Skull Base Radiology and Ddx.pptx

“Don’t read success stories, you will only
get a message. Read failure stories, you
will get some ideas to get success.”
A.P.J. Abdul Kalam (15 October 1931 – 27 July 2015)
“The People's President” and “Missile Man of India”

SKULL BASE IMAGING:
TUMORS & RADIOLOGICAL D-Dx
VASU NALLALUTHAN
MS NEUROSURGERY (USM)
SUPERVISOR: DR. NUR ASMA SAPIAI/ PROF. MOHD SHAFIE ABDULLAH

DISCLAIMER:
The depicted information and the images contained in this presentation
is to be used only for educational and teaching purposes only.
It is intended for the development of knowledge and stimulate discussion of
Neurosurgery Residents of Neuroscience Dept. of HUSM.

OBJECTIVE
• Able to understand the radiological features of lesion at skull
base area related to anatomical region
• Able to list the possible diagnosis for lesion in specific region of
the skull base
• Able to identify the features of imaging of each skull base lesion

OUTLINE
• Introduction
• Purpose of Imaging
• Imaging Modalities Available
• Anatomy Approach
• Anterior
• Anterior-Middle
• Middle
• Middle-Posterior
• Posterior
• Anywhere
• References

INTRODUCTION
• Cross-sectional imaging became a key factor in the management of skull
base pathology:
• Narrows down differential diagnoses, according to
• Site of origin
• Pattern of growth
• Imaging features of a given lesion
• Allows accurate delineation of tumour margins
• Determines the precise relationship between lesions and important surrounding
structures
• CT Scan and MR imaging  one complements the other.
• Detailed knowledge of skull base anatomy is a pre-requisite for correct
imaging diagnosis and for accurate delineation of skull base lesions.

PURPOSE OF IMAGING
• The purpose of CT and MR imaging is to evaluate
a. Lesion characterization
b. Involvement
a. Paranasal sinus
b. Extracranial soft tissues
c. Bone
d. Neurovascular
c. Invasion to brain
d. Variation of skull base anatomy
• Imaging is used to
• Anticipate the morbidity and mortality of surgical procedures
• Delineate the therapeutic target for focused radiation therapy
• Determine the best approach for tissue sampling  CT/ MR guided FNAB

GLIMPSE of SKULL BASE REGIONS
Skull base formed by the
• Frontal
• Ethmoid
• Sphenoid
• Temporal
• Occipital
Skull base can be subdivided into 3 regions:
• ANTERIOR
• Frontal & Ethmoid bone
• CENTRAL
• Sphenoid & Ant aspect Temporal bone
• POSTERIOR
• Occipital bone & Post aspect Temporal bone
Álvarez Jáñez et al. Diagnosis of Skull Base Osteomyelitis. RadioGraphics 2021; 41:156–174
Kunimatsu A. et al. Skull base tumors and tumor-like lesions: A Pictorial Review. Polish Journal of Radiology, 2017;
82: 398-409

BONE AND SPACE
Bello et al. Skull Base–related Lesions at Routine Head CT from the Emergency Department: Pearls, Pitfalls, and Lessons Learned.
RadioGraphics. 2019; 39:1161–1182
Axial CT image with color-coded
overlay shows the skull base bones.
Blue = temporal bones,
Fuchsia = nasal bones
Green = ethmoid bone,
Light pink = vomer,
Purple = occipital bones
Teal = sphenoid bone
Yellow = zygomatic bones.
Axial CT image with color-coded
overlay shows the extracranial
spaces.
Blue = masticator space
Dark yellow = parotid space
Fuchsia = parapharyngeal space
Green = nasal cavity,
Light yellow = maxillary sinus
Pink = carotid space
Purple = perivertebral space
Red = spinal canal and spinal cord
Teal = nasopharynx.

INTRACRANIAL

EXTRACRANIAL

IMAGING MODALITIES – CT
• CT scans  skull base must include at least 2 different planes (axial and coronal
planes) and slices < 3 mm thick (1.5 – 3 mm).
• Multiplanar reconstructions of variable thickness in both bone and soft tissue acquired.
• IV iodinated contrast mandatory
• to delineate tumour margins and adjacent vascular structures
• to access lesions’ vascularity
• to obtain perfusion studies  differentiating benign and malignant lesions.
• CT  well suited to define the bony anatomy of the skull base.
• Axial study  Reid baseline plane (line drawn parallel to orbitomeatal line)
• From foramen magnum to the suprasellar cistern
• Direct coronal images obtained  perpendicular to the Reid baseline.
• Significant artifact (dental amalgam) or if the patient cannot tolerate the coronal head position
reconstructed images  thin (1.5 - 2.0mm) axial scans

IMAGING MODALITIES - CT
• High-resolution bone algorithms  thin cortical margins of
neurovascular foramina.
• Good specificity  diagnosis of fibro-osseous and primary bone lesions and
in determining the pattern of bone involvement.
• The effect of a tumour - adjacent bone  important clues – nature of a
lesion and is used to narrow down differential diagnoses, namely
determining  aggressive and rapidly growing or is slow growing apparently
benign.
• CT surpasses MR imaging
• Evaluating  Intra-tumoral calcification, bone destruction or osteosclerosis.
• Example: Dural- based tumors with hyperostosis of the underlying bones
(meningiomas)

IMAGING MODALITIES - MRI
• Suspected to involve the intracranial compartment.
• More sensitive then CT in detecting dural, leptomeningeal and cranial
nerves involvement
• To depict bone marrow invasion
• To discriminate between retained secretions and tumour within sinonasal
cavities
• Routine examination  midsagittal, axial, and coronal planes.

• T1-weighted images  repetition times of 600 - 1,000 msec and echo
times of 17-20 msec for anatomic definition.
• A section thickness of 3-5 mm is used.
• A mid-sagittal image is first obtained and serves as a scout view.
• It also shows the superior and inferior extent of disease at midline.
• Little use is made of parasagittal sections because of the confusing aspects of anatomy
• Axial images  repeated after the IV administration of gadolinium
diethylenetriaminepentacetic acid (DTPA)(0.1mmol/kg)
• Coronal images  from the anterior aspect of the sphenoid sinus to the foramen
magnum
• Conventional or fast spin echo T1W images are the best sequences to
depict bone marrow invasion.
• Most tumours  low to intermediate signal intensity on T1W images
• Easily differentiated from the high signal intensity of fatty marrow.

