglobin is slowly broken down into hemichromes which produce only mild T1
shortening. Hematomas at this end stage are slightly high signal on T1-weighted images and
remain high signal on the T2-weighted images. Another interesting phenomenon occurs around
the periphery of hematomas. Macrophage activity results in degradation of the methemoglobin
and conversion of the iron moiety to hemosiderin. Hemosiderin shortens T2 and produces a black
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ring around the hematoma on T2-weighted images. We have observed this ring as early as nine
days after hemorrhage, and the ring becomes thicker over time. The amount of hemosiderin
varies from one hematoma to another, and the specific physiologic and chemical factors that
influence this are unknown. In small hematomas (less than 1 cm), we have noted low signal
intensity from hemosiderin throughout the cavity. The length of time that the hemosiderin will
remain in the area of a hematoma is also unknown, but we have observed hemosiderin at the site
of a

previous hematoma as long as four years following the primary hemorrhage. From this
discussion, it is apparent that the specific signal intensities of a hematoma on T1- and T2-
weighted images provide a clue as to the age of the hemorrhage.

Hypertensive Hemorrhage

The criteria for hypertensive hemorrhage include a hypertensive patient, 60 years of age or
older, and a basal ganglia or thalamic location of the hemorrhage. A CT scan is the procedure of
choice for evaluating these patients. Arteriography is necessary only if one of these criteria is
missing. Hypertensive hemorrhages are often large and devastating. Since they are deep
hemorrhages and near ventricular surfaces, ventricular rupture is common. One-half of
hypertensive hemorrhages occur in the putamen; the thalamus in 25%; pons and brainstem, 10%;
cerebellum, 10%, and cerebral hemispheres, 5%.

VASCULAR MALFORMATIONS
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Arteriovenous Malformation

The arteriovenous (AV) malformation consists of a congenital abnormality of anomalous,


dilated capillaries that result in shunting of blood from the arterial to venous side. AV
malformations are by far the most common of the cerebrovascular malfor mations. One-half of
patients present with seizures or a neurological deficit due to compression of normal brain or a
steal phenomenon. The other half presents with hemorrhage. The hemorrhage is usually more
benign than that due to a ruptured aneurysm. Ninety-five percent of AV malformations are in the
supratentorial compartment, either in a lobar or deep location and 10% are in the infratentorial
region. Dural supply is more commonly found with infra tentorial lesions although it is important
to remember than any AV malformation adjacent to a dural surface can receive dural
contributions.

CT features of an AV malformation on plain scan include a high- absorption irregular mass


with large feeding arteries and draining veins, focal areas of calcification and no surrounding
edema or mass effect. The contrast scan shows serpiginous enhancement with prominent arteries
and veins. Due to the rapidly flowing blood from these lesions, a flow void is observed on MR
scan. As a result, the characteristic feeding arteries and draining veins can be imaged without any
injection of contrast material.
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One should suspect AV malformation as a cause of an intracerebral hemorrhage if the


hemorrhage is lobar and away from the territory of the anterior communicating and middle
cerebral arteries, and also in deep hemorrhages in younger, normotensive patients. It is important
to remember that the hematoma may compress a small AV malformation. If the initial angiogram
is negative, a follow-up study should be done one to two months later, after the hematoma and
mass effect have resolved. AV malformations can thrombose either spontaneously or due to
compression by the hematoma.

Cavernous Angioma

They are characterized by a honeycomb of endothelium-lined vascular spaces, separated by


fibrous, collagenous bands with no intervening neural tissue. Most cavernous angiomas are
asymptomatic and are noted incidentally on MR scans. They may cause seizures or a focal
neurologic deficit, and on occasion they will be of sufficient size to produce symptoms by mass
effect. The intralesional hemorrhages are usually small and occult clinically. Multiplicity is
common.
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Cavernous angiomas invariably contain hemosiderin from chronic hemorrhage and are
distinctly hypointense on T2-weighted MR images. Lesion margins are "fuzzy" due to the
magnetic susceptibility effect of the hemosiderin, and a "blooming effect" occurs with gradient-
echo sequences. Calcification is often present. Mild enhancement can be obscured by the
hemosiderin.

Larger cavernous angiomas have a more complex appearance from multiple hemorrhages of
varying ages. Hemosiderin lines the perimeter of these lesions and also outlines the internal
compartments that contain various components of hemorrhage.

CT of Subarachnoid Hemorrhage

The CT scan is important, first of all, to document the subarachnoid hemorrhage and to
assess the amount of blood in the cisterns. Detection of subarachnoid blood is very dependent on
how early the scan is obtained. Data in the literature vary from 60-90%. If the scan is obtained
within four to five days, the detection rate is very high. Secondly, the CT helps localize the site
of the aneurysm. This can be done by the distribution of blood within the cisterns and also with
dynamic scanning following an IV bolus of contrast. Thirdly, the CT is important to evaluate
complicating factors such as cerebral hematoma, ventricular rupture, hydrocephalus, cerebral
infarction, impending uncal herniation and re-bleed.

Regarding CT patterns of ruptured aneurysm, an anterior communicating aneurysm is


suggested by blood in the cisterna lamina terminalis, anterior pericallosal cistern, and
interhemispheric fissure. Identification of clot within a cistern makes this sign more specific.
There may be extension of blood into the septum pellucidum and lateral ventricle, and hematoma
in the inferomedial frontal lobe. Localizing posterior communicating artery aneurysms is more
difficult because the blood is usually diffuse within the cisterns. Intracerebral hematoma or
ventricular rupture is unusual with posterior communicating aneurysms. Rupture of a middle
cerebral aneurysm is characterized by blood in the sylvian fissure and a hematoma in the
temporal lobe, which may also rupture into the adjacent temporal horn. Posterior fossa
aneurysms often do not have good localizing findings on the CT scan.

It is not uncommon to find a small amount of blood in the ventricles in patients with
subarachnoid hemorrhage. That does not necessarily mean that direct ventricular rupture has
occurred because subarachnoid blood can enter the ventricular system in a retrograde manner.
Ventricular rupture from a bleeding aneurysm is usually more dramatic, often showing a cast of
blood or clot in a lateral ventricle. A subarachnoid hemorrhage with blood in the lateral ventricle
is usually due to an anterior communicating aneurysm. Middle cerebral aneurysm is another
possibility, but that should be associated with a temporal hematoma. Similarly, pericallosal
aneurysms can rupture into the ventricle but then there should be hematoma in the corpus
callosum as well.

