Radiology | Medicine-3

Dr. Jose P. Rizal School of Medicine

Xavier University – Ateneo de Cagayan
Normal Cranial
CT/MRI

Aubrey A. Encong
 CT scan
• Technique of choice
– Acute trauma
– Acute intracranial hemorrhage
– Diseases, base of the skull
– With contraindications to MRI
• Normal CT scan of the head; this slice shows the cerebellum, a small portion of each
temporal lobe, the orbits, and the ethmoid sinuses.
• LEGEND: + - border of maxillary sinus, * - maxillary sinus ostium, U - uncinate
process, E - ethmoid sinuses, IT- inferior turbinate, MT- middle turbinate, S -
septum, C - concha bullosa.
 MRI

• Preferred technique for diagnostic evaluation

of most pxs with neurologic disease
Axial
sagittal
frontal
Arteries and Veins
of the Head

Christine L. Namoc
Arteries of the Head
Common Carotid Artery – divides into:
Internal Carotid Artery supplies the brain
Opthalmic artery
Post. Communicating artery
Anterior cerebral artery
Middle cerebral artery
Arteries of the Head
External Carotid Artery supplies structures
external to the
skull
Superior thyroid artery
Ascending pharyngeal artery
Lingual artery
Facial artery
Occipital artery
Posterior auricular artery
Superficial temporal artery
Maxillary artery
 Ant. Cerebral artery
Circle of Willis Left middle cerebral
Right middle artery
cerebral artery
Ant. Communicating
Basilar artery artery

External Carotid Posterior cerebral artery

arteries Post. Communicating artery
Common Carotid
Arteries Internal Carotid
Artery
Veins of the Head
Veins of the brain Diploic veins
Cerebral veins Emissary veins
Cerebellar veins
Veins of brainstem
Veins of the sinuses
Superior sagittal
Inferior
Straight
Transverse
Sigmoid
Occipital
Cavernous
Superior and inferior petrosal
Veins of the Head
External Jugular Vein Internal Jugular Vein
Posterior external Inferior petrosal sinus
jugular vein Facial vein
Superficial cervical vein Pharyngeal veins
Suprascapular vein Lingual vein
Anterior jugular vein Superior thyroid vein
Middle thyroid vein
Circle of Willis
Anastomosis between branches of 2 internal carotid
arteries and the 2 vertebral arteries
Arteries involved:
Anterior communicating
Anterior cerebral
Internal carotid
Posterior communicating
Posterior cerebral
Basilar (formed by
junction of 2
vertebral arteries)
Normal MR arteriogram, axial slab, MR arteriogram demonstrating markedly
through the circle of Willis diminished left middle cerebral artery flow as
a result of internal carotid occlusion
Normal MR venogram, median sagittal slab MR venogram demonstrating lack of flow in the
superior sagittal and straight sinuses because of
dural sinus thrombosis
 Cranial Nerves

Kenneth Nomer E. Escalante

 Cranial Nerves
I Olfactory Cribriform Plate of Ethmoid
II Optic Optic Canal
III Occulomotor x Superior Orbital Fissure
IV Trochlear Superior Orbital Fissure
V Trigeminal
Opthalmic Superior Orbital Fissure
Maxillary Foramen Rotundum
Mandibular Foramen Ovale
VI Abducens Superior Orbital Fissure
VII Facial Internal Acoustic Meatus
Facial Canal
Stylomastoid Foramen
VIIIVestibulocochlear Internal Acoustic Meatus
IX Glossopharyngeal Jugular Foramen
X Vagus Jugular Foramen
XI Spinal Accessory Jugular Foramen
XII Hypoglossal Hypoglossal Canal
 Skull, from the front
Supraorbital foramen

Frontal bone

Frontal Notch Glabella

Orbit Nasion

Infraorbital margin
Infraorbital foramen
 Foramen magnum

Occipital condyle

Jugular foramen

Carotid canal

Foramen lacerum
 Palatine bone

Foramen ovale

Foramen spinosum
 Foramen ovale

Foramen spinosum

Foramen lacerum

Occipital bone
Jugular Foramen

Parietal bone
 Midbrain (Ventral)
Optic Nerve
(CN II)

Optic Chiasma
Optic Tract

Mamillary body
(not part of midbrain) Cerebral peduncle

Interpemdicular
fossa
Trochlear Nerve
(CN IV)
Occulomotor
Nerve (CN III)
 Pons (Ventral)
Superior pontine
sulcus

Trigeminal Nerve
(CN V)
Eminentia
pyramidalis

Vestibulocochlear
Nerve (CN VIII)