• T2-weighted sequence  a repetition time of 2,000 – 3,000msec with a
double-echo time of 20-45msec (1st echo) and 90msec (2nd echo)
• Lesser value in examine skull base  add significant time to the total examination
 can be achieved with shorter T1 sequences & Gd-DTPA enhancement
• Solid tumors
• Marked hyperintensity likely to contain chondroid, chordoid or myxoid matrix
• Hypointensity suggests abundant fibrous tissue or hemosiderin within the tumor.
• Combination of T1W, T2W and contrast enhanced T1W sequences
• Discriminate between tumour and retained secretions.
• Retained secretions  show variable signal intensities
• Depend on the degree of hydration and protein content  unusual share the exact same signal
intensity as tumour on both T1 and T2W sequences.
• As opposed to neoplasm, retained secretions do not enhance.

MRI - GADOLINIUM ENHANCEMENT
• Depict meningeal invasion & perineural spread of disease
• To maximize tumour contrast.
• Gadolinium enhanced fat suppressed T1W images
• Enhancing tumours are in close contact with fat containing spaces
• Orbit, exocranial openings of neurovascular foramina, pterygopalatine fossa, retro-
antral fat and bone marrow within the skull base namely in the clivus and petrous
apices.
• Failure of fat suppression  mimic tumour enhancement
• Near bone–air and bone–fat interfaces at skull base region.
• STIR technique should be preferred Not based on frequency selective pulses

IMAGING MODALITIES - ANGIOGRAPHY
• Plays a role mainly for endovascular interventional procedures which are
used as
• An adjunct to surgical treatment of highly vascular tumours such as juvenile
angiofibromas, paragangliomas, and a few hypervascular meningiomas and
metastases.
• When a carotid artery needs to be sacrificed, a balloon test occlusion is used to
determine the ability of collateral circulation to supply that carotid territory

IMAGING MODALITIES - PET SCAN
• Positron emission tomography using flurodesoxyglucose (18 FDG-PET)
• Useful in patients follow up to differentiate between post-treatment
changes and recurrent neoplasm
• No routine role in the primary evaluation of skull base lesions has been
found.

ANTERIOR
SKULL BASE
 Sinonasal neoplasms
 Squamous Cell Ca (SCC)
 Adeno-Ca
 Esthesioneuroblastoma
 Malignant Melanoma
 Lymphoma
 Orbital Tumors
 Pseudotumors

SINONASAL NEOPLASMS
• Most are epithelial in origin
• Order of frequency
• Squamous cell carcinoma
• Adenocarcinoma
• Intestinal type adenocarcinoma (ITAC)
• Minor salivary gland neoplasms
• Neuroendocrine Neoplasms

SQUAMOUS CELL CARCINOMA
• The most common epithelial neoplasm
• Accounting for over 70% of all malignancies
• Imaging features are non-specific
• T2W images  Intermediate signal intensity
• Reflecting high cellularity and aggressive bone destruction occasionally with
small bony fragments engulfed within the lesion.
• Large tumours  heterogeneous due to the presence of necrosis and
haemorrhage.
• These neoplasms show intermediate gadolinium enhancement usually
to a lesser degree then normal sinonasal mucosa

SQUAMOUS CELL CARCINOMA
Coronal T2W (a) and gadolinium enhanced T1W (b) images show a large nasoethmoidal neoplasm invading the anterior skull base through the cribiform
plate and the orbit through lamina papyracea, on the right side. The frank displacement of the medial rectus, compressed against the optic nerve (black
arrow), with loss of its convex contour towards the bony orbit and complete effacement of the extraconal fat, indicate orbital invasion. The intracranial
component of the tumour is separated from the adjacent frontal lobe by a thin rim of CSF best seen on the T2W image (white arrows). No vasogenic
edema or contrast enhancement of the brain parenchyma is noted. The high T2 signal intensity of retained secretions within the right maxillary sinus can
be clearly separated from the neoplasm which is seen to grow along the ethmoid infundibulum and to obstruct the maxillary ostium (diagnosis:
moderately differentiated SCC).
A. Borges. Skull base tumours Part I: Imaging technique, anatomy and anterior skull base tumours. European Journal of Radiology.
2008; 66: 338 - 347

ADENOCARCINOMAS
• Comprise 10% of all sinonasal tumours
• Minor salivary gland tumours
• Most common
• Origin in the hard palate and spread secondarily to the paranasal
sinuses.
• Primary sinonasal lesions arise more often in the maxillary sinus followed by the
nasal cavity.
• Imaging features
• T2W prolongation
• Low grade (less aggressive pattern) tumours  bone involvement
• Remodelling and thinning rather then permeative destruction of surrounding bone.
• These tumours are also known for their propensity to spread perineurally.

OLFACTORY NEUROBLASTOMA
• a.k.a ESTHESIONEUROBLASTOMA
• Malignant neoplasm of the neural crest origin
• Arising from the olfactory epithelium located in the nasal vault and
cribriform plate.
• It accounts for 3–5% of all intranasal neoplasms.
• Bimodal incidence peaks in the teens and 40s with a slight female
predominance
• Presentation is nasal stuffiness and bleeding  mimic inflammatory polyp.
• Requires en-bloc resection  treatment of choice & long term survival
• High local recurrence rate  surgery and radiation therapy even for a small
tumor confined to the nasal cavity.