What is the role of a contrast scan in subarachnoid hemorrhage? The combination of clinical
and plain scan findings is often fairly conclusive that a subarachnoid hemorrhage has occurred. If
emergency arteriography is considered, contrast limitations need to be considered. We obtain the
contrast scan if the diagnosis is in doubt, or if the plain scan shows a large intracerebral
hematoma that needs emergency evacuation and there is no time for the angiogram. The
detection rate of aneurysms with contrast scanning ranges from 40% for posterior
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communicating to 80% for anterior communicating, middle cerebral and basilar aneurysms. A
common problem is that the subarachnoid blood obscures the enhancing aneurysm.

Conventional MR sequences are very insensitive for detecting subarachnoid hemorrhage.


Clots within cisterns can be detected, but in general, MR is not the procedure of choice in the
work-up of patients with subarachnoid hemorrhage. Due to the flow void phenomenon,
aneurysms about the circle of Willis can be identified on spin-echo MR images. With fluid-
attenuated inversion recovery (FLAIR) sequences, the CSF is dark, so that subarachnoid
hemorrhage can be seen more easily. These sequences may be helpful for detecting subarachnoid
blood in the posterior fossa where CT has difficulty and in the sulci over the cerebral convexities.

MULTIPLE SCLEROSIS

On histologic examination, acute MS plaques show partial or complete destruction and loss
of myelin with sparing of axon cylinders. They occur in a perivenular distribution and are
associated with a neuroglial reaction and infiltration of mononuclear cells and lymphocytes. The
perivascular demyelination gives the appearance of a finger pointing along the axis of the vessel.
In the pathologic literature these elongated lesions have been named "Dawson's fingers." Active
demyelination is accompanied by transient breakdown of the blood-brain barrier. Chronic lesions
show predominantly gliosis. MS plaques are distributed throughout the white matter of the optic
nerves, chiasm and tracts, the cerebrum, the brain stem, the cerebellum and the spinal cord.

Imaging Features

MS plaques are hyperintense on T2-weighted and FLAIR images and hypointense on T1-
weighted scans. Specific signal intensities of MS lesions will vary depending on the magnetic
field strength, the pulse sequence parameters, and partial volume effects. Occasionally, acute
plaques may have a thin rim of relative T2 hypointensity or T1 hyperintensity. The T1
hyperintensity is attributed to free radicals, lipid-laden macrophages, and protein accumulations.

MS plaques are usually discrete foci with well-defined margins. Most are small and irregular,
but larger lesions can coalesce to form a confluent pattern. Multiple focal periventricular lesions
can give a "lumpy-bumpy" appearance to the ventricular margins. As a result of their perivenular
distribution, many periventricular plaques have an ovoid configuration, with their long axis
oriented transversely on an axial scan. The ovoid lesion is the imaging correlate of "Dawson's
finger." In general, MS plaques have a homogeneous texture without evidence of cystic or
necrotic components. Hemorrhage is not a feature of MS lesions. Edema and mass effect are also
uncommon.

The periventricular white matter is a favorite site for MS plaques, particularly along the
lateral aspects of the atria and occipital horns. The corpus callosum, corona radiata, internal
capsule, visual pathways, and centrum semiovale are also commonly involved. When more than
a few lesions are present, symmetric involvement of the cerebral hemispheres seems to be the
rule. Any structures that contain myelin can harbor MS plaques, including the brain stem, spinal
cord, subcortical U-fibers, and even within the gray matter of the cerebral cortex and basal
ganglia. A distinctive site in the brain stem is the ventrolateral aspect of the pons at the fifth
nerve root entry zone. Brain stem and cerebellar plaques are more prevalent in the adolescent age
group.
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Lesions of the corpus callosum have been a special focus of study. On axial sections, plaques
in the corpus callosum above the lateral ventricles have a transverse orientation along the course
of the nerve fiber tracts and vessels. Sagittal FLAIR images are especially helpful to depict the
small callosal lesions closely apposed to the superior ependymal surface of the lateral ventricles.
Early edema and demyelination along subependymal veins produce a striated appearance.
Atrophy of the corpus callosum is common in long-standing, chronic MS and is seen best on T1-
weighted sagittal images.

Involvement of the visual pathways, particularly the optic nerves, frequently occurs
sometime during the course of disease. Patients may present with optic neuritis, although in
about half of those cases, MRI will unveil other silent lesions in the brain. Imaging plaques in the
optic nerves is a challenge even for MRI. Unenhanced spin-echo sequences are not very
sensitive, and generally some type of fat suppression is required. Probably the most sensitive
method for detecting acute MS of the optic nerves is the combination of gadolinium
enhancement and fat suppression.

Gadolinium enhancement

Since acute MS plaques are associated with transient breakdown of the blood-brain barrier,
gadolinium contrast agents will produce enhancement of these lesions on T1-weighted images.
Enhancement will be observed for 8 to 12 weeks following acute demyelination. Thus, Gd-
enhanced MR can be used to assess lesion activity just like contrast-enhanced CT. Either nodular
or ringlike enhancement may be seen early after contrast injection, but the central areas tend to
fill in and become more homogeneous on delayed scans. Immediate postcontrast scans are most
sensitive for detecting MS, and delayed scanning is not necessary. Contrast-enhanced MR can be
used to follow the progression of disease and to assess the response to therapy.

Occasionally, large plaques, also called tumefactive MS, may produce mass effect and
simulate other mass lesions. However, compared with neoplastic or inflammatory processes, MS
plaques have minimal surrounding edema and relatively less mass effect for the overall size of
the white matter lesions. Balo's concentric sclerosis has a unique MR appearance. Like
tumefactive MS, the plaques usually are quite large, but in addition, a concentric laminated
pattern is seen on T2 and T1-weighted images. Similarly, post-contrast images often show rings
of enhancement alternating with non-enhancing regions during the acute phase.

