CNS RADIOLOGY 1st sem SY 2014

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NERVOUS SYSTEM

Looking at the brain:
Midline
Symmetry
Basal Cisterns
o Quadrigeminal Plate
o Suprasellar
Ventricles
o Suprasellar
o Pineal
o Craniocervical region

EXAMINATION OF THE CENTRAL NERVOUS SYSTEM
skull radiograph
ultrasound
Cranial Ultrasound:
CSF black
Hemorrhage white
computed tomography (CT)
Cranial CT Scan
Brain window brain is being assesed
Bone window bone is being assesed
Punched-out lesion metastasis or
meningioma
angiography
radionuclide (nuclear imaging)
magnetic resonance (MR) for soft tissue imaging
MR Spectroscopy (MRS)
o Newer modality
o Each peak of metabolites has corresponding
pathologic diagnosis
o Available in 1.5 3.0 TESLA machine
o Metabolites
Choline tumor
N-acetyl aspartate (NAA)
Creatine
Lactic Acid inflammation
Diffusion-Weighted MR Imaging
o Used by neurologists to diagnose ischemic strokes
o <6 hours of infarct/ischemia is diagnostic on
DWI/ADC-time restricted diffusion
o FMRI (functional MR imaging)
CT SCAN IS THE TECHNIQUE OF CHOICE FOR:
evaluation after acute trauma
suspected acute intracranial hemorrhage
diseases of the skull base or calvaria
when MRI is contraindicated
REASONS FOR THE USE OF INTRAVENOUS CONTRAST
MEDIUM
iodinated contrast (for CT) and gadolinium paramagnetic
contrast (for MR) do not cross the blood brain barrier
in the presence of pathology/ disruption of the BBB,
contrast will localize in the site of pathology
also improves definition of vascular and dural structures

X-RAY AND ULTRASOUND
x-ray has no meaningful role
ultrasound has limited use because of thick calvaria
in neonates and infants, use the open fontanels
transcranial doppler probes for intracranial evaluation

ANGIOGRAPHY AND RADIONUCLIDE IMAGING
many of the indications for cerebral angiography have been
eliminated by CTA, MR and MRA
radionuclide imaging has specific roles in seizure disorders,
dementia, psychiatric disorders, brain death

MRA
Analysis of the abnormality
o Intraaxial in the parenchyma
o Slightly, moderate, or markedly enhanced?
o Cystic or fluid?
o Solid or heterogenous?


INTRACRANIAL CALCIFICATION AND OSSIFICATIONS

Physiologic Intracranial Calcifications
pineal gland
habenular commissure
choroid plexus
dura
Pacchionian bodies
basal ganglia and dentate nucleus

PINEAL GLAND CALCIFICATION
almost always present in the adult
Rare before 6 years old
cluster of amorphous irregular calcifications, or may be
solitary
usually 10-12 mm in greatest diameter; usually 3-5 mm
calcifications greater than 1 cm, suspect pineocytoma or
AVM
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CHOROID PLEXUS CALCIFICATION
almost all adults; also frequent in children
frequently seen at the glomera (atria of lateral ventricles)
DURAL CALCIFICATIONS
plaque-like calcification
common in the falx and in the edges of the tentorium
free edges of the tentorium posterior to the sella (the
petroclinoid ligaments) are prone to dense calcifications
may be part of the basal cell nevus syndrome

CEREBROVASCULAR DISEASES
Ischemic Stroke
Etiology
CT Scan
Hypodense artery sign
MRI is superior
Normal black signal

EDEMA
increase in fluid in the brain tissue
primarily intracellular because of some insult to the cell =
cytotoxic edema
may be extracellular related to loss of blood-brain barrier =
vasogenic edema

CYTOTOXIC EDEMA
seen in strokes, hypoxemic injury (near-drowning), viral
cerebritis, cortical edema from status epilepticus
seen in neuronal cell bodies ( in gray matter)
on CT, leads to diminished density of gray matter
blurring or loss of distinction between gray and white
matter
on MRI, diminished signal on T1-weighted images, and
increased signal on T2-weighted images

VASOGENIC EDEMA
seen in metastatic or primary neoplasm, infections
primarily a white matter phenomenon because the
intercellular spaces are larger in the white matter, with
notable exception of the corpus callosum

EDEMA
increased brain volume versus fixed volumes of the
intracranial compartments
may cause brain tissue to be deformed or to herniate from
one compartment to another

EDEMA INJURY
may lead to death with downward brainstem herniation or
cerebellar tonsillar herniation, which compromise the
medulla
death through an overall pressure effect
death from ischemia when intracranial approaches or
exceeds arterial perfusion pressure
direct physical deformation of the brain parenchyma
injury of the brain along the edges of the dural reflections
across which it is squeezed
pressure on other portions of the brain
compromise of the vascular supply
compromise of other structures (ie. cranial nerves)