Sulcus basilaris
Facial Nerve (CN
VII)

Inferior pontine
Abducens Nerve sulcus
(CN VI)
 Medulla (Ventral)
Inferior pontine
sulcus
Glossopharyngealn
erve (CN IX)
Pyramids

Vagus nerve (CN Olivary body

XI)
Post-olivary sulcus
Pre-olivary sulcus
Hypoglossal nerve
(CN XII) Pyramidal
decussation
Anterior median
fissure
Spinal accessory
nerve (CN XI)
Olfactory Bulb, Nerve
• Originates as the central process of the olfactory
receptor nerve cells in the mucus membrane above
the superior concha
• Bundles of nerve fibers pass through openings in
the cribriform plate of Ethmoid
• Ends in the Olfactory Bulb in the anterior canial
fossa
• The Olfactory tract runs from the posterior end of
the Olfactory bulb towards the olfactory area in the
cerebral cortex
• MRI of the brain pre and post gadolinium
demonstrates a T1 dark, T2 intermediate to
hyperintense lesion emanating from the anterior
cranial fossa into the left nasal region with moderate,
homogeneous contrast enhancement. There is also a
T1 dark, T2 bright signal present in the left maxillary
sinus, sphenoid sinus, and the left frontal ethmoid
recess, which demonstrates a peripheral rim of
enhancement.
Optic Nerve
• Optic nerve Leaves the orbital cavity through the
Optic Canal with the Ophthalmic Artery
• Optic nerves on both sides join into the Optic
Chiasma
• Optic Tract emerges from the lateral sides of the
chiasma and passes through the lateral side of the
midbrain to the lateral geniculate body and then to
the optic radiation
• Optic radiation curved backwards to the visual
cortex
Optic Schwannoma
Occulomotor, Trochlear, Abducens
• Occulomotor nerve
emerges from the anterior midbrain and divides
into superior and inferior rami which enter the orbit
through the Superior Orbital Fissure
• Trochlear nerve
emerges from the posterior midbrain, lies below
the Occulomotor and enters the orbit through the
Superior Orbital Fissure
• Abducens
emerges from the anterior midbrain and enters
the orbit through the Superior Orbital Fissure
Trigeminal
Trigeminal Neurilema
Facial
Vestibulocochlear
Acoustic Schwannoma
• BrainTF10-Acoustic Schwannoma
• Clinical Profile:
• There was a H/O decreased hearing and tinnitus on the left side with headaches. 
• Findings:
• There is evidence of an extra-axial mass lesion located in the cerebellopontine angle cistern with an
intracanalicular component. This lesion is of intermediate signal intensity on the T1W images and
enhances intensely after contrast administration.    
• Discussion: 
• They account for approximately 7% to 8% of all primary intracranial tumors. They usually arise from the
vestibular portion of the eighth cranial nerve. When bilateral, they are usually associated with
neurofibromatosis type II. They usually involve the intracanalicular portion of the nerve (20% do not have
an intracanalicular component). A mass may also be seen in the cerebellopontine angle cistern.
• MRI:    
• On the T1W images, the lesions are usually hypointense or of intermediate signal and show variable signal
pattern on the T2W images. They are usually well demarcated from CSF, more so on the MR cisternogram
images. Cystic and hemorrhagic changes are more commonly seen, than in meningiomas. Focal/nodular
calcifications may be seen. Widening of the internal auditory canal may be seen. The lesion usually shows
homogeneous contrast enhancement. Occasional inhomogeneous contrast enhancement may be seen.
Tumors without an intracanalicular component may be difficult to differentiate from a meningioma. 
Glossopharyngeal
Vagus
Spinal Accessory, Hypoglossal
 Neural Tube
Disorders