Adrenoleukodystrophy

Adrenoleukodystrophy is a peroxisomal disorder that results in abnormal accumulation of


very long chain fatty acids. Several forms have been described, but x-linked
adrenoleukodystrophy is the classic form that presents in males between the ages of 4 and 8. The
neurologic findings of visual and behavioral problems, intellectual impairment and long tract
signs can appear before or after adrenal gland insufficiency. Adrenoleukodystrophy is both a
demyelinating and dysmyelinating disorder. Initially, it involves predominantly the parietal-
occipital lobes and posterior visual pathways, but it extends forward into the frontal and temporal
lobes as the disease progresses. Unlike the focal plaque-like character of multiple sclerosis,
adrenoleukodystrophy tends to be contiguous within fiber tracts and often is confluent within the
larger white matter bundles of the centrum semiovale. Both periventricular and subcortical white
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matter are affected, and in advanced disease the internal capsule, corpus callosum, corticospinal
tracts and other white matter fiber tracts in the brain stem can be involved.

The typical MR findings are large, symmetric, hyperintense lesions on T 2-weighted


images that are also clearly visible as hypointense areas on T 1-weighted scans. The white matter
abnormalities tend to be confluent and of homogeneous signal intensity. Sites of active
demyelination along the advancing edges may be associated with blood-brain barrier disruption
and enhance with paramagnetic contrast agents. Atypical features include frontal lobe
involvement, unilateral involvement, calcifications and mass effect.

INFECTIOUS AND INFLAMMATORY DISORDERS

Inflammatory diseases of the brain include abscess, meningitis, encephalitis and


vasculitis. The brain is protected from invading infectious agents by the calvarium, dura and
blood- brain barrier. Moreover, the cerebral tissue itself is relatively resistant to infection. Most
pyogenic infections are hematogenous and related to septicemia and endocarditis. Direct
extension from an infected paranasal sinus or middle ear/mastoid is less common than in the pre-
antibiotic era. Fungal infections are less common than bacterial infections, but are taking on
more importance in AIDS patients and those immunocompromised by way of chemotherapy,
neoplasia, or immunosuppressive therapy for organ transplantation. The most important viral
infections of the central nervous system from an imaging point of view are aseptic meningitis,
encephalitis, and progressive multifocal leukoencephalopathy (PML). Herpes simplex is
responsible for a fulminant viral encephalitis, and both the human immunodeficiency virus
(HIV) and cytomegalovirus (CMV) produce a white matter encephalitis associated with the
AIDS epidemic.

ABSCESS

Bacterial

Brain abscesses may be related to infections of the paranasal sinuses, mastoids, middle
ears as well as hematogenous seeding, but in 20% of cases a source is not discovered. Very rarely
an abscess is secondary to meningitis. In children, more than 60% of cerebral abscesses are
associated with congenital heart disease and right to left shunts. Presenting symptoms of a
cerebral abscess include headache, drowsiness, confusion, seizures and focal neurologic deficits.
Fever and leukocytosis are common during the invasive phase of a cerebral abscess but may
resolve as the abscess becomes encapsulated. Organisms most frequently cultured from brain
abscesses in otherwise immunocompetent individuals are staphylococcus and streptococcus.

When the brain is inoculated with a pathogen, a local cerebritis develops. Pathologically,
an area of cerebritis consists of vascular congestion, petechial hemorrhage and brain edema. The
infection goes through a stage of cerebral softening, followed by liquefaction and central
cavitation. With time, the central necrotic areas become confluent and are encapsulated after one
to two weeks. Edema, a prominent feature of cerebral abscess, may actually subside after the
capsule forms.

In the cerebritis stage, MR reveals high signal intensity on T2-weighted images, both
centrally from inflammation and peripherally from edema. Areas of low signal are variably
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imaged on T1-weighted scans. As the progression to abscess ensues there is further prolongation
of T1 and T2 centrally. The capsule becomes highlighted as a relatively isointense structure
containing and surrounded by low signal on T1- weighted images, and high signal on T2-
weighted images. Mottled areas of enhancement are seen with gadolinium-enhanced MR during
the cerebritis stage, with an enhancing rim developing as the abscess matures. The enhancing rim
may appear late in the cerebritis stage, prior to actual central necrosis. In some instances, the
central area of necrosis has also enhanced on delayed scans, but not as commonly as is seen in
necrotic tumors.,

Cysticercosis

Neurocysticercosis is the most frequently encountered parasitic infestation of the CNS.


Originally endemic in underdeveloped countries, predominantly Latin America, Africa, Asia and
some portions of eastern Europe, it is becoming increasingly frequent in North America in
immigrant populations. Humans become accidental hosts for the larval stage of Taenia Solium,
the pork tapeworm, by ingesting contaminated material. The eggs hatch in the stomach and
larvae burrow through the gut wall and become distributed by the circulatory system. There is a
predilection for involvement of the brain. Patients most often present with seizures, elevated
intracranial pressure, focal neurologic abnormalities and altered mental status. Asymptomatic
infections are common.

Four forms of neurocysticercosis are described: meningeal, parenchymal, ventricular and


mixed. In all locations, death of the larva provokes a more intense inflammatory response, and in
the case of an intraventricular lesion may lead to ependymitis. Parenchymal lesions consist of
small cysts, large cysts and calcified lesions. Small (approximately 1.5 cm. in diameter) cysts
may have a central area of relatively shorter T1 (isointense or hyperintense to cortex) and are
uniformly hyperintense on T2-weighted images. Large (4-7 cm) cysts are usually multiloculated,
adjacent to the subarachnoid space and may contain a mural nodule. The presence of a mural
nodule or a T2-hypointense rim in encapsulated lesions may correlate with larval death.
Visualization of calcified lesions has been variable with MR; overall there is an advantage for CT
in this regard. Sometimes, calcified lesions are surrounded by edema, making them more
conspicuous on MR. Basal cistern lesions can be difficult to identify but have been visualized as
areas of intermediate signal intensity on T1-weighted images. Intraventricular cysticercosis
results in deformable and mobile cysts that may cause intermittent hydrocephalus.