• CT
• Non-contrast CT  Iso- to slightly hyperdense
• Solitary, polypoid, expansile soft tissue mass centred in the nasal vault and cribiform plate
• Intracranial extension through the cribiform plate
• Orbital invasion through lamina papyracea
• Meningeal spread and parenchymal invasion of the olfactory bulbs and inferior frontal lobes
• MRI  Small peripheral cysts at the interface with brain parenchyma, with their
broadest base at the tumour mass  hallmark
• T1-weighted: Iso- to hypointense; T2-weighted: hyper- to isointense
• On contrast-enhanced T1-weighted: homogeneous enhancement
• Can be inhomogeneous with necrosis.
• Diffusion-weighted imaging: Restricted diffusion
• Other features:
• Intratumoral cyst formation or necrosis is not uncommon
• Intracranial extension has characteristic marginal cysts where the tumor approaches the brain.
• Calcification – uncommon but typical feature

2008; 66: 338 - 347
Axial T2W (a) and (b) and coronal contrast enhanced T1W images without (c) and with fat suppression (d) show a large neoplasm
occupying the nasoethmoidal region bilaterally centred at the nasal vault, clearly invading the anterior cranial fossa through the cribiform
plate. A small erosion of lamina papyracea is also noted on the left side but the neoplasm is confined by the periorbita, with no signs of
orbital invasion. The T2W images provide an accurate mapping of tumour extent as the intermediate signal intensity of the lesion can be
nicely separated from the high signal intensity of retained secretions within the adjacent obstructed sinuses (white arrows). Vasogenic
brain edema is also best depicted on the T2W images reflecting cortico-pial invasion (long black arrows). Also note the presence of small
cysts at the tumour–brain interface (short black arrows) which are typical for an olfactory neuroblastoma (courtesy from Dr. Se ́rgio
Cardoso).

Olfactory neuroblastoma in a 38-year-old man.
Coronal post-contrast, fat-suppressed, T1-weighted image shows
homogenously enhancing tumor in the right nasal cavity with
intracranial extension (arrow).
Kunimatsu A. et al. Skull base tumors and tumor-like lesions: A Pictorial Review. Polish Journal of Radiology, 2017; 82: 398-409

LYMPHOMA
• Common location for extranodal lymphoma particularly in Asian
populations.
• B cell lymphoma
• slight western predominance
• Involves the paranasal sinuses
• On imaging
• Bulky expansile,
• Homogeneous soft tissue mass that erodes adjacent bone and extends into
surrounding soft tissues,
• Not uncommonly presenting as a facial bulge or proptosis.

LYMPHOMA
• T cell lymphoma
• More common in Asians
• Affects primarily the nasal cavity  origin - At the midline nasal septum.
• Distinctive features  an aggressive angiocentric growth pattern resulting in
chondro and osteo-necrosis.
• Changes pattern
• Limited to nodular or lobulated mucosal thickening (early stages)
• indistinguishable from chronic inflammation.
• Disease progresses, bone destruction begins  nasal septum  auto rhinectomy with complete
destruction of the nasal turbinates or sinus walls
• Mimicking post-surgical changes.
• Hallmark T cell- lymphoma  presence of bone destruction in excess to the soft
tissue component.
• Main differential diagnoses include Wegener’s granulomatosis and cocaine abuse.

T CELL LYMPHOMA
2008; 66: 338 - 347
Contrast enhanced, fat suppressed coronal T1W images (a) and (b) show thick irregular enhancement of the sinonasal mucosa without a
bulky mass lesion and extensive bone destruction that includes large dehiscence of the nasal septum, absent nasal turbinates and partial
destruction of the medial walls of the maxillary sinuses, resembling post-surgical changes. Of note is the discrepancy between the sparse
soft tissue component and the extensive bone destruction. Smooth, thin and linear dural enhancement along the floor of the anterior
cranial fossa reflects fibrovascular changes (short white arrows). Also note the artefacts related to failure of fat suppression at the air–fat
interface adjacent to the medial and inferior walls of the orbits (long white arrows) (pathologic diagnosis: sinonasal T cell lymphoma).

ORBITAL TUMORS
• Benign lacrimal gland tumours
• Manifest as mass lesions
• Originating in the superior and outer aspect of the orbit  the normal anatomic
location of the lacrimal gland.
• When large enough  displace the globe and extra-ocular muscles inferior and
medially and remodel and erode the orbital roof
• Malignant neoplasms
• Arising in the orbital compartment
• Aggressive features
• May extend posteriorly through the orbital apex and orbital fissures into the medial
cranial fossa

BENIGN LACRIMAL GLAND TUMOURS
2008; 66: 338 - 347
Coronal CT sections through the orbits (a) and (b) show a soft tissue mass in the upper lateral quadrant of the left orbit in the region of the lacrimal fossa.
The lesion thins and remodels the roof of the orbit and displaces the extraocular muscles and globe inferiorly. No intracranial extent is noted (pathologic
diagnosis: pleomorphic adenoma of the lacrimal gland).

MALIGNANT NEOPLASMS OF LACRIMAL GLAND
2008; 66: 338 - 347
Contrast-enhanced sagittal T1W images (a) and (b) show a large enhancing soft tissue mass with infiltrative borders occupying most of the orbit, both the
extra- and intraconal compartments. The tumour extends posteriorly into the middle cranial fossa through the orbital apex and superior orbital fissure (long
black arrows) and breaches the superior orbital wall extending into the anterior skull base (short black arrows). Vasogenic brain oedema is seen in the basal
temporal and frontal lobes (diagnosis: recurrent adenoid cystic carcinoma of the lacrimal gland).

PSEUDOTUMOURS
• Infectious inflammatory conditions
• Mucoceles
• Sinonasal polyposis
• Abscesses
• Fungal infection
• Osteomyelitis
• Several granulomatous diseases including Wegener’s
• Correlation with clinical history and laboratory findings is mandatory to
reach the diagnosis.

