Subject: radiology
Topic: neurology 1
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
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PENG KARLA ALPHE AARON KYTH ANNE EISA KRING CANDY ISAY MARCO JOSHUA FARS RAIN JASSIE MIKA SHAR ERIKA MACKY VIKI JOAN PREI KATE BAM AMS HANNAH MEMAY PAU
RACHE ESTHER JOEL GLENN TONI
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2t Shifting /sept 6 ‘08
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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 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 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
Subject: radiology
Topic: neuro 1
Page 2 of 14
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
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.
Subject: radiology
Topic: neuro 1
Page 3 of 14
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.

Vascular Patterns IMAGING OF CEREBRAL HEMORRHAGE and AV

MALFORMATIONS
Since most infarcts result from occlusion of vessels, INTRACEREBRAL HEMORRHAGE
the CT or MR pattern of abnormality should follow one of CT Features
the major vascular territories, such as the anterior
cerebral, middle cerebral or posterior cerebral arteries. Together, hypertension, aneurysm, and vascular
Infarcts can usually be distinguished from inflammatory malformations account for 80% of intracerebral
and neoplastic disease because unlike the white matter hemorrhages. All cerebral hematomas, whatever the
pattern of edema found with tumors and abscesses, cause, have a similar
infarcts involve the cortex as well and, therefore, the resolution pattern on
abnormal density or signal intensity should extend CT. The rate of
peripherally to involve the cortex. As mentioned above, resolution depends
the enhancement pattern of infarcts is also fairly on the size of the
characteristic, having a gyral pattern of enhancement hematoma, usually
along the cortex. If a stroke is due to systemic within one to six
hypotension or hypoxia, the area of infarction is weeks, and they
commonly found in watershed areas between the major resorb from the
vascular territories. outside toward the
center.
Lacunar infarction results from occlusion of the small Perihematoma low
penetrating arteries at the base of the brain, including density appears in
the lenticulostriate and thalamoperforating arteries. 24-48 hours. Rim
They are smaller infarcts (less than 1 cm) and are found enhancement appears in one week and persists for six
in the basal ganglia, thalamus and brainstem. MR is far weeks. The end result of a hematoma is decreased
more sensitive than CT for detecting small lacunar parenchymal density, focal atrophy and local ventricular
infarcts, particularly in the brainstem where CT scans are dilatation.
often degraded by artifacts from the bone at the skull
base. MR Appearance

Intracerebral hematomas have a very dynamic

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
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 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%.
Subject: radiology
Topic: neuro 1
Page 4 of 14
VASCULAR MALFORMATIONS
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.
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.
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.
Subject: radiology
Topic: neuro 1
Page 5 of 14
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 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.
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.
Subject: radiology
Topic: neuro 1
Page 6 of 14
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 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 T2-weighted images that are also

clearly visible as hypointense areas on T1-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
Subject: radiology
Topic: neuro 1
Page 7 of 14
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 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.
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
Subject: radiology
Topic: neuro 1
Page 8 of 14
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.
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,
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
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Topic: neuro 1
Page 9 of 14
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
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-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.
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Topic: neuro 1
Page 10 of 14
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
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 clinical trials have also shown
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Topic: neuro 1
Page 11 of 14
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 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
Subject: radiology
Topic: neuro 1
Page 12 of 14
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
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. 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
Subject: radiology
Topic: neuro 1
Page 13 of 14
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-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.
Subject: radiology
Topic: neuro 1
Page 14 of 14
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.
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