ACUTE MCA ISCHEMIA ON CT
Insular ribbon sign
Lentiform nucleus edema sign

CT SCAN AND MRI IN ISCHEMIA
Left temporoparietal lobe thrombus

CNS NEOPLASMS
Approach to radiographic abnormality
Is it a mass?
Intraaxial or extraaxial?
Tumor margins
MRI is modality of choice for intracranial neoplasm

NEOPLASMS: GENERALITIES
classified by anatomic location and cell of origin
o intraaxial = lesion within the brain
o extraaxial = lesion outside the brain
70% of tumors in adults are supratentorial
most tumors in children are infratentorial
most common primary tumors in adults - astrocytomas,
glioblastomas
most common primary tumor in children - astrocytoma of
the cerebellum or brainstem
extraaxial location of tumor = more favorable prognosis

NEOPLASMS: INCIDENCE
gliomas = 43%
meningiomas = 15%
pituitary adenomas = 13%
acoustic neuromas = 6.5%
congenital tumors = 4%
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blood vessel tumors = 3%
miscellaneous = 9%

INTRACRANIAL TUMORS

GLIOMAS
graded from 1 to 4, grade 4 being most malignant
grade 1 and 2 are the more benign astrocytomas
grade 3 are anaplastic astrocytomas
grade 4 are glioblastoma multiforme
classification may include cell morphology (fibrillary or
pilocytic), and site of origin (supra- or infratentorial)
gliomas seldom of pure histologic type

GLIOBLASTOMA MULTIFORME
invasive, malignant tumor of astrocytic origin
most common supratentorial glioma
Butterfly glioma
between 40-60 years
rapid onset of symptoms; infiltrative; spread rapidly
involvement of both cerebral hemispheres via spread
through corpus callosum common
may spread through ventricular system or subarachnoid
space
true multicentric tumors are rare
MR - increased signal intensity is related to vasogenic
edema
show marked enhancement on contrast
enhancement because of tumor neovascularity and the
resulting increased permeability of the BBB
margins of the tumor are irregular
pattern of contrast enhancement is heterogenous
mass effect is usually present
if the frontal or parietal lobes are involved, usually crosses
midline and deformity of both ventricles occur
central necrosis of the tumor occurs
cysts sometimes occur
difficult to accurately differentiate the infiltrating margin of
the tumor form adjacent normal brain tissue
CT demonstrates less of the pathologic findings than MR
o Ring enhancing lesions (MAGIC DR)
o Contralateral heterogenous enhancing margins

ANAPLASTIC ASTROCYTOMA
second most common supratentorial glioma
less infiltrative and less rapid than glioblastoma multiforme
comprise 32% of all supratentorial tumors

LOW-GRADE ASTROCYTOMA
symptoms duration to the time of diagnosis usually 3 years
large cysts usually form in astrocytomas
cystic element may predominate in the pathologic and
radiographic appearance
calcification occurs in the minority
variable degree of enhancement on contrast
for small lesions, CT may be normal or show only mass
effect, with displacement, distortion or compression of the
ventricles
MR is more accurate than CT in demonstrating the borders
of the lesion

JUVENILE PILOCYTIC ASTROCYTOMA
variety of low-grade astrocytoma that occurs in children
occurs in or adjacent to the visual pathways or posterior
fossa
well-defined; enhance markedly on CT and MR
cyst formation is common

OLIGODENDROGLIOMA
7% of supratentorial gliomas
average age at time of diagnosis is 45 years
grow slowly, duration of symptom to diagnosis is 11 years
occurs almost exclusively in the cerebral
hemispheres
predilection for frontal lobes
calcification (course, irregular strands within the tumor
occurs frequently) on CT Scan
lack of neovascularity and minimal disruption of BBB,
contrast enhancement is slight
cystic and necrotic changes are rare

INTRAAXIAL TUMORS: NON-GLIAL AND MIXED GLIAL

PRIMARY CNS LYMPHOMA

EPENDYMOMA
5% of supratentorial gliomas
duration of symptom to diagnosis is short, usually 1 year
average age at diagnosis is 30 years
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infratentorial ependymomas occur in children and
adolescents; more common than the supratentorial form
arise from ependymal cell nests at margin of lateral
ventricles
occur near the atrium of the lateral ventricles
often contain scattered small or punctate calcium deposits
cystic changes may occur
enhances on contrast