MENINGITIS

Bacterial

Bacterial meningitis is an infection of the pia and arachnoid and adjacent cerebrospinal
fluid. The outer arachnoid serves as a barrier to the spread of infection, but involvement of the
subdural space can occur, resulting in a subdural empyema. This complication is more common
in children than adults. The most common organisms involved are Hemophilus influenza,
Neisseria meningitides (Meningococcus) and Streptococcus pneumoniae. Patients present with
fever, headache, seizures, altered consciousness and neck stiffness. The overall mortality rate
ranges from 5 to 15% for H. influenza and meningococcal meningitis to as high as 30% with
streptococcal meningitis. In addition, persistent neurologic deficits are found in 10% of children
after H. influenza meningitis and in 30% of patients with streptococcal meningitis.
14

The ability of nonenhanced MR to image meningitis is extremely limited, and the


majority of cases are normal or have mild hydrocephalus. In severe cases, the basal cisterns may
be completely obliterated, with high signal intensity replacing the normal CSF signal on proton
density images. Intermediate signal intensity may be seen in the basal cisterns on T1-weighted
images in these cases. Meningeal enhancement often is not present, unless a chronic infection
develops. Infection within the ventricles, either from direct extension from a shunt or abscess or
progression of meningitis, may lead to ependymitis, resulting in hyperintensity outlining the
ventricles on T2- weighted images and enhancement of the ependyma on T1-weighted images
with gadolinium. Subdural empyemas are better seen with MR than with CT, and the signal
characteristics of the exudate in subdural empyema (higher signal than CSF) helps to
differentiate it from benign extra-axial collections.

Tuberculosis

Tuberculous meningitis remains an important disease, becoming more common as an


infectious agent in AIDS patients. As a rule, the evolution is less rapid than in pyogenic
infections. Vasculitis and cerebral infarction, caused by inflammatory changes in the basal
cisterns, are more prevalent. The MR features of tuberculous meningitis are similar to the
bacterial agents, but the chronic inflammation induces thick granulation tissue that produces a
more striking enhancement pattern. Actual intracranial tuberculomas are rare in the United
States. Mature tuberculomas are T2 hypointense. Central necrosis in some lesions results in a T2
bright core with a low signal intensity rim.
15
ENCEPHALITIS

Encephalitis refers to a diffuse parenchymal inflammation of the brain. Acute encephalitis


of the non-herpetic type presents with signs and symptoms similar to meningitis but with the
added features of any combination of convulsions, delirium, altered consciousness, aphasia,
hemiparesis, ataxia, ocular palsies and facial weakness. The major causative agents are
arthropod-borne arboviruses (Eastern and Western equine encephalitis, St. Louis encephalitis,
California virus encephalitis). Eastern equine encephalitis is the most serious but fortunately also
the least frequent of the arbovirus infections. The enteroviruses, such as coxsackie-virus and
echoviruses, can produce a meningoencephalitis, but a more benign aseptic meningitis is more
common with these organisms. MR reveals hyperintensity on T2-weighted scans within the
cortical areas of involvement, associated with subcortical edema and mass effect.

Herpes Simplex

Herpes simplex is the commonest and gravest form of acute encephalitis with a 30-70%
fatality rate and an equally high morbidity rate. It is almost always caused by Type 1 virus except
in neonates where Type 2 predominates. Symptoms may reflect the propensity to involve the
inferomedial frontal and temporal lobes- hallucinations, seizures, personality changes and
aphasia. MR has demonstrated positive findings in viral encephalitis as soon as 2 days after
symptoms, more quickly and definitively than CT. Early involvement of the limbic system and
temporal lobes is characteristic of herpes simplex encephalitis. The cortical abnormalities are
first noted as ill-defined areas of high signal on T2-weighted scans, usually beginning
unilaterally but progressing to become bilateral. Edema, mass effect and gyral enhancement may
also be present. Since MR is more sensitive than CT for detecting these early changes of
encephalitis, hopefully it will improve the prognosis of this devastating disease.

CONGENITAL INFECTIONS

Congenital infections refer to maternally transmitted infections, which are most


frequently caused by the group of TORCH pathogens, which include Toxoplasma, Others
(Listeria, Treponema), Rubella, Cytomegalovirus, and Herpes simplex type 2. Nowadays, maybe
another “H” should be added to emphasize the common occurrence of HIV in this subgroup of
CNS infections. Congenital infections of the brain may produce diffuse, parenchymal
inflammation with some unique characteristics, such as microcephaly, brain atrophy,
hydrocephalus, neuronal migrational anomalies and cerebral calcifications. The degree of the
destructive brain process and the resultant developmental abnormalities depend on the timing of
the infection. The earlier in gestation the CNS involvement occurs, the more profound the brain
destruction will be. In cases of congenital infections, where the prerequisite is involvement of the
mother, even in a subclinical form, the causative agents may reach the fetus, either during the
gestation via a hematogenous - transplacental route, or during the birth as the fetus passes
through the infected birth canal.

Toxoplasmosis

Toxoplasmosis is caused by the parasite Toxoplasma gondii, which is typically passed


hematogenously through the placenta to the fetus. There is a large percentage of the population,
16
approaching 50%, which has been infected by the parasite sometime in their life, but congenital
toxoplasmosis occurs only when the mother becomes infected during pregnancy. Infected fetuses
have a high incidence (almost 50%) of CNS involvement. Early infection before 20 weeks of
pregnancy is associated with severe, persistent neurologic abnormalities, whereas late infection
after 30 weeks is rarely associated with deficits. Neuroimaging of congenital toxoplasmosis may
reveal a whole spectrum of findings such as intracranial calcifications, hydrocephalus, brain
atrophy, microcephaly and neuronal migrational anomalies.

Cytomegalovirus

Cytomegalovirus (CMV) is a member of the herpesvirus family, which subclinically


infects nearly all the population at some time in their life and is the most frequent cause of a
congenital viral infection. Congenital infection occurs after primary or secondary (reactivation)
maternal infection, and the virus reaches the fetus via the transplacental route. CNS involvement
is a very important manifestation of the disease, and as with toxoplasmosis, earlier infection
results in poorer outcome with more severe and persistent neurologic sequelae.

CMV produces a diffuse encephalitic infectious process, which results in multifocal


destructive changes in the brain that lead to calcifications and microcephaly. The immature cells
in the germinal matrix region are the first involved areas in the brain. Necrosis and calcifications
of those areas explain the predilection for thick or nodular calcifications in the periventricular
area. Intracranial calcifications may also be found in the cortical and subcortical region, as well
as in the basal ganglia, so differentiation between congenital infection from CMV or
toxoplasmosis is not certain based on imaging criteria alone.

