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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
Circle of artery
Left middle cerebral
Willis
Right middle artery
cerebral artery
Ant. Communicating
Basilar artery artery

External Posterior cerebral


Carotid artery
Post. Communicating
arteries artery
Common
Carotid Internal
Arteries 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 Internal Jugular Vein
Inferior petrosal sinus
Vein
Facial vein
Posterior external Pharyngeal veins
jugular vein Lingual vein
Superficial cervical Superior thyroid vein
vein Middle thyroid vein
Suprascapular vein
Anterior jugular
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 MR arteriogram demonstrating
slab, through the circle of Willis markedly diminished left middle
cerebral artery flow as a result of
Normal MR venogram, median MR venogram demonstrating lack of
sagittal slab 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
VIII Vestibulocochlear 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

Nasion
Orbit

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
Malformation
s
(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
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

spleniu
m

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 Sagittal T2-weighted MR image


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

Sagittal T1-weighted MR Axial T2-weighted MR image


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

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
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
b fossa cyst (yellow arrow)
• Cerebellar hemispheres
and brainstem (b) are
hypoplastic
• Thinned occipital squama
Magnetic Resonance
ImagingPicture 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.
Neurofibromato
sis

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 births number during late childhood
and adolescence

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


live births early twenties, but occa. as
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
Hemorrhag
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.
Subarachno
id
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.
Craniocerebr
al 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
Astrocytom
a
& 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
Nonastrocyti
c 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
Neuroepitheli
al 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.
Medulloblasto
ma. 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