PSEUDOTUMOURS
• Imaging features that might suggest inflammatory pseudotumour include
the
• Presence of MR signal changes, particularly on long TR images, in excess to the
amount of soft tissue mass seen on CT and the presence of vessel occlusion.
• Neoplasms invading the cavernous sinus  narrow or compress the internal carotid
artery
• Infection and inflammation reaching the skull base may rapidly extend to
the petrous or cavernous segments of the carotid artery, leading to
inflammation of the vessel wall (endarteritis) and occlusion

PSEUDOTUMOURS
A. Borges. Skull base tumours Part II: Central skull base tumours and intrinsic tumours of the bony skull base. European Journal of
Radiology. 2008; 66: 348–362
Axial T1W (a) and axial T2W (b) MR images show
heterogeneous soft tissue filling in the left nasal cavity
and paranasal sinuses with a permeative pattern of
bone destruction. There is destruction of the posterior
wall of the maxillary sinus with abnormal soft tissue
seen within the PPF, replacing the retro-antral fat,
infiltrating the infratemporal fossa, the left cavernous
sinus and middle cranial fossa. Luminal irregularity
and pre-occlusive stenosis of the left cavernous
carotid artery is also seen. There is also extensive
bone marrow replacement of the sphenoid body and
clivus. Coronal fat-suppressed contrast-enhanced T1W
image (c) clearly depicts the extent of the
inflammatory changes and the encasement of the
cavernous carotid artery (black arrow). MR
angiography of the circle of Willis (d) shows a large
segment of luminal irregularity and stenosis of the left
petrous and cavernous carotid artery (diagnosis:
invasive aspergillosis in a HIV positive patient).

BASAL CEPHALOCELES
• Cephaloceles account for 10%-20% of all craniospinal malformations. Most
cephaloceles are thought to represent a failure of neural tube fusion.
• Basal cephaloceles  10% of cephaloceles
• 75% for occipital forms and 15% for those around the nose and orbit.
• Basal cephaloceles are subdivided into five major categories  the site of the
defect:
a) Sphenopharyngeal, through the sphenoid body
b) Sphenorbital, through the superior orbital fissure
c) Sphenoethmoidal, through sphenoid and ethmoid bones
d) Transethmoidal, through the cribriform plate
e) Sphenomaxillary, through the maxillary sinus
• Cephaloceles  a mass in the nose, nasopharynx, mouth, or posterior portion of
the orbit.
• The most common type sphenopharyngeal mass airway obstruction and act as
a site of cerebrospinal fluid (CSF) rhinorrhea and meningitis.

BASAL CEPHALOCELES
• CT.
• The aperture is smooth and defined by a rim of cortical bone.
• The bone margins of the defect, as well as the soft-tissue component.
• CT contrast  differentiation of a simple meningocele from an
encephalocele.
• Cortical sulci bathed in contrast material would be evident  encephalocele
• MR imaging- in the evaluation of the soft-tissue component of
the lesion.

PSEUDOTUMORS
Laine FJ et al. CT and MR Imaging the Central Skull of Base. Part 2: Pathologic Spectrum. RadioGraphics 1990; 10: 791 - 821
Basal cephalocele with persistent craniopharyngeal canal in an 8-year-old
child with recurrent bouts of meningitis. (a) Plain radiograph of the skull,
submentovertex view, demonstrates a well-defined area of decreased
opacity surrounded by a thin rim of cortical bone projected over the skull
base (arrow) . Axial CT scan (b) photographed with bone window and
coronal CT scan (c) photographed with soft-tissue window reveal the
presence of a persistent craniopharyngealcanal (arrow) in the sphenoid
bone. Coronal (d) and midsagittal (e) T1 -weighted MR images through the
central skull base demonstrate herniation of the pituitary gland into the
craniopharyngeal canal through the sphenoidal defect (arrow) . Note the
proximity of the pituitary gland to the roof of the nasopharynx. (Courtesy
of Dr Lakshmana Das Narla, Medical College of Virginia, Richmond)

PSEUDOTUMORS
Biopsy-proved encephalocele in a 35-year-old man who underwent CT for evaluation of headache. Axial (a) and coronal (b) CT scans through the central
skull base and sphenoid sinus reveal the presence of a soft-tissue mass within the left sphenoid sinus (arrow) . The mass involves the base of the pterygoid
plates on the left in the region of the Vidian canal. A smooth, well circumscribed defect is suggestive of a benign

CAVERNOUS CAROTID FISTULA
Cavernous carotid fistula in an 1 8-year-old man after a motor vehicle accident. Axial CT scans photographed with soft-tissue (a) and bone (b) windows show
subarachnoid hemorrhage and extensive basilar skull fracture, which extends obliquely along the sphenoid bone (straight arrows) across the cavernous sinus
and into the petrous tip (curved arrow) . (c) Lateral subtraction view from a left carotid angiographic study reveals a cavernous carotid fistula. Contrast material
from the arterial system has extravasated into the cavernous sinus (straight arrow) and subsequently into the petrosal sinuses (curved arrow).

ANTERIOR AND MIDDLE
SKULL BASE
 Skull base invasion from head and
neck tumor
 Fibrous dysplasia
 Paget’s Disease
 Giant cavernous carotid aneurysms
 Sphenoid Sinus Tumor

CENTRAL/ MIDDLE SKULL BASE APPROACH
KEY TO REMEMBER:
The central skull base may be affected by systemic
conditions, from lesions arising from the skull base
proper, from the intracranial compartment or from
the extracranial head and neck
For diagnostic imaging purposes central skull base
sub-divide into
• MIDLINE SAGITTAL: medial to the
petroclival fissure
• Off-middline PARASAGITTAL: Petro- clival
fissure and foramen ovale
• LATERAL: External to foramen ovale
*** Different compartments have different 
possible differential diagnoses

SKULL BASE INVASION FROM HEAD AND NECK TUMOR
• Head and neck tumors sometimes invade the anterior or the middle skull
base by either direct invasion or perineural tumor spread.
• Perineural tumor spread into the intracranial space can occur in adenoid
cystic carcinoma, squamous cell carcinoma, lymphoma and melanoma.
• Most common in patients aged 40 to 60 years
• A male predominance
• Typically spreads along the branches of the trigeminal nerve or the facial
nerve.

SKULL BASE INVASION FROM HEAD AND NECK TUMOR
•CT
• Expansion of the skull base foramen with an enlarged nerve in
it.
•MR
• Non-contrast T1-weighted: hypointense, enlarged nerve with a
loss of perineural fat.
• T2-weighted : Enlarged nerve shows variable intensity.
• Contrast-enhanced: A tubular, enhanced mass.