MENINGIOMA
extraaxial tumors that arise from the arachnoid
majority are benign
common sites
along superior sagittal sinus
region of tuberculum sellae or anterior to the
tuberculum along the olfactory groove
edge of sphenoidal ridge
margin of falx cerebri and tentorium
derive blood supply from arteries supplying the dura
may parasitize vasculature of adjacent brain
may obstruct dural sinuses
most incite osseous response (ie. hyperostosis) and may
invade bone producing hyperostotic density on outer table
may produce bone destruction
some completely destroys bone, with a soft-tissue mass
bulging externally
calcification found in 15-20%
small punctate densities
sand-like deposits = psammoma bodies
some form densely calcified masses
homogeneous enhancement on contrast administration,
with well defined margin and with an adjacent dura tail
MR shows hypointense lesion (T1W) and hyperintense
(T2W), with sharply defined magins

PITUITARY ADENOMA
classified as hormonally active versus hormonally inactive
hormonally active adenomas are further subdivided
according to the hormone they secrete
depending on size , classified as
o macroadenoma (>1cm)
o microadenoma (<1cm)
macroadenomas, usually hormonally inactive, become
clinically manifest as a result of their size, compressing
adjacent neural structures (ie. Optic chiasm)
microadenomas seek medical attention because of
abnormal hormone secretion
o prolactinomas - galactorrhea and amenorrhea;
hypogonadism in male
o growth-hormone-secreting adenomas - gigantism;
acromegaly
o ACTH-secreting adenomas - Cushings disease

PITUITARY MICROADENOMA
contrast MR - reduced signal intensity (on T1W) on top of
an enhancing pituitary gland
increased height of the gland (usually <10mm) with
alteration in contour of the upper margin of the gland
erosion of the floor of the sella turcica
displacement of the normally midline pituitary stalk

PITUITARY MACROADENOMA
contrast MR - marked homogeneous enhancement
cystic or necrotic areas in large macroadenomas

CRANIOPHARYNGIOMA
congenital tumor which arises from remnants of Rathkes
Pouch
tumor of childhood and adolescence
In young children, clinical complaints are related to
increased intracranial pressure
In older children and adults, symptoms are visual or
endocrine in nature (ie. Delayed growth)
calcification occurs in 80%
most are suprasellar; 10-15% within the pituitary fossa
cystic changes may occur
variable appearance on MR depending on the amount of
calcification (low intensity on T1w and T2W) and cystic
change (high signal on T1W and T2W)
solid portions of the tumor enhance in a homogeneous
manner

SCHWANNOMA
benign tumors occuring along the course of cranial, spinal
and peripheral nerves
previously called neuromas or neurilemmomas which are
misleading
adults; 2W:1M
eighth cranial nerve most frequently involved; fifth nerve
also
of the VIII CN - hearing loss, tinnitus, vertigo or dizziness
most common tumor of the cerebellopontine angle
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CT - large lesions will obliterate the CP angle, displace
brainstem and IV ventricle, and widen the contralateral CP
angle cistern
small lesions may only enlarge the internal auditory canal
enhances considerably on contrast
MR - reduced signal on T2W; intense enhancement on
contrast
Acoustic Schwannoma CT angle : pontine involvement

METASTASIS TO THE CNS FROM EXTRACRANIAL SITES
o Intraaxial
o Extraaxial
o Hemorrhagic
o On CT and MRI
o Intense enhancement

Leptomeningeal Carcinomatosis

METASTASIS
most arise from hematogenous spread
tends to occur in the distribution of the end-arteries, hence
at the gray-white matter junction, and in the distribution of
the deep perforating arteries
melanoma, lung, breast, colon, kidneys
CT and MR findings vary, depending on the primary source
(ie. cellularity), vascularity and biological behavior, number
and location of tumors, and previous treatment
CT - often multiple, fairly discrete, surrounded by low
density edema
calcification is unusual (except osteogenic sarcoma)
tendency to hemorrhage spontaneously (melanoma, renal
cell, choriocarcinoma)
contrast CT - most will enhance, though variable in pattern
MR - hypointense on T1W, heterogenously hyperintense on
T2W
most enhance on contrast administration

POSTERIOR FOSSA TUMORS
Choroid Plexus Papilloma
Carcinoma
Colloid Cyst

HEAD TRAUMA
MRI is not needed in Acute Head Trauma
Skull Xray is not helpful
Assess whether scalp injury or skull injury
CT is the diagnostic method of choice; MRI slowly
supplanting CT
detection of hemorrhages - subarachnoid,
intraparenchymal, extraaxial (subdural, epidural)
contusions, diffuse axonal (shearing) injury, diffuse brain
swelling