Josie Mae N. Taghoy

• Cause: incomplete development of the
brain, spinal cord and/or their protective
coverings
• Occurs when the fetus' spine fails to close
properly during the early stages of
pregnancy (first 28 days).
• Accdng to the Spina Bifida Association of
America (SBAA), spina bifida is the most
common NTD.
• Other types: anencephaly and
encephaloceles
 SPINA BIFIDA
• Has the best prognosis
• Spine fails to close properly during the
first few weeks of pregnancy, causing
damage to the nerves and spinal cord.
• No cure
• Prognosis depends largely on the
number and severity of abnormalities
• Outlook is poorest for those with
complete paralysis, hydrocephalus and
other problems.
A. Surface of the myelomenigocele has become covered with skin through secondary
epithelization from the margins of the defect B. Sagittal T1-weighted MR demonstrates features
of untreated myelomeningocele: dehiscence of high signal subcutaneous fat (F), fascia, muscle,
and bone in the zone of spina bifida; low position of the spinal cord (C); acute angulation (arrow)
of the cord under the last intact lamina at the upper margin of the spina bifida; and posterior
herniation of the neural tissue (white arrow-heads) forming the dorsal wall of the cerebrospinal
fluid space (S) that protrudes through the spina bifida. This patient also exhibits thoracolumbar
kyphos.
Repaired myelomeningocele with epidermoid inclusion, 4 year old child. Sagittal T1-weighted (A) and T2-
weighted (B) MRI disclose a repaired lumbosacral myelomeningocele. The low-lying spinal cord (c) is
tethered inferiorly by a mass (arrowhead) that is nearly isotense to the cord on the T1- and T2-weighted
images. Closure of the sac has created dorsal fluid compartments with restricted communication. Such
compartments appear brighter on T2-weighted images because of reduced dispersal of signal by the
cerebrospinal fluid pulsations and perhaps because of higher protein concentrations within them.
Spina bifida patient with a congenital
kyphosis (Gibbus) deformity.
ANENCEPHALY
ENCEPHALOCELE
HYDROCEPHALUS
 Chiari
Malformations
(kee-AR-ee)

Paul Carlo P. Araneta

Maureen Irish C. Sambaan
 What are Chiari malformations?

 Chiari malformations (CMs) are

structural defects in the cerebellum
 Normally the cerebellum and parts of
the brainstem sit in an indented space
at the lower rear of the skull, above the
foramen magnum
 When part of the cerebellum is located
below the foramen magnum, it is called
a Chiari malformation
 How does it develop?

 CMs may develop when the bony space

is smaller than normal, causing the
cerebellum and brainstem to be pushed
downward into the foramen magnum and
into the upper spinal canal
 What causes these
malformations?
 Structural defects in the brain and spinal
cord that occur during fetal development
– called primary or congenital CM
 Later in life if spinal fluid is drained
excessively from the lumbar or thoracic
areas of the spine either due to injury,
exposure to harmful substances, or
infection – called acquired or secondary
CM
 Primary CM is much more common than
secondary CM
Classification

Type I involves the extension of the cerebellar tonsils (the lower

part of the cerebellum) into the foramen magnum, without
involving the brainstem

Type II, also called classic CM, involves the extension of both
cerebellar and brainstem tissue into the foramen magnum

Type III is the most serious form of CM.  The cerebellum and
brainstem protrude, or herniate, through the foramen magnum
and into the spinal cord

Type IV involves an incomplete or underdeveloped cerebellum

— a condition known as cerebellar hypoplasia
 Cephaloceles

Candy T. Cahilog
Livey A. Aleria
Cephalocele refers to a defect in the skull and
dura with extracranial herniation of intracranial
structures.

1-3 in 10,000 live births

• incidence of occipital cephaloceles to be 70 – 90% of all
cephaloceles

Development attributed to:

failure of primary neurulation (Van Allen)
result of a postneurulation event in which the brain
tissue herniates through a defect in the mesenchyme
that is to become the cranium and dura (Gluckman, et
al)
US - for antenatal diagnosis
CT - demonstrates the osseous defect
MR- definitive role in demonstrating contents of the sac
MR venogram - shows the assoc. venous sinus abn

4 Types based on Contents

Meningoencephaloceles
Meningocele
Atretic cephaloceles
Glioceles
Ultrasound images (sagittal and axial sections) showing a cystic mass placed in
the anterior part of the ethmoid bone (arrow).
3D ultrasound view of the fetal face (29 weeks)
Thin axial T2 weighted FSE images shows mixed intensity tissue within the cephalocele.
Axial T2 weighted images of the posterior fossa reveal abnormal band of tissue
surrounded by CSF extending from the brainstem to the occipital cephalocele.
Corpus Callosum
Anomalies

Kelvin C. Nacalaban
Yasmin Grace Y. Lao
 Agenesis of the Corpus Callosum
• Absence (may be complete or partial) of the
corpus callosum
• Etiology
– Disturbance of embryogenesis in the first
trimester of gestation by some unknown
insult leads to failure of the callosal axons
to pass across the midline.
• Its incidence is usually sporadic; may be
increased in patients with Trisomy 8, 13, and
18.
• Associated with other diseases: Dandy-Walker
Malformations, Lipomas, Arnold-Chiari
Malformation, Hydrocephalus, etc.
MRI is the diagnostic imaging of choice
Sagittal T1-weighted MRI of the brain shows complete absence of the corpus
callosum.
Axial T1-weighted MRI shows that the lateral ventricles are parallel to each other and do not come into contact
with each other as they normally should.
Sagittal T1-weighted MRI of the brain. Parasagittal section through the lateral ventricle shows dilatation of the atrium
and occipital horn (colpocephaly).
Axial nonenhanced CT of the brain shows colpocephaly due to dilated atria and occipital horns of the lateral ventricle. Lateral
ventricles are parallel in configuration.
 anterior body
genu