PERINEURAL SPREAD
• Cardinal signs  solid or hematological malignancies and to several
infectious/inflammatory conditions
• Cranial nerve enhancement
• Loss of fat adjacent to the extracranial openings
• Abnormal enlargement of neural foramina  Depending on the degree of enlargement of the nerve
• Clinical history is crucial to achieve a correct diagnosis as imaging features are non-
specific.
• MR imaging is mandatory to detect subtle thickening and enhancement of cranial
nerves.
• Denervation atrophy may also be a clue to the diagnosis.
• Cranial nerves are a common route of spread of extracranial head and neck cancers.
• Salivary gland malignancies (adenoid cystic and mucopepidermoid carcinomas)
• Perineural spread reflects direct tumour extent

PERINEURAL SPREAD
Trust SC and Yousry T. Imaging of skull base tumours. Reports of practical oncology and radiotherapy. 2016; 21: 304–318.
Perineural tumor spread of nasopharyngeal carcinoma in a 63-year-old woman. (A) Coronal, non-contrast, T1-weighted, MR image shows nasopharyngeal
mucosal wall thickening. The tumor invades into the basisphenoid and spreads through the left Vidian canal (arrow) to the pterygopalatine fossa (not
shown), and then goes up to the left cavernous sinus along the maxillary branch of the left trigeminal nerve. The left cavernous sinus is also replaced by the
tumor (arrow head). (B) Axial, T2-weighted MR image shows the mass with intermediate intensity along the maxillary branch of the left trigeminal nerve
(arrows). (C) Coronal post Gadolinium T1 image showing SCC perineural spread along the left mandibular nerve (V3) characterised by nerve thickening with
avid perineural enhancement.

PERINEURAL SPREAD
Radiology. 2008; 66: 348–362
Coronal pre- (a) and (b) and post-gadolinium (c) T1W images demonstrate enlargement and abnormal enhancement along the maxillary
division of the trigeminal nerve from the pterygopallatine fossa (short white arrow), to foramen rotundum (long white arrow), inferior
orbital fissure (thick white arrow) and cavernous sinus (short black arrow). Note the normal non-enhancing right V2 (long black arrow).
(Diagnosis: perineural spread of nasopharyngeal carcinoma.)

FIBROUS DYSPLASIA
• Affect any bones in the body May involve the skull base either focal or
diffusely
• The skull and the facial bones  leontiasis ossea (facial deformity produced by
lesions)
• 10–25% of patients with monostotic FD
• 50% of patients with polyostotic FD.
• Most commonly in the teens or 20s (children and young adults)
• Can be incidentally found in the elderly on CT or MR imaging
• Female predominance.
• Symptoms depend on the site of the lesion.
• Cranial nerve deficits  CT: Bone expansion  Stenosis of neurovascular foramina
• Observation is chosen in asymptomatic patients.
• Curettage or volume reduction surgery  bone pain, skeletal deformity or
progressive neurological deficit.

FIBROUS DYSPLASIA
• CT
• Expands the medullary cavity of bones  replaced by myxofibrous tissue and
woven bone trabecula containing spindle cells and cysts.
• The cortical margin is usually spared (distinctive feature from Paget’s disease).
• The involved bone tends to merge imperceptibly with normal adjacent bone and no
periosteal reaction is seen.
• The presence of aggressive periosteal reaction should raise the suspicion for a pathologic
fracture or malignant degeneration into a sarcoma, most often an osteosarcoma
• Several patterns of bone involvement are seen in different stages of the disease or
all together  three dominant patterns
• Ground-glass pattern (56%)
• Homogeneously sclerotic pattern (23%)
• Predominantly cystic pattern (21%).
• FD often appears as a mixture of these patterns and may show variable appearances on CT.

FIBROUS DYSPLASIA
• MRI
• Predominantly hypointense on both non-contrast T1W and T2W.
• Diffuse replacement of the fatty marrow by tissue of intermediate SI on T1W
images
• T2-W: Hyperintensity at non-mineralized areas and regions of cystic
changes
• Contrast-enhanced T1W: Heterogeneous enhancement (strong) 
active phase of the disease
• Can be easily confused with a skull base neoplasm.
• In the absence of a pertinent clinical history  CT scan is
mandatory to make the diagnosis and to exclude neoplasm

FIBROUS DYSPLASIA
Fibrous dysplasia of the sphenoid in a 61-year-old man.
(A, B) Axial, T1-weighted (A) and T2-weighted (B) MR images show a mass lesion (arrows) of the sphenoid with mixed intensity ranging
from hypo- to hyperintense.
(C) Axial, fat-suppressed, contrast-enhanced MR image reveals inhomogeneous but strong enhancement of the mass (arrows).
(D) Sagittal-reformatted bone window CT image shows a mixed ground-glass and cystic appearance that is typical of fibrous dysplasia. A
convex margin (arrows) also suggests fibrous dysplasia rather than arrested pneumatization.
Fibrous dysplasia incidentally found in the elderly can be mistaken for a neoplasm on MR images.

FIBROUS DYSPLASIA
Radiology. 2008; 66: 348–362
Axial CT section in bone window (a) demonstrate diffuse structural changes of the skull base, facial bones and calvarium shown as a sclerotic ground-glass
pattern, expanding the medullary cavity and sparing the cortex. The affected bone merges imperceptibly with the normal adjacent bone. Note the involvement
of the clivus, nasal turbinates, maxillary sinus and left temporal bone leading to stenosis of the middle ear cleft on the right side. T2W MR images (b) and (c) of
the same patient demonstrate areas of very low signal intensity consistent with sclerotic bone and areas of inhomogeneous signal intensity due to cystic
change, more striking in the frontal calvarium. Note the obliteration of the right orbital apex leading to slight proptosis and the mass effect upon the anterior
frontal lobe. (Diagnosis: polyostotic fibrous dyplasia—leontiasis ossea.)