Herpes Simplex Virus

Herpes simplex virus (HSV) is a DNA virus and a member of the herpesvirus family,
which has two different serotypes, herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2).
They produce the most important acute viral encephalitis in the neonate. In over 80% of cases of
herpes simplex encephalitis, HSV-2 is the causative agent. The infection is most commonly
acquired during delivery through an infected birth canal, although hematogenous transmission
through the placenta does occur. An explanation for the observed rarity of early transplacental
infection is that it causes severe destruction in the fetus, resulting in spontaneous abortions rather
than maldevelopment of the CNS. However, if infants survive the early hematogenous infection,
the devastating effect of the panencephalitis results in findings similar to those of other
placentally transmitted infections, such as microcephaly, cerebral atrophy and necrosis, and
intracranial calcifications, but to a greater degree and with more severe neurological sequelae.
An important and unique imaging finding in HSV-2 encephalitis is a linear, gyriform cortical
pattern of increased attenuation on CT and hyperintensity on T1-weighted images, overlying
abnormal edematous and/or necrotic white matter. The cortical imaging features have been
attributed to the presence of microcalcifications or to changes in local vascularity.

SUPRATENTORIAL BRAIN TUMORS


17
In the diagnostic work-up of intracranial tumors, the primary goals of the imaging studies
are to detect the abnormality, localize and determine its extent, characterize the lesion, and
provide a list of differential diagnoses or, if possible, the specific diagnosis. Correlative studies
have proved that MR is more sensitive than CT for detecting intracranial masses. Moreover, the
multiplanar capability of MR is very helpful to determine the anatomic site of origin of lesions
and to demarcate extension into adjacent compartments and brain structures. The superior
contrast resolution of MR displays the different components of lesions more clearly. MR can
assess the vascularity of lesions without contrast infusion. On the other hand, CT detects
calcification far better than MR, a useful finding for differential diagnosis. Gradient-echo
techniques improve MR detection of calcification by accentuating the diamagnetic susceptibility
properties of calcium salts, but the observed low signal on T2-weighted images is nonspecific, in
that any accompanying paramagnetic ions would produce the same effect.

Contrast enhancement with gadolinium increases both the sensitivity and specificity of
MR. Gadolinium is a blood-brain barrier (BBB) contrast agent like iodinated agents for CT. It
does not cross the intact BBB, but when the BBB is absent or deficient, gadolinium enters the
interstitial space to produce enhancement (increased signal) on T1-weighted images. All the
collective knowledge learned from contrast-enhanced CT can be applied directly to the
gadolinium-enhanced MR images. Although the enhancement patterns are not tumor specific,
the additional information is often helpful for diagnosis. Lesions can be classified as
homogeneous or heterogeneous, and necrotic and cystic components are seen more clearly. The
margins of enhancement provide a gross measure of tumor extension. Contrast MR is
particularly valuable for extra-axial tumors because they tend to be isointense to the brain on
plain scan.

CEREBRAL GLIOMAS

Gliomas are malignant tumors of the glial cells of the brain and account for 30-40% of all
primary intracranial tumors. They occur predominantly in the cerebral hemispheres, but the brain
stem and cerebellum are frequent locations in children, and they are also found in the spinal cord.
The peak incidence is during middle adult life, when patients present with seizures or symptoms
related to the location of the gliomas and the brain structures involved.

Astrocytomas are graded according to their histologic appearance. Grade 1


astrocytomas have well-differentiated astrocytes and well-defined margins. The clinical course
often proceeds over many years and complete cures are possible. The pilocytic variant is a low-
18
grade tumor with a distinct capsule that is commonly found in children. The giant cell
astrocytoma is a specialized tumor that develops from pre-existing hamartomas in patients with
tuberous sclerosis. Grade 2 astrocytomas are well-differentiated but diffusely infiltrating tumors.
The fibrillary type is most common, and although initially benign, they may evolve into a higher
grade tumor over time. This changing character of gliomas makes histological classification
difficult from sample biopsies, because different parts of the tumor often exhibit varying degrees
of malignancy. The higher grade astrocytomas are very cellular and pleomorphic. Anaplastic
astrocytomas (Grade 3) are very aggressive tumors, readily infiltrate adjacent brain structures,
and have a uniformly poor prognosis. Glioblastoma multiforme (Grade 4) has the added
histologic features of endothelial proliferation and necrosis. Multicentric foci of tumor may be
seen in 4 to 6% of glioblastomas. Gliomatosis cerebri is an unusual condition with diffuse
contiguous involvement of multiple lobes of the brain.

Oligodendrogliomas are the most benign of the gliomas. Calcification is common, and
they occur predominantly in the frontal lobes. The mixed neuronal and glial tumors are found
mostly in children and young adults. They are slow-growing and are found predominantly in the
temporal lobes and around the third ventricle. Intratumoral cysts and calcification are common.

The common signal characteristics of intra-axial tumors include high signal intensity on
T2-weighted images and low signal on T1-weighted images, unless fat or hemorrhage is present.
Fat and subacute hemorrhage (methemoglobin) exhibit high signal on T1-weighted images, and
acute hemorrhage (deoxyhemoglobin) and chronic hemorrhage (hemosiderin/ferritin) show low
signal intensity on T2-weighted scans. Gliomas have poorly defined margins on plain MR. They
infiltrate along white matter fiber tracts, and the deeper lesions have a propensity to extend
across the corpus callosum into the opposite hemisphere. They are often quite large by the time
of clinical presentation.

The higher grade gliomas, particularly glioblastomas, appear heterogeneous due to central
necrosis with cellular debris, fluid, and hemorrhage. Peritumoral edema and mass effect are
common features. Following injection of gadolinium, T1-weighted images show irregular ring
enhancement, with nodularity and nonenhancing necrotic foci. As mentioned above,
gliomas are infiltrative lesions, and microscopic fingers of tumor usually extend beyond the
margin of enhancement. Enhanced scans are particularly helpful to outline subependymal spread
of tumor along a ventricular surface, as well as leptomeningeal involvement. Although
highly malignant, anaplastic astrocytomas may or may not exhibit breakdown of the blood-brain
barrier. In general, the presence or lack of enhancement alone is not helpful in grading
astrocytomas.

The lower grade astrocytomas tend to be more homogeneous without central necrosis.
Large cystic components may be present. The cysts have smooth walls, and the fluid is of
uniform signal, to distinguish them from necrosis. Enhancement is variable, depending on the
integrity of the blood-brain barrier.