Sagittal T1-weighted MRI of the brain shows partial agenesis of the corpus callosum. The genu and anterior body of the
corpus callosum are visualized, while the posterior body, splenium, and the rostrum are absent.
 body

splenium

Sagittal T1-weighted MRI of the brain shows apparent atypical callosal dysgenesis in lobar holoprosencephaly. The body
and splenium of the corpus callosum are well formed while the genu and rostrum are hypoplastic.
A patient with Dandy-Walker malformation. The corpus callosum is present but thinned.
 Marchiafava-Bignami Disease (MBD)
• a progressive neurological disease characterized
by corpus callosum demyelination and necrosis
and subsequent atrophy
• Alcoholism is the greatest risk factor
• MBD is dintinguished from other diseases that
may affect the CC (ischemic stroke, lymphoma,
etc) by lesions that are symmetrical and located
at the anterior portion
Multiple T1 dark and T2 bright lesions within the corpus callosum and frontal lobe
Multiple T1 dark and T2 bright lesions within the corpus callosum and frontal lobe
Severe atrophy of the body and splenium of the corpus callosum
FLAIR shows periventricular white matter degeneration
Sagittal T1-weighted MR image shows corpus callosum atrophy (short arrow), which is characteristic of
chronic form. Involvement of central layers of corpus callosum, indicated by hypointensity, with
sparing of dorsal and ventral layers results in the sandwich sign (long arrow).
 Other Diseases with Involvement of the
Corpus Callosum
LIPOMA

Coronal T1-weighted MR
image shows large well-
defined homogeneous
midline mass lesion in
region of corpus callosum
with characteristic bright
signal of lipoma. Note
associated dysgenesis of
corpus callosum.
PILOCYTIC ASTROCYTOMA

Sagittal T1-weighted MR image

shows well-circumscribed
hypointense lesion in body of
corpus callosum.
 MULTIPLE SCLEROSIS

Sagittal fluid-attenuated inversion recovery Sagittal T2-weighted MR image shows

paramedian image obtained through multiple hyperintense lesions in corpus
corpus callosum shows multiple ovoid callosum.
hyperintense lesions (arrow).
 HYDROCEPHALUS

Sagittal T1-weighted MR image shows Axial T2-weighted MR image shows

well-defined cystic lesions (arrows) of abnormal signal throughout corpus
corpus callosum. callosum, which has persisted for
many years.
Holoprosencephaly

Adlee W. Hassannoor
Vincent Mari Angelo W. Laguardia
• denotes an incomplete or absent division of
the embryonic forebrain (prosencephalon)
into distinct lateral cerebral hemispheres

Epidemiology:
– US: 1 in 10,000-20,000 neonates at birth
Internationally: similar to that in the US
– At birth, the ratio of females to males is 2:1
– Age of onset: 3-4 weeks of gestation
Pathogenesis
Types (from most severe to least):
(1)alobar (2) semilobar (3) lobar

Facial phenotypes (from most severe to least):

(1)cyclopia
(2)ethmocephaly
(3)cebocephaly
(4)ocular hypotelorism and midline clefting
(5) milder facial dysmorphic features in
combination or in isolation
 Most severe

Wide spectrum of
HPE phenotypes

Mild forms
Alobar HPE
MRI: Coronal fluid-attenuated inversion recovery image
showing alobar holoprosencephaly
Fetal MRI shows alobar holoprosencephaly
Early fetal MRI shows alobar holoprosenscephaly
Semilobar HPE
Lobar HPE