PAGET’S DISEASE
• Fibrous Osseous condition
• Involve the skull base and calvaria,  focal or diffusely.
• Appearance similar to fibrous dysplasia
• Often beyond the 5th decade.
• Paget’s tends to thicken cortical bone.
• The most common is that of bone sclerosis with coarse trabecula.
• As opposed to fibrous dysplasia, Paget’s disease may affect the otic
capsule, another distinctive feature

GIANT CAVERNOUS CAROTID ANEURYSM
• It is mandatory to rule out this condition before any attempts to
get a tissue diagnosis.
• Imaging features  quite variable depending on the degree of
thrombosis and luminal patency.
• It expand the cavernous sinus with outward bowing of its lateral
wall
• Longstanding  can remodel the medial wall of the sphenoid
sinus due to the effect of arterial pulsations.

• CT
• Blends with the enhancing sinus
• Mistaken for other enhancing mass lesions such as cavernous meningioma.
• Early arterial phase scans or a CT angiogram (CTA)  to make this
distinction and to separate the aneurysm from the cavernous sinus
proper
• Completely thrombosed aneurysms present as hypodense lesions with
an enhancing rim
• Partially thrombosed aneurysms  heterogeneous masses partially
hypodense with an enhancing “nodule” reflecting the patent lumen.
• Marginal calcifications are common and reflect calcified atheromatous
plaques.

• On MR
• The patent lumen  signal void, unless turbulent flow is present
resulting in variable signal intensities.
• The thrombosed portion of the aneurysm  a variety of signal
intensities depending on the different stages of hemorrhage.
• Blood degradation products within a thrombus layer in a centrifugal pattern,
according to age.
• “early” thrombus containing metahemoglobin is usually seen adjacent to the
patent lumen
• “older” thrombus containing hemossiderin, at the periphery of the aneurysm.

GIANT CAVERNOUS CAROTID ANEURYSMS
Axial CT image from a CT angiogram of the circle of Willis shows a right parasellar lesion predominantly hypodense with an area of early arterial
enhancement and extensive peripheral onion-like calcifications. Coronal pre- (b) and post-contrast (c) T1W images on another patient show a complex,
right parasellar lesion that expands the cavernous sinus and bulges its lateral wall. Medially, it occupies most of the sella displacing the pituitary gland and
pituitary stalk. Note the heterogeneous signal intensity with a signal void on the plain T1W image which enhances vividly after gadolinium, corresponding
to the patent lumen of the aneurysm. (Diagnosis: largely thrombosed giant cavernous carotid aneurysms.)
Radiology. 2008; 66: 348–362
(a) (b) (c)

SPHENOID SINUS TUMORS
• Similar to those arising from other paranasal sinuses but much less
common.
• The main diagnostic challenge is to differentiate primary tumours from
those arising from adjacent structures and invading the sphenoid sinus
secondarily.
• Tumours in this location can easily spread intracranially and are associated
with worse prognosis.

MIDDLE/ CENTRAL
SKULL BASE
 Pituitary Adenoma
 Craniopharyngioma
 Chondroid Tumor
 Chondrosarcoma
 Clival Chordoma
 Giant Cell Tumor
 Juvenile nasopharyngeal angiofibroma (JNA)

PITUITARY ADENOMA
• Benign - Site specific tumors
• Arising from the anterior lobe of the pituitary gland.
• Most common cause of sellar masses  invade from above
• Occur from the age of 20 years
• Up to 10% of all intracranial neoplasms.
• Intrasellar or combined intra- and suprasellar location  most common form
• Pituitary adenomas
• Macroadenomas: Larger than 10 mm
• Giant macroadenomas: size exceeds 40 mm
• Clinical Sign & Symptom  in diagnosis.

PITUITARY ADENOMA
• Clinical symptoms
• Local mass effects and/ or
• Hormonal abnormalities  hypersecretion
• Prolactin-producing adenoma accounts for 57% of all pituitary adenomas.
• A dopamine agonist should be used for initial treatment for prolactin-
producing pituitary adenomas.
• Trans-sphenoidal surgery is most commonly employed for initial treatment
of other pituitary adenomas.
• Radiation therapy is employed when a residual tumor grows progressively.

PITUITARY ADENOMA
• Characteristics
• The tumors can exhibit aggressive behavior, with invasion of the dura,
sphenoid bone, cavernous sinus, or surrounding structures.
• It tend to fill and expand the sella
• Extend superiorly into the suprasellar cistern through the diaphragm sella.
• Lateral growth  cavernous sinus
• May contact or even surround the cavernous carotid artery without narrowing its lumen, a
distinctive feature of these neoplasms.
• Preferential inferior growth, destroy the sellar floor and extend into the
sphenoid body and sinus (invasive pituitary adenoma).
• subgroup of giant pituitary adenomas

PITUITARY ADENOMA
• CT
• Non-Contrast: Iso- to mild hyperdensity
• When the origin of the lesion is doubtful on axial scans, coronal and sagittal
sections are particularly useful.
• MRI
• T1W: Iso- to hypointensity
• T2W: Mild hyper- to isointensity.
• Features:
• They sometimes contain intratumoral cysts or hemorrhage.
• Contrast enhancement of the tumor is moderate and mostly homogeneous.
• Large adenomas expand the sella.
• Invasive pituitary adenomas may erode or destroy adjacent bones.

PITUITARY ADENOMA
(a) Coronal post Gadolinium T1 image demonstrating a pituitary microadenoma (arrow). (b) Pituitary macroadenoma with suprasellar
extension and encroachment on the optic chiasm. The lesion extends to the medial surface of the right cavernous ICA.

PITUITARY ADENOMA
Pituitary adenoma in a 38-year-old man.
(A) Axial, non-contrast, T1-weighted MR image shows a large, infiltrating, hypointense mass (arrows) at the central skull base. Bone invasion can be
confirmed by the loss of normal high signals from fatty bone marrow. Intratumoral hemorrhage (arrow head) can be also seen.
(B) On coronal-reformatted, contrast-enhanced MR image, the mass shows moderate enhancement with a very indistinct margin (arrows).
(C) Axial, bone window CT image shows bone destruction of the central skull base (arrows). A pathological analysis revealed a prolactin-producing
pituitary adenoma.