LYMPHOMA
19
Primary malignant lymphoma is a non-Hodgkin's lymphoma that occurs in the brain in
the absence of systemic involvement. These tumors are highly cellular and grow rapidly. Favorite
sites include the deeper parts of the frontal and parietal lobes, basal ganglia, and hypothalamus.
Most occur in patients who are immunocompromised secondary to chemotherapy or acquired
immunodeficiency syndrome (AIDS) or in organ transplant recipients who are on
immunosuppressant drugs. Cerebral lymphomas are very radiosensitive and respond dramatically
to steroid therapy.

Lymphomas typically appear as homogeneous, slightly high signal to isointense masses


deep within the brain on T2-weighted images. The observed mild T2 prolongation is probably
related to dense cell packing within these tumors, leaving relatively little interstitial space for
accumulation of water. They are frequently found in close proximity to the corpus callosum and
have a propensity to extend across the corpus callosum into the opposite hemisphere, a feature
that mimics glioblastoma. Multiple lesions are present in as many as 50%. Despite their rapid
growth, central necrosis is uncommon. They are associated with only a mild or moderate amount
of peritumoral edema. By time of presentation they can be quite large and yet produce relatively
little mass effect, a feature that sets lymphoma apart from glioblastoma and metastases.
Intratumoral cysts and hemorrhage are unusual. Most lymphomas show bright homogeneous
contrast enhancement.

The pattern is modified somewhat in AIDS patients. Multiplicity seems to be more


common. Moreover, lymphomas exhibit more aggressive behavior and readily outgrow their
blood supply. As a result, central necrosis and ring enhancement are often seen in lymphomatous
masses in AIDS patients. On MR spectroscopy, lymphomas exhibit elevated choline little or no
NAA.

METASTATIC DISEASE

Metastases to the brain occur by hematogenous spread, and multiple lesions are found in
70% of cases. The most common primaries are lung, breast, and melanoma, in that order of
frequency. Other potential sources include the gastrointestinal tract, kidney, and thyroid.
Metastases from other locations are uncommon. Clinical symptoms are nonspecific and no
different from primary brain tumors. If a parenchymal lesion breaks through the cortex, tumor
can extend and seed along the leptomeninges.

Metastatic lesions can be found anywhere in the brain but a favorite site is near the brain
surface at the corticomedullary junction of both the cerebrum and cerebellum. They are
hyperintense on plain T2-weighted images. Areas of necrosis are prevalent in the larger lesions,
accounting for their heterogeneous internal texture. Peritumoral edema is a prominent feature,
but multiplicity is the most helpful sign to suggest metastatic disease as the likely diagnosis.
Correlative studies have shown MR to be more sensitive than CT for detecting metastases,
particularly lesions near the base of the brain and in the posterior fossa. One limitation of plain
MR is the frequency of periventricular white matter hyperintensities found in the same older age
group at risk for metastatic disease.

Gadolinium enhanced MR has resulted in improved delineation of metastatic disease


compared with nonenhanced scans. Moderate to marked enhancement is the rule, nodular for the
smaller lesions and ringlike with central nonenhancing areas for the larger ones. Controlled
20
clinical trials have also shown that contrast-enhanced MR is more sensitive than both plain MR
and contrast-enhanced CT for detecting cerebral metastases. In patients with a known primary,
T1-weighted enhanced MR is probably sufficient to screen the brain for metastatic disease.

Hemorrhage is present in 3 to 14% of brain metastases, mainly in melanoma,


choriocarcinoma, renal cell carcinoma, bronchogenic carcinoma, and thyroid carcinoma. The
presence of nonhemorrhagic tissue and pronounced surrounding vasogenic edema are clues to
the underlying neoplasm.

Metastatic melanoma has been a topic of special interest in the MR literature because of
the presence of paramagnetic, stable free radicals within melanin. The MR appearance is variable
depending on the histology of the melanoma and the components of hemoglobin. Most are
hyperintense to white matter on T1-weighted scans and hypointense on T2-weighted scans. Atlas
and coworkers observed three distinct signal intensity patterns. Nonhemorrhagic melanotic
melanoma was markedly hyperintense on T1-weighted images and isointense or mildly
hypointense on T2-weighted images. Nonhemorrhagic amelanotic melanoma appeared isointense
or slightly hypointense on T1-weighted scans and isointense or slightly hyperintense on T2-
weighted scans. The signal pattern for hemorrhagic melanoma was variable depending on the
components of hemoglobin. Some uncertainty remains as to whether the predominant effect on
signal intensity within melanomas is due to stable free radicals, chelated metal ions, or
hemoglobin.

INTRAVENTRICULAR TUMORS

The intraventricular location is unique in that many of the tumor types are more
commonly associated with extra-axial locations. Patients often present with obstructive
hydrocephalus. Most intraventricular tumors are relatively benign and have well-defined
margins. As they grow, the tumors expand the ventricle of origin. With malignant degeneration,
extension into the brain parenchymal occurs. The primary blood supply to intraventricular
lesions is derived from the choroidal arteries.

MENINGIOMA

Meningiomas account for 15% of all intracranial tumors and are the most common extra-
axial tumor. They originate from the dura or arachnoid and occur in middle-aged adults. Women
are affected twice as often as men. Meningiomas are well-differentiated, benign, and
encapsulated lesions that indent the brain as they enlarge. They grow slowly and may be present
for many years before producing symptoms. The histologic picture shows cells of uniform size
that tend to form whorls or psammoma bodies.

The parasagittal region is the most frequent site for meningiomas, followed by the
sphenoid wings, parasellar region, olfactory groove, cerebello-pontine angle, and rarely the
intraventricular region. Meningiomas often induce an osteoblastic reaction in the adjacent bone,
resulting in a characteristic focal hyperostosis. They are also hypervascular, receiving their blood
supply predominantly from dural vessels.

Most meningiomas are isointense with cortex on T1- and T2-weighted images. A
heterogeneous internal texture is found in all but the smallest meningiomas. The mottled pattern
21
is likely due to a combination of flow void from vascularity, focal calcification, small cystic foci,
and entrapped CSF spaces. Hemorrhage is not a common feature. An interface between the brain
and lesion is often present, representing a CSF cleft, a vascular rim, or a dural margin. MR has
special advantages over CT in assessing venous sinus involvement and arterial encasement.
Occasionally, a densely calcified meningioma is encountered that is distinctly hypointense on all
pulse sequences.