A B

C D
Dorsal Lobar HPE
Dandy Walker Complex
and Posterior Fossa
Malformations

Chrismarie Joy L. Bugayong

Ahliah E. Ibrahim
 Dandy-Walker Complex

• Dandy-Walker malformation
• Dandy-Walker variant
• Mega cisterna magna

Precisely differentiating the malformations may not

be possible using imaging methods!
Dandy-Walker Complex
• Enlarged posterior fossa
• High position of tentorium with upward
displacement of the lateral sinuses
• Torcular herophili associated with varying
degrees of vermian aplasia or hypoplasia
• Cystic dilatation of the fourth ventricle that
nearly fills the entire posterior fossa
 Dandy-Walker Malformation
• Rare congenital malformation (US: 1/ 35,000 live births)
• Accounts for approximately 1-4% of
hydrocephalus cases
• Nature and cause of the insult are unknown
• Characterized by:
– Agenesis or hypoplasia of the cerebellar vermis
– Cystic dilatation of the fourth ventricle
– Enlargement of the posterior fossa
Magnetic Resonance Imaging
Picture 1. Sagittal T1-weighted
MRI in a 5-year-old girl shows:
• Large posterior fossa cyst
elevating the torcular herophili
and sinus rectus (blue arrow)
• Hypoplastic vermis is everted
over the posterior fossa cyst
(yellow arrow)
b
• Cerebellar hemispheres and
brainstem (b) are hypoplastic
• Thinned occipital squama is seen
(green arrowheads)
Magnetic Resonance Imaging
Picture 2. Axial T2-weighted
MRI shows:
• Hydrocephalus
• Large cerebrospinal fluid
cyst in the posterior fossa
• Thinned occipital bone
(arrows)
C C
• Hypoplastic cerebellar
hemispheres with a winged
appearance (c)
Magnetic Resonance Imaging
Picture 3. Axial T1-
weighted MRI shows:

• Ventriculomegaly
• Superiorly displaced
posterior fossa cyst
 Dandy-Walker variant
• More likely to present in adulthood than in
infancy or childhood
• Consist of:
– Vermian hypoplasia
– Cystic dilatation of the fourth ventricle
– Without enlargement of the posterior fossa
Magnetic Resonance Imaging
Picture 4. Dandy-Walker variant in a
13-year-old girl with thoracal
scoliosis. Sagittal T1-weighted MRI
shows:
• Agenesis of the corpus
callosum
• Hypoplastic inferior vermis
• Fourth ventricle slightly
enlarged
• Posterior fossa typically
normal in size
 Mega Cisterna Magna

• Consist of:
– normal cerebellar vermis and fourth
ventricle
– enlarged posterior fossa 2o to enlarged
cisterna magna
Magnetic Resonance Imaging
Picture 6. Sagittal T1-
weighted MRI shows:
• Large retrocerebellar
cerebrospinal fluid
collection
• Normal fourth ventricle
and vermis
 Posterior Fossa Arachnoid Cysts

• Displacement of the fourth ventricle and

cerebellum anteriorly
• Produces significant mass effect
Sagittal (left) and axial (right) MR views of the brain revealing a large posterior fossa
arachnoid cyst and caudal displacement of the cerebellar tonsils
CT scan of an
infratentorial
posterior fossa
arachnoid cyst with
obstructive
hydrocephalus.
Neurofibromatosis

Lathefa L. Pescadero
Jeanette A. Venancio
 • Group of neurocutaenous syndromes primarily
affecting tissues derived fro the neural crest
• Consists primarily of distinct neuroectodermal
disorders (phakomatoses) which are inherited as
autosomal dominant traits

EPIDEMIOLOGY
Incidence Prevalence Age
NF-1: 1:2500 1:5,000 Always present at birth, in
live number during late childhood
births
and adolescence