PITUITARY ADENOMA
• Intraosseous pituitary adenoma
• Rare  pituitary adenomas arising within the sphenoid bone.
• Presents as a soft tissue mass replacing the fatty marrow of the
sphenoid
• Imaging
• Hypointense on T1W
• Heterogeneously hyperintense on T2W images.
• Bone is often slightly expanded with areas of cortical erosion but its original
morphology is retained.
• Main clues to the diagnosis include an empty sella, off-midline deviation of the
pituitary stalk and an intact sellar floor.

INTRAOSSEOUS PITUITARY ADENOMA
Axial CT section in bone window (a) shows a “vanishing” sphenoid body and clivus, completely replaced by a mass lesion. The outer
margins of the sphenoid body retain their original shape. MR coronal T1W (b) and contrast-enhanced sagittal T1W image (c) show
expansion and replacement of the shenoid body and clivus by an enhancing soft tissue mass. Of note is the presence of an empty sella,
inferior displacement of the sellar floor, leftward deviation of the pituitary stalk (long white arrow) and the inferior displacement of the
optic chiasm (short white arrow). (Diagnosis: intraosseous pituitary adenoma).
Radiology. 2008; 66: 348–362

CRANIOPHARYNGIOMA
• Benign tumour
• Arises from remnants of the pharyngohypophyseal canal (Rathke’s pouch)
• May occur anywhere from the nasopharynx to the hypothalamus.
• Rare occasions  tumours may be completely within the sphenoid bone
extending upward into the pituitary fossa.
• Typical features
• Largely cystic or mixed
• Partially calcified  showing a thin calcified rim or chunks of calcium within the
solid component

CRANIOPHARYNGIOMA
• On MR
• T1W  Cystic component may have variable signal intensity depending
on the protein content of the fluid
• T2W images hyperintense.
• Post gadolinium  a thin, smooth rim of peripheral enhancement is
seen.

CRANIOPHARYNGIOMA
(a) and (b) Sagittal pre and post Gadolinium T1 images demonstrating a cystic-solid craniopharyngioma with intrinsic T1 shortening and
heterogeneous enhancement.

CHONDROID TUMOURS
• Relatively rare.
• Arise from skull base synchondroses 
• Most commonly – petroclival synchondrosis.
• The second most  chondro-vomerian synchondrosis, the junction between the
posterior nasal septum and the rostrum of the sphenoid.

CHONDROID TUMOURS
• CT Scan
• Chondroid type calcifications  hallmark
• MRI
• Delineation of the neoplasm and its relationships with adjacent
neurovascular structures.
• Expansile lesions of intermediate signal intensity on T1W
• Calcifications (depend on their size and composition)  signal voids or
punctate hyperintense foci on T1W images.
• Extremely hyperintense on T2W images, more than CSF, a distinctive
feature.

CHONDROSARCOMA
• Arise from the cartilage, bones with endochondral ossification
• Origin primitive mesenchymal cells of the meninges.
• It accounts for 6% of skull base tumors
• Can occur at all ages from the teens into the 90s.
• No sex predominance has been reported.
• Location  Most commonly occurs along the petro-occipital fissure.
• The sphenoid is the next most common location but is far rarer .
• Typical clinical symptoms include abducens nerve palsy and headache.
• Surgery and adjuvant radiation therapy are most commonly employed for
treatment.
• Skull base chondrosarcoma is well-differentiated, grade 1 chondrosarcoma in
many cases, and the prognosis is rather favourable.

CHONDROSARCOMA
• Skull base chondrosarcoma typically forms an expansile mass with
multilobulated margins.
• CT
• An osteolytic mass.
• Typical ring and arc calcification can be seen in 41% of the tumors.
• MR:
• The tumor demonstrates iso- to hypointensity on non-contrast T1-weighted
and hyperintensity on T2-weighted MR images.
• Hypointense foci on T2-weighted images  hemorrhage or fibrous tissue.
• The contrast enhancement pattern is heterogeneous with a predominance at
the periphery in 73% of patients and homogenous in 27%.

CHONDROSARCOMA
Skull base chondrosarcoma in a 46-year-old woman.
(A) Axial, non-contrast, T1-weighted MR image shows an expansile, hypointense mass (arrows) engulfing the left petrous apex and the
clivus. The epicenter of the tumor is likely located at the left petroclival fissure.
(B) On an axial, fat-suppressed, T2-weighted MR image, most of the tumor shows very high signals (arrows). The left mastoid air cells lose
aeration, likely because the Eustachian tube is obstructed.
(C) Axial, contrast-enhanced, MR image with fat suppression shows peripheral enhancement (arrows).
(D) On an axial, bone window CT image, punctuate calcification is seen in the tumor (black arrow). The margin of the tumor is rather
distinct (white arrows).

CHONDROSARCOMA
Chondrosarcoma of the sphenoid in a 56-year-old man.
(A) Axial, T2-weighted MR image shows a lobulated mass at the sphenoid (arrows). The mass contains abundant intermediate signals
but also includes hyperintense foci.
(B) Axial, contrast-enhanced, MR image with fat suppression shows peripheral enhancement that indicates chondrogenic tumor. A
pathological analysis revealed grade 1 chondrosarcoma.

CHONDROSARCOMA
MR axial gadolinium enhanced T1W image (a) and axial T2W image (b) through the skull base show an expansive, moderately enhancing
lesion, centred at the petroclival synchondrosis. The lesion is noticeable for its high signal intensity on the T2W images, brighter then CSF.
CT scan of another patient in bone window (c) demonstrates an expansive lesion in the right parasagittal central skull base with multiple
popcorn-shaped calcifications, typical for chondroid tumours (Diagnosis: chondrossarcoma).
(a) (b) (c)
Radiology. 2008; 66: 348–362

CLIVAL CHORDOMA
• Expansile, Low to intermediate, locally aggressive malignancy  histologically benign
• Bone destruction  replacement of the clival bone marrow and erosion of its cortical margins.
• Arise from embryonic remnants of the primitive notochord (or benign notochordal cell
tumors)
• Entrapped within the basisphenoid and basi-occiput (typical midline sagittal central
skull base located tumours).
• Account for 1% of primary brain tumors
• Incidence peak at 30 to 50 years with Male-to- female ratio  2: 1.
• Typical clinical symptoms of clival chordomas include headache and diplopia.
• May grow
• Laterally  cavernous sinus; Superiorly  sella turcica; Anteriorly  sphenoid sinus; Anterior and
inferiorly  nasopharynx; Posterior and inferiorly  jugular foramen, pre-pontine cistern and
foramen magnum.
• Surgery and adjuvant radiation therapy are most frequently employed.