HEAD TRAUMA: PARENCHYMAL HEMATOMA
increased density on CT
margins are irregular but very distinct
homogeneous in character
occur most frequently in the inferior frontal and temporal
lobes, and basal ganglia
extraventricular obstructive hydrocephalus arachnoid
scarring lead to blockage of CSF absorption

SUBARACHNOID HEMORRHAGE


HEAD TRAUMA: BRAIN CONTUSION
may not be visualized on CT initially, unless large or
associated with hemorrhage
become apparent 1-2 hours after injury
mixed high and low density - small hemorrhages with
surrounding edema
frontal and temporal lobes adjacent to calvaria
CORTICAL CONTUSIONS
in the brain cortex
Areas
Multiple
Common sites
On CT
Salt and pepper pattern
On MRI

SUBDURAL HEMATOMA
bleeding into subdural space
over the convexity of the cerebral hemisphere
early detection by CT has reduced mortality in acute
subdural hematomas
appearance varies on
o age of blood
o whether repeated episodes of bleeding occurred
o unilateral or bilateral
o level of patients hematocrit (has haematocrit
effect)
hyperdense, isodense, hypodense
o hyperdense in early stage - 1 to 10 days
o isodense - 1 to 3 weeks
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o hypodense - after 1 month
crescentic configuration crescent shape bleeding
mass effect is greater than the size of the hematoma;
reflect underlying brain swelling and injury that accompanies
the hematoma
in large hematomas, medial margin may be straight or
convex, simulating epidural
hematoma may be heterogeneous even in acute bleed if
there is incomplete clotting due to disorder of clotting
mechanism
chronic subdural hematoma

EPIDURAL HEMATOMA
result of injury to meningeal vessels (arterial)
most commonly occur in the lateral surface of cerebral
hemisphere
hyperacute hematoma - first hour of injury - portions of
low density blood indicating bleed has not yet clotted or is
still bleeding; neurosurgical emergency!
acute hematoma - 1 to 2 hours - hyperdense (but may be
hypodense in px with anemia or DIC)
occur between the dura and calvaria constrained resulting
in biconvex configuration
may cross the midline because they are external to the falx
do not cross sutures

INTRAVENTRICULAR HEMORRHAGE
may puti

DIFFUSE AXONAL INJURY
m

INTRACEREBRAL HEMORRHAGE
Subcortical gray matter injury
Multiple petechial hemorrhage

CNS INFECTION
pyogenic
atypical bacterial
fungal
viral
parasitic
prion (slow virus)

Viral Meningoencephalitis
diagnostic neuroimaging is optimized by clinical
information
neuroimaging patterns are limited

MENINGITIS
infection in the subarachnoid space - leptomeninges
secondary involvement of the epidura, dura, subdura,
brain parenchyma
severe cases
o pial and ependymal enhancement
o abnormal signal or density of CSF because of high
protein content or frank pus
o brain edema
o stroke from vasospasm

SUBDURAL AND EPIDURAL EMPYEMA
in untreated, high mortality rates
develops in association with osteomyelitis of the skull,
sinusitis, meningitis or penetrating trauma
extraaxial fluid collections
may extend to interhemispheric fissure or margin of
tentorium

CEREBRITIS AND BRAIN ABSCESS
cerebritis/encephalitis
most frequently from hematogenous dissemination of
infectious agents, often from the lung
direct extension from sinuses or middle ear
none produce totally characteristic radiographic finding
immunosuppression, cyanotic heart disease, pulmonary AV
fistula predispose patients to develop brain abscess
initially consist of small, scattered foci of cerebritis
mature into well-demarcated, encapsulated lesion
central portion with suppurative material and debris
CT - areas of hypodensities, with little enhancement on
contrast
later, neovascularity and collagen capsule develop; ring
enhancement become apparent

ATYPICAL BACTERIA, FUNGI AND PARASITES
taenia solium
o cysticercosis
o multiple small larvae are asymptomatic when alive
o encysted larvae dies eliciting inflammatory
reaction leading to seizures and ring enhancing brain
lesions

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CEREBRAL INFARCTION
ischemic brain infarcts commonly due to atherosclerosis
embolic brain infarcts result from emboli from the heart
other causes - primary arterial diseases such as
fibromuscular hyperplasia, arterial dissections and arteritis;
venous occlusive disease; septic or tumor emboli
CT most commonly employed
MRI is superior
CT scan findings depend on
o size of the abnormality
o association with significant hemorhage
o time interval between the time of infarct and the
time of CT scan
o location of the infarct
CT scan finding may be normal within the first 24 hours if
nonhemorrhagic, small, or located in the brainstem
infarcts involving the cerebral hemispheres are
evident within the first few hours after onset
CT findings
o loss of distinction with the gray and white matter
o subtle obliteration of the cortical sulci
o reduced density related to vascular distribution
o poorly defined, heterogeneous reduced density;
may or may not cause mass effect
o may have sharp margin and homogeneous
attenuation
MRI findings
o demonstrates ischemic changes earlier than CT
o on T1-weighted images - decreased signal intensity
with loss of normal signal difference between gray
and white matter
o on T2-weighted images - increased signal intensity
o small hemorrhages in the infarcts are seen on MRI
but not seen on CT