NF-2: 1:33,000 1:210,000 Symptoms begin in teens or

live early twenties, but occa. as
births
early as 1st and as late as 7th
decade of life
 CLASSIFICATION
Neurofibromatosis 1 ( NF-1 )
• More common type
• AKA Peripheral neurofibromatosis and von
Recklinghausen’s Neurofibromatosis
• The skull and brain manifestations are protean
and highly variable penetrance
• Classic skull malformations include hypolplasia of
the sphenoid bone  poorly separated orbit and
middle cranial fossa and to sutural defects
• Optic gliomas are common, as are other low-
grade gliomas and hammartomas in the white
matter and basal ganglia
Left, Plain radiograph of the left forearm
in a 15-year-old boy shows hypoplasia
and deformity of the radius and ulna.
Note the intramedullary sclerotic streaks
within the radius and periosteal dysplasia.
Right, Compare these findings with the
normal right forearm, and note the
unrelated exostosis of the distal radius.
T1-weighted MRI in a 7-year-old
girl with a family history for the
disease and who had been blind
for 18 months shows bilateral optic
nerve gliomas (arrows) (same
patient as in Image 12).
A 7-year-old girl with a family
history of neurofibromatosis
type 1 had been blind for 18
months. T2-weighted
transaxial MRI shows
bilateral optic nerve gliomas
(arrows).
CT scan through the orbits
in a patient with the
disease shows a right
optic glioma.
A 66-year-old woman with
neurofibromatosis type 1
presented with paresthesia down
the right arm. T1-weighted
transaxial MRI through the cervical
spine shows a low-signal-intensity
mass extruding through the left
foraminal canal at vertebral level
C5-6; the mass appears to be
eroding the vertebral body. The
final diagnosis was a
neurofibroma.
Neurofibromatosis 2 ( NF-2 )
• Less common type
• AKA central neurofibromatosis
• Bilateral acoustic neuroma
• Characterized by bilateral 8th cranial
nerveschwannomas as well as schwannomas of
other cranial nerves and multiple meningiomas
Axial and coronal T1-weighted images with gadolinium demonstrating bilateral
acoustic schwannomas.
Coronal T1 with gadolinium showing extra-axial meningioma located in right
frontal cortex (left) and sagittal T1 with gadolinium showing small enhancing
lesion on the posterior aspect of the medulla (right).
Sagittal T1-weighted
postcontrast image in a
patient with known
neurofibromatosis type 2 that
demonstrates 2 midline
meningiomas (arrowheads),
one over the convexity and
one along the vein of Galen.
The enhancing mass in the
medulla (arrow) most likely is
an ependymoma.
Axial postcontrast T1-weighted image
demonstrates a large enhancing sellar
meningioma surrounding both internal
carotid arteries in this case of
neurofibromatosis type 2 (NF2) (black
arrows). Enhancing tissue in the ethmoid
air cells also represents a meningioma
extending through the cribriform plate.
Meningiomas in patients with NF2 can
be more aggressive and invasive than
spontaneous meningiomas. Note the
small, round, enhancing extra-axial mass
posterior to the tectum (white arrows).
Although this could represent another
meningioma, the shape and location
suggest it is a trochlear (CN IV)
schwannoma instead.
Sagittal T1-weighted postcontrast
image of the thoracic spine
demonstrates an enhancing extra-
axial meningioma (arrow) anterior
to the cord with a complex
enhancing mass (arrowheads)
that represents a conus
ependymoma filling the spinal
canal in the lower thoracic spine.
 Intracranial
Hemorrhage

Mary Claudette M. Abad

Melissa A. Corinales
 Intracranial Hemorrhage
• the pathological accumulation of blood
within the cranial vault
• occurs when a blood vessel in the head
is ruptured or leaks
• from physical trauma (head injury) or
nontraumatic causes (hemorrhagic
stroke) such as a ruptured aneurysm
 Subdural
Hemorrhage
 Subdural Hemorrhage
• form of traumatic brain injury in which
blood collects between the dura (the
outer protective covering of the brain)
and the arachnoid (the middle layer of
the meninges)
• arise from bleeding from small veins
between the dura and the brain
• occur when physical injury results in the
development of shearing forces
• Acute subdural hematoma. Note
the bright (white) image
properties of the blood on this
noncontrast cranial CT scan.

• MR examination shows bilateral

fluid collections as a result of
chronic bilateral subdural
hematomas and new subdural
hematomas in the right frontal
and posterior interhemispheric
region.
Subarachnoid
Hemorrhage
 Subarachnoid Hemorrhage
• bleeding of an artery in the area between
the brain and the thin tissues that cover
the brain
• may arise due to trauma or
spontaneously, and is a medical
emergency which can lead to death or
severe disability
• most frequent cause of subarachnoid
hemorrhage is bleeding from an
aneurysm
• CT scan of the brain
showing subarachnoid
hemorrhage as a white
area in the center
The pathological accumulation of blood within
the cranial vault.

Epidemiology
 ICH accounts for 8-13% of all strokes
 30-day mortality rate of 44%.
Age:  - >55 years and doubles with each
decade until age 80 years.
Sex: slight male predominance
Race: higher incidence in Asian countries
 Pathophysiology
 hypertensive damage to  arteriopathy
blood vessel walls  cerebral amyloid angiopathy
 Hypertension
 moyamoya
 eclampsia
 drug abuse  altered hemostasis
 autoregulatory dysfunction  thrombolysis
with excessive cerebral  anticoagulation
blood flow  bleeding diathesis
 reperfusion injury
 hemorrhagic  hemorrhagic necrosis
transformation  tumor
 cold exposure  infection
 rupture of an aneurysm or  venous outflow obstruction
arteriovenous  cerebral venous thrombosis
malformation (AVM)
 Nonpenetrating and
penetrating cranial trauma
CT scan of right frontalintracerebral hemorrhage complicating
thrombolysis of an ischemic stroke
 Fluid-attenuated inversion-recovery, T2-weighted, and gradient
echo MRI illustration of intracerebral hemorrhage associated with
a right frontal arteriovenous malformation.
Fluid-attenuated inversion-recovery, T2-weighted, and gradient
echo MRI depiction of left temporal intracranial hemorrhage
due to sickle cell disease
EDH occurs in the potential space between
the dura and the cranium.

