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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.
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.
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.
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.
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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INTRACEREBRAL HEMORRHAGE
CT Features
MR Appearance
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
Cavernous Angioma
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.
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.
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
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
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.
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Tuberculosis
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
Toxoplasmosis
Cytomegalovirus
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.
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.
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
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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.
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.
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
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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.
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.
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
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.
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.
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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%.
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-
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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.
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
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.