Meningiomas show intense enhancement with gadolinium and are sharply circumscribed.
They have a characteristic broad base of attachment against a dural surface. Associated
hyperostosis may result in thickening of low signal bone as well as diminished signal from the
diploic spaces. Although meningiomas are not invasive, vasogenic edema is present in the
adjacent brain in 30% of cases. Contrast scans are especially helpful for imaging the en plaque
meningiomas that occur at the skull base. MR spectroscopy shows elevated alanine and
glutamates, no NAA, and markedly decreased creatine.

BRAIN STEM AND POSTERIOR FOSSA

CRANIAL NERVES

ANATOMY

The cranial nerve nuclei are located in the tegmentum of the brainstem, just ventral to the
cerebral aqueduct and 4th ventricle. The 3rd nerves (oculomotor) pick up parasympathetic fibers
from the Edinger-Westfall nucleus and course ventrally through the substance of the midbrain to
exit in the interpeduncular cistern. The cisternal segments continue ventrally between the
posterior cerebral and superior cerebellar arteries and enter the cavernous sinuses. The 4th nerves
(trochlear) are the only cranial nerves to cross the midline. They course dorsally and cross behind
the aqueduct, exit the dorsal midbrain, and travel forward in the ambient cisterns to reach the
cavernous sinuses. Other major structures within the midbrain include the pyramidal
(corticospinal and corticobulbar) tracts within the cerebral peduncles, the substantia nigra, the
red nuclei, the decussation of the superior cerebellar peduncles, and the superior and inferior
colliculi of the quadrigeminal plate.

The pons contains the nuclei for the 5th (trigeminal), 6th (abducens), 7th (facial), and the
8th (acoustic) cranial nerves. The 5th nerve enters the mid-portion of the pons ventrolaterally.
The spinal tract and nucleus of the 5th nerve extends from the upper pons all the way down into
the upper spinal cord. The 6th exists ventrally at the pontomedullary junction. Both the 5th and
6th nerves course through the cavernous sinus. The 7th nerve loops posteriorly around the 6th
nerve nucleus and indents the floor of the 4th ventricle (facial colliculus). The 7th and 8th nerves
exist the inferior pons inferiolaterally, traverse the cerebellopontine cistern and enter the internal
auditory canal. The anterior pons (basis pontis) contains a large number of transverse fibers from
the middle cerebellar peduncles and longitudinal, dispersed bundles of the pyramidal tracts.

The medulla contains the remaining cranial nerves. Nerves 9 (glossopharyngeal), 10


(vagus), and 11 (spinal accessory) exist laterally just posterior to the olivary nucleus and course
toward the jugular foramen. The 12th cranial nerve (hypoglossal) exists the medulla ventral to
the olive and courses ventrally to the hypoglossal canal. The medulla also contains the
22
decussation of the pyramids (corticospinal tracts) ventrally and the inferior cerebellar peduncles
posteriorly.

Two other important fiber tracts are the medial longitudinal fasciculus (MLF) and the
medial lemniscus. The MLF, which connects the 3rd, 4th, and 6th cranial nerve nuclei, lies in a
paramedian position just ventral to the aqueduct and 4th ventricle. The medial lemniscus, the
major sensory tract, ascends through the brainstem just ventral to the MLF.

Pathology

Nerve sheath tumors

Tumors of schwann cell origin include schwannoma and neurofibroma. Schwannomas


are more common and most arise from the 8th cranial nerve. Neurofibromas are usually
associated with neurofibromatosis. Acoustic neuromas originate on the vestibular division of the
eighth cranial nerve just within the internal auditory canal. Bilateral lesions are common with NF
2. They usually present in middle-aged adults with a sensorineural hearing loss, but other
symptoms include headache, vertigo, tinnitus, unsteady gait, and facial weakness. Large tumors
may fill the cerebellopontine angle cistern and compress adjacent brain structures, producing
additional symptoms.

Most schwannomas are isointense to the brain on MR images, but some are distinctly
hyperintense with T2-weighted sequences. Occasionally, a schwannoma will be hyperintense on
T1-weighted images owing to foci of hemorrhage. They may be heterogeneous on T2-weighted
images as well, particularly the larger ones, due to necrosis, hemorrhagic components, and
occasional calcification. With small intracanalicular tumors, partial voluming effects may result
in uneven signal intensity.

Gadolinium causes approximately 50% shortening of the T1 relaxation time of


schwannomas, making them appear very bright on T1-weighted images. Those lesions that are
heterogeneous on plain scan will likely exhibit heterogeneous enhancement as well.

Meningioma

Meningiomas originate from the dura or arachnoid and occur in middle-aged adults. In
the posterior fossa, most meningiomas are found in the cerebellopontine angle. Women are
affected twice as often as men. Meningiomas are well-differentiated, benign, and encapsulated
lesions that indent the brain as they enlarge. They grow slowly and may be present for many
years before producing symptoms. The histologic picture shows cells of uniform size that tend to
form whorls or psammoma bodies. They are hypervascular, receiving their blood supply
predominantly from dural vessels.

Most meningiomas are isointense with cortex on T1- and T2-weighted images. A
heterogeneous internal texture is found in all but the smallest meningiomas. The mottled pattern
is likely due to a combination of flow void from vascularity, focal calcification, small cystic foci,
and entrapped CSF spaces. Hemorrhage is not a common feature. An interface between the brain
and the lesion is often present, representing a CSF cleft, a vascular rim, or a dural margin. MR
has special advantages over CT in assessing venous sinus involvement and arterial encasement.
23
Occasionally, a densely calcified meningioma is encountered that is distinctly hypointense on all
pulse sequences.

Meningiomas show intense enhancement with gadolinium and are sharply circumscribed.
They have a characteristic broad base of attachment against a dural surface. Contrast scans are
especially helpful for imaging the en plaque meningiomas that occur at the skull base.

Arachnoid Cyst

Arachnoid cysts are benign but slowly grow as they accumulate fluid, compressing
normal brain structures. Most are smoothly marginated and homogeneous. They are not calcified
and do not enhance. The cyst fluid is usually isointense with CSF on all pulse sequences. The
cysts may appear higher signal than CSF on intermediate T2-weighted images due to dampening
of the CSF pulsations that normally results in signal loss in the ventricles and cisterns. This effect
will be less apparent with pulse sequences that incorporate flow compensation techniques.