Epidemiology
 As many as 10-20% of all patients with head
injuries are estimated to have EDH.
 Approximately 17% of previously conscious
patients who deteriorate into coma
following a trauma have EDH.
Pathophysiology
 Mainly caused by structural disruption of
the dural and skull vessels commonly
associated with calvarial fractures.
 Most common etiology – lacerationof the middle
meningeal artery
 In the posterior fossa
 Disruption of dural venous sinuses (eg,
transverse or sigmoid sinus) by fracture may lead
to EDH
 Disruption of the superior sagittal sinus may
cause vertex EDH.
 In the absence of trauma
 infectious diseases of the skull
 vascular malformations of the dura mater
 metastasis to the skull
 Spontaneous EDH
 Px’s with coagulopathies associated with
other primary medical problems
– end-stage liver disease
– chronic alcoholism
– other disease states associated with
dysfunctional platelets
CT scan of an acute left-sided epidural hematoma. Note the typical convex or lens-
shaped appearance. The hematoma takes this shape as the dura strips from the
undersurface of the cranium, limited by the suture lines. A midline shift of the ventricular
system is present. This hemorrhage requires immediate surgical evacuation.
Nontraumatic epidural hematoma in a young woman. The grey area in the top left
is organizing hematoma, causing midline shift and compression of the ventricle.
 Craniocerebral
Trauma

Jan Idrian C. Algar

Mark Renier B. Rebolos
 Injuries related to skull fracture:
 Scalp injuries
 Axonal injury
 General penetrating injuries
 Missile wounds
 Stab wounds
 Nonaccidental trauma
 Intracranial hemorrhages related to skull fracture:
 Extradural hemorrhage
 Subdural hemorrhage
 Subarachnoid hemorrhage
 Intracerebral hemorrhage
 Frequency: >60% are simple linear

 Sex: Men twice likely to have injury

 Risk of head injury: Peaks at 15-30 years old

 Head trauma: Most common cause of morbidity and

mortality in infants

 Preferred examination: CT is the modality of choice

in evaluating head injuries
Occipital Skull Fracture in
Nonaccidental Injury
Linear Temporoparietal Fracture
Baseball bat assault:
Depressed fracture
Intracranial injury from a golf club
Stab wound to the head from a large
knife
Gunshot wound to the right
temporoparietal region
Open comminuted fracture with
underlying extradural hematoma
Multiple fractures, soft tissue swelling,
air in cranial cavity, contusional
hemorrhage
Multiple fractures, soft tissue swelling,
air in cranial cavity, contusional
hemorrhage
Bilateral contusion and intracerebral
hematoma
Penetrating injury from a low velocity
bullet
Plastic bullet
Left subfrontal subdural hematoma
with active hemorrhage
 Extracranial hematoma and
intracranial extradural hematoma
Right frontal extradural hematoma
8-week-old baby after forceps delivery
Ax attack with open midline frontal
fracture
Missile injury through the frontal bone
Missile injury through the frontal bone
with intracerebral
hematoma/infarction
 Astrocytoma
& Variants

Grystel G. Gadian
Ma. Florelyn S. Datu
 ASTROCYTOMA
• CNS neoplasms
• Derived from an immortalized astrocyte
• Etiology:
– associations with various disorders and
exposures
– genetic
• Two classes of astrocytic tumors
– narrow zones of infiltration
– diffuse zones of infiltration
 ASTROCYTOMA
PATHOPHYSIOLOGY

• compression, invasion, and destruction of

brain parenchyma
• Disruption of normal parenchymal function
• Mediation of secondary clinical sequelae
• perturbation of CNS function
– Neurological signs and symptoms
– Focal neurological deficits and seizures
ASTROCYTOMA
variants
 NARROW ZONES OF
INFILTRATION
ASTROCYTOMA
• pilocytic astrocytoma
• subependymal giant cell astrocytoma
• pleomorphic xanthoastrocytoma
 PILOCYTIC ASTROCYTOMA

• Benign tumor of childhood

• Cerebellum (MC), brainstem, hypothalamic region, optic
pathways, cerebral hemispheres and the spinal cord
• Peak incidence is 5-14 years
• Grade I
 SUBEPENDYMAL GIANT CELL
ASTROCYTOMA