CLIVAL CHORDOMA
• CT
• Forms a multilobulated expansile mass in the clivus
• 1/3 of skull base chordomas occur in off-midline positions.
• Non-contrast CT: Mild hyper- to hypodensity.
• Bone destruction may be more aggressive in chordomas than in chondrosarcomas.
• MR (imaging characteristics similar with chondrosarcomas)
• T1W – Non-Contrast: Iso- to hypointensity
• High signal intensity  reflect hemorrhage or cystic areas filled with mucinous/proteinaceous
fluid.
• Very useful in determining the exact amount of bone marrow involvement.
• T2W: Hyperintensity (To differentiate them from osteomyelitis)
• T1W – Contrast-enhanced: Moderate-strong enhancement with a typical
honeycomb appearance.

CLIVAL CHORDOMA
Clival chordoma in a 40-year-old man.
(a) Axial contrast-enhanced CT image shows destruction of the sphenoid bone in the sellar region and clivus, occupied by a soft-tissue
mass (arrows).
(b) Sagittal T2-weighted MR image shows a mass with high signal intensity and septa (green arrows) and pontine compression (orange
arrows).

CLIVAL CHORDOMA
A soft tissue mass replacing the fatty marrow and expanding the clivus with focal areas of cortical disruption (white arrow). The lesion extends superiorly to
the floor of the sella and inferiorly to the nasopharynx. The pre-pontine cistern remains patent and the sphenoid sinus is not invaded by tumour. The lesion is
of intermediate signal intensity on T1W images and heterogeneous on T2W. (Diagnosis: clival chordoma).
Sagittal
T1W
MR
image
Aaxial
T2W
image
Radiology. 2008; 66: 348–362

CLIVAL CHORDOMA
Clival chordoma in a 67-year-old man.
(A) Axial, non-contrast, T1-weighted MR image shows a lobulated, hypointense mass lesion (arrow) in the upper part of the clivus.
(B, C) The mass shows hyperintensity on an axial, T2-weighted MR image
(B) and honeycomb-like enhancement on a sagittal, fat-suppressed, contrast-enhanced T1-weighted MR image (C).
(D) Axial bone window CT shows cortical bone destruction of the clivus and likely a residual bone fragment within the tumor (arrow).
The pathologic analysis demonstrated chordoma.

GIANT CELL TUMOR
• A rare benign intraosseous neoplasm containing multinuclear giant cells.
• It is rare in the skull base
• Most commonly occurs in the sphenoid bone followed by temporal bone.
• Most common in young adults, with a slight female predominance.
• CT: An expansile intraosseous mass with reactive bone remodeling.
• MR Images
• Low to intermediate signal intensity on both T1-weighted and T2-weighted MR
images.
• Intra-lesional hypointensity on T2-weighted  to hemosiderin or calcification
• Contrast-enhanced T1-weighted MR imaging shows variable enhancement patterns.

JUVENILE NASOPHARYNGEAL ANGIOFIBROMA (JNA)
• Benign tumour  In adolescent boys
• Fibrous tissue and abundant endothelial lined vascular spaces  ? vascular
malformation.
• Arise in the posterolateral wall of the nasal cavity near or within the
sphenopalatine foramen
• Tend to follow vessels along natural foramina and fissures.
• From the sphenopalatine foramen  grows laterally  pterygopallatine fossa 
the pterygomaxillary fissure infratemporal fossa.
• May access the orbit through the inferior orbital fissure
• To middle cranial fossa through foramen rotundum and vidian canal.
• Embolization prior to surgical treatment is standard of care  to significantly
decrease hemorrhage related surgical morbidity and mortality

• CT
• Anterior bulging of the posterior wall of the maxillary sinus, best seen on axial and
sagittal planes is a typical feature.
• Tumour location and imaging features, in the adequate clinical setting, are diagnostic.
• On MRI
• Highly vascular lesions show a “salt and pepper” appearance on T2W images
reflecting the stromal elements of the tumour and vascular flow voids, respectively.
• Vivid contrast enhancement is also seen both on CT and MRI.

Juvenile nasopharyngeal angiofibroma (JNA) in 12 year old child in whom mass was noted at adenoidectomy. Axial CT scan shows a tumor within the left
nasal fossa (t) with lateral extension through the widened pterygopa!atine fossa (*) into the infratemporal fossa (black arrow) . Note the characteristic
anterior displacement of the posterior wall of the maxillary antrum (white arrow) . (b) Coronal contrast- enhanced study reveals tumor extending through
the skull base (*) into the sphenoid sinus with cxtension into the cavernous sinus (arrow) . (c) Lateral subtraction view from an internal carotid artery
angiographic study reveals the supply to this juvenile angiofibroma via dural branches of the cavernous carotid artery (arrow), a finding consistent with
tumor invasion of cavernous sinus.

MIDDLE AND POSTERIOR
SKULL BASE
 Schwannoma
 Other Fibrous Osseous Condition
 Nasopharyngeal Ca (NPC)
 PVNS - TMJ

SCHWANNOMA
• Skull base schwannomas include
• Subfrontal
• Trigeminal
• Facial
• Vestibular
• Jugular foramen
• Hypoglossal
• Facial nerve (CN VII) schwannoma commonly occurs within the temporal
bone.
• Most commonly  between the ages of 20 to 60 years
• Women are more commonly affected.

SCHWANNOMA
• Subfrontal schwannomas  Rare neoplasms