INTRAAXIAL TUMORS

Except for hemangioblastoma and metastatic disease, the majority of intra-axial posterior
fossa tumors occur in children. Cerebellar astrocytoma accounts for 33% of these childhood
tumors, medulloblastoma 26%, brain stem glioma 21%, ependymoma 14% and choroid plexus
papilloma, only 2%.

Brain Stem Glioma

Most brain stem gliomas are relatively benign initially but frequently evolve to a higher
grade. They usually present with a cranial nerve palsy, most often involving the 6th or 7th
nerves. The pons is the common location, but they also occur in the medulla and midbrain. These
tumors infiltrate the brain stem and induce surrounding vasogenic edema in the brain
parenchyma. Since both the tumor and edema are hyperintense on T2-weighted images, tumor
margins tend to be indistinct and poorly defined.

Brain stem gliomas are relatively homogeneous masses without much cystic change,
necrosis, vascularity or calcification. About 50% of cases will show mild enhancement. As the
gliomas grow, they enlarge the brain stem, producing effacement of the basal cisterns, anterior
displacement of the basilar artery against the clivus, and compression and posterior bowing of
the fourth ventricle. Hydrocephalus is often present. Exophytic growth is a well-known feature
of these tumors.

Cerebellar Astrocytoma

Cerebellar astrocytoma is the most common CNS tumor in children. They tend to be
lower grade than the supratentorial variety found in adults and are often quite large by time of
presentation. The majority are hemispheric in location, a helpful but not absolute criterion to
distinguish them from medulloblastoma.

More than 50% of cerebellar astrocytomas are cystic, and the cyst contents often have
elevated protein, making them slightly higher signal than CSF but lower signal than brain on T1-
24
weighted images. The solid components are hyperintense to brain on proton density-weighted
images. Both solid tumor and cyst are bright on T2-weighted scans. Calcification is occasionally
present. Peritumoral edema is not pronounced, and in general, their margins are defined better
than in supratentorial gliomas. Cerebellar astrocytomas exhibit nodular or ringlike enhancement.
Since these tumors are frequently large, mass effect is a prominent feature. Anterior and lateral
displacement of the fourth ventricle is common. Upward herniation of the superior vermis and
downward herniation of the cerebellar tonsils can also occur.

Medulloblastoma (and PNET)

The majority of medulloblastomas occur in children between four and eight years old,
and males outnumber females three to one. Primitive neuro-ectodermal tumors (PNET) may
present at birth or early infancy. Medulloblastomas and PNETS arise from remnants of primitive
neuro-ectoderm in the roof of the fourth ventricle. These tumors are very malignant and exhibit
an aggressive biologic behavior, commonly invading the adjacent brain stem and leptomeninges.
Widespread dissemination through the ventricular system and distant seeding to other areas of
the neuraxis occurs in as high as 30%.

Medulloblastomas are primarily midline vermian lesions, but hemispheric locations are also
possible. Since they arise close to the fourth ventricle, growth predominantly into the ventricle
may make them simulate an intraventricular mass. Necrosis, hemorrhage and cavitation are
common features, giving these tumors a heterogeneous appearance on MR, but not to the same
degree as seen with ependymomas. Calcification is rare in medulloblastomas. They are
hypervascular lesions and show moderate contrast enhancement.

Ependymoma

About 70% of ependymomas are found in the fourth ventricle. The atria of the lateral
ventricles are another common site. Males are affected twice as often as females. They originate
from the ependyma of the ventricles but may grow either into the ventricle or into the brain
substance. Ependymomas are slow-growing, but malignant, tumors and grow by expansion and
infiltration. Ventricular and subarachnoid seeding are not infrequent.

Most ependymomas arise in the floor of the fourth ventricle. They have a propensity to extend
through the foramina of Luschka and Magendie into the basal cisterns. They tend to be well
defined, particularly if they are marginated by CSF within a ventricle or cistern. Calcification is
present in 50%, cysts and necrotic areas are common, and most are moderately vascular. These
properties account for their heterogeneous internal texture on both plain and contrast scans.

Hemangioblastoma

Hemangioblastoma is a benign tumor of middle age. In fact, it is the most common


primary intra-axial tumor of the posterior fossa in adults. About 20% are associated with Hippel-
Lindau disease, and hereditary factors have been implicated in another 20%. The cerebellum and
vermis are the common sites, but hemangioblastomas can also be found in the medulla and spinal
cord. Multiplicity is a well-known feature but is present in only about 10% of cases. Histologic
examination reveals a meshwork of capillaries and small vessels.
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The classic MR appearance of hemangioblastoma is a cystic mass with a brightly enhancing
nodule. About 60% are cystic, so solid lesions are not uncommon. Calcification is rare.
Hemangioblastomas are sharply marginated and induce minimal surrounding parenchymal
reaction. The tumor nodules are hypervascular and the vascular pedicle often produces a
characteristic flow void on MR.

Metastatic disease

Metastases to the brain occur by hematogenous spread, and multiple lesions are found in
70% of cases. The most common primaries are lung, breast, and melanoma, in that order of
frequency. Other potential sources include the gastrointestinal tract, kidney, and thyroid.
Metastases from other locations are uncommon. Clinical symptoms are nonspecific and no
different from primary brain tumors. If a parenchymal lesion breaks through the cortex, tumor
can extend and seed along the leptomeninges.

Metastatic lesions can be found anywhere in the brain but a favorite site is near the brain surface
at the corticomedullary junction of both the cerebrum and cerebellum. They are hyperintense on
plain T2-weighted images. Areas of necrosis are prevalent in the larger lesions, accounting for
their heterogeneous internal texture. Peritumoral edema is a prominent feature, but multiplicity is
the most helpful sign to suggest metastatic disease as the likely diagnosis. Hemorrhage is present
in 3 to 14% of brain metastases, mainly in melanoma, choriocarcinoma, renal cell carcinoma,
bronchogenic carcinoma, and thyroid carcinoma. The presence of nonhemorrhagic tissue and
pronounced surrounding vasogenic edema are clues to the underlying neoplasm.

Gadolinium enhanced MR results in improved delineation of metastatic disease compared with


nonenhanced scans. Moderate to marked enhancement is the rule, nodular for the smaller lesions
and ringlike with central nonenhancing areas for the larger ones. Correlative studies have shown
MR to be more sensitive than CT for detecting metastases, particularly lesions near the base of
the brain and in the posterior fossa.