• Benign large subependymal nodule (SEN)

• Lateral ventricle, attached to caudate head
• Children, young adults
• Grade I
 PLEOMORPHIC XANTHOASTROCYTOMA

• Cerebral hemispheres, meninges and spinal column (rare)

• Affect males and females equally
• Children and young adults (peak 20 years)
• Grade II-III
PLEOMORPHIC XANTHOASTROCYTOMA
 DIFFUSE ZONES OF
INFILTRATION
ASTROCYTOMA

• low-grade astrocytoma
• anaplastic astrocytoma
• glioblastoma multiforme
 LOW-GRADE ASTROCYTOMA

• Slow growing primary tumor

• Brain and spinal cord
• Slight male predominance (1.18:1)
• Peak incidence 30-40 years
• Grade II
 ANAPLASTIC ASTROCYTOMA

• Rapidly growing tumor

• Cerebral hemispheres (MC), thalamus and hypothalamus,
cerebellum and brain stem
• Male predominance (1.87:1)
• Children and adults
• Grade III
 GLIOBLASTOMA MULTIFORME

• MC and most malignant

• Cerebral hemispheres (adults, MC), brain stem (children) and
spinal cord
• Primary (>50 years) and secondary (<45 years)
• Any age (peak incidence 45-70 years)
• Male predominance (3:2)
• Grade IV
GLIOBLASTOMAMULTIFORME
GLIOBLASTOMA MULTIFORME
GLIOBLASTOMAMULTIFORME
GLIOBLASTOMA MULTIFORME
 Nonastrocytic
Glial Tumors

Lucio V. Temonio, Jr.

Melissa T. Sy
Melissa T. Sy
Oligodendroglioma

• 7% of supratentorial gliomas
• Found in middle-aged adults,
45 y.o.
• Slow growing tumor
• Duration of symptoms before
dx = 11 yrs
Oligodendroglioma

• Calcifications
in plain skull
radiograph
• Lesion occur at:
cerebral
hemisphere,
white matter
• MC: frontal lobe
• Calcification
within the
tumor
• Frequently
occur but a
non-specific
sign
Calcium = coarse, irregular
strands
COMPARATIVE STUDY

2000 2005 2006

EPENDYMOMA

Lucio Temonio Jr.

 Ependymoma
• from cells lining the ventricles
(fluid filled spaces w/in the
brain) OR spinal cord’s central
canal
• Duration of symptoms before
dx= <1 yr
• Arise in children & young adults
– Infratentorial ependymomas
– Supratentorial ependymomas
• Isodense/ slightly hyperdense
• w/ scattered small/ punctuate Ca
deposits
• Lines the ventricle
 Primitive
Neuroepithelial
Tumors

Wilhema M. Villan
Marco Po D. Dela Cruz
• Applied to a tumor that cannot be sharply
differentiated from other embryonal cell
types
• Includes neuroblastoma, pineoblastoma,
ependymoblastoma, polar
spongioblastoma, & medulloblastoma
• Incidence: common CNS tumor in children
– 25% of all intracranial tumors
• Age & gender: Majority - < age of 5 years
– Males = Females
• Location: MC in posterior fossa
• Imaging:
– Computed Tomography
• Large, irregular, heterogeneous mass deep in the cerebral
white matter
• Solid component of mass is usually hyperdense
• Necrosis, cyst formation, calcification, & hemorrhage seen
• Enhancement is seen & may be heterogeneous / ringlike
– Magnetic Resonance Imaging
• Large, heterogeneous mass w/ necrosis. Cyst formation,
calcification, / hemorrhage
• Solid component of mass is slightly hypointense on T1-
weighted images & slightly to moderately hyperintense on
T2-weighted images
 Cerebellar medulloblastoma. This MRI
(axial view, T2-weighted image)
demonstrates the heterogeneity of the
tumor.

Cerebellar medulloblastoma. This axial

view CT scan with contrast shows a
partially enhancing mass arising in the
midline from cerebellum and filling the
fourth ventricle.
Medulloblastoma.
Axial T2 weighted
image reveals a
predominantly
isointense mass to
grey matter with
small foci of cystic
changes
T1-weighted sagittal
MRI of an 8-year-old
boy who presented
with nausea and
vomiting reveals an
enhancing tumor
within the fourth
ventricle. The child
underwent a
suboccipital
craniotomy and
resection of his
medulloblastoma.
pineoblastoma
 Radiology | Medicine-3
Dr. Jose P. Rizal School of Medicine
Xavier University – Ateneo de Cagayan
© SY 2007-2008