BRAIN INFARCTION
Loss of
Subtle
Reduced density
Infarction black on CT Scan

VASCULAR INJURIES
Arterial
Internal carotid injury
Carotid cavernous fistula
o On MRI
o Proptosis
o Selective carotid angiography with rapid
flowing
Cavernous sinus in middle portion
Inferior Carotid Artery

Hemorrhagic Transformation of Infarction
Peak time is 1-10weeks, 2 weeks most infarction
happen
Petechial gyral pattern
Large cortical infarcts

Watershed (Borderzone) Infarction
Infectious
Rosary head sing

SMALL VESSEL ISCHEMIA
Lacunes little lakes as a result of
Differentiated from Virchow robin spaces which is
benign

Venous Infarction
Venous clot scar

Empty delta sign
Pattern of hemorrhagic infarction

Parenchymal Hemorrhage

Vascular Malformations
Primary hemorrhage VS hemorrhagic neoplasms
Primary hemorhhage VS hemorrhagic transformation of
infarction (infarct that becomes hemorrhagic again)

HYPERTENSIVE HEMORRHAGES 200/100mmHg
often occur in the
o external capsule
o thalamus
o internal capsule
o cerebellum
o pons
o lobar white matter
frequently rupture into the ventricular system
areas of high density with sharply defined borders
no edema in acute bleed; edema develops after several days

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INTRACRANIAL ANEURYSM
dilatation of an artery
saccular/berry aneurysm - result of hemodynamic stresses
other types - atherosclerotic, mycotic (infectious),
posttraumatic
become symptomatic because of rupture leading to
subarachnoid and intraparenchymal hemorrhage

SACCULAR ANEURYSMS berry aneurysm
very common, up to 5-9% of the adult population
most aneurysms never rupture
once rupture occurs, 60% will either die or develop
neurologic dysfunction
occur at points of major arterial branching
most common sites
o proximal segment of middle cerebral artery
o anterior communicating artery
o junction between the internal carotid and
posterior cerebral artery
size from less than 1 mm to more than 5 cm
those > 2.5 cm = giant aneurysm

INTRACRANIAL ANEURYSMS
suspected subarachnoid hemorrhage - do NECT (non
enhanced CT)
unilateral location, above or below the tentorium gives
evidence as to where the lesion is most likely located

SECONDARY HEAD INJURIES
Diffuse Cerebral Swelling
Brain Herniation
Hydrocephalus
I?
CSF Leak
Leptomeningeal cyst
Encephalomalacia

Diffuse Cerebral Swelling

Brain Herniation
Subfalcine (cingulate) herniation
Uncal herniation medal temporal lobe downward
Transtentorial herniation upward or downward
External outward through skull defect
Tonsillar herniation downwad to craniocervical
junction

Hydrocephalus

I?

CSF Leak
Dural Tear
Calvaria
CSF rhinorrhea
CSF otorrhea

Leptomeningeal cyst
Growing fracture
Traumatic tear in the dura

Encephalomalacia
Focal

Penetrating Wound
Gunshot wound

Child Abuse
Skull fracture
Subdural hematoma
Whiplash shaken injury
Chronic subdural hematoma
Diffuse brain swelling

MULTIPLE SCLEROSIS
most common demyelinating disease
onset at age 20-50 years
women > men
manifest with clinical exacerbations and remissions
multiple plaques representing areas of demyelination and
varying inflammatory activity
tendency to involve periventricular white matter,
corpus callosum and visual system from the optic nerve to
the occipital lobe; spinal cord
MRI used to demonstrate plaques; follow up of therapy
response
number and distribution areas do not correlate with clinical
severity of disease

MULTIPLE MYELOMA
Salt and pepper appearance

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PARANASAL SINUSES
Frontal, maxillary, sphenoid, ethmoids
AP, Waters view and Lateral view ON X-RAY
CT SCAN and MRI

CROUP (Laryngotracheobronchitis)
AP view of the neck
NORMAL versus ABNORMAL (steeple sign)

Source:
-Old trans
-Brant and Helms Diagnostic Radiology 4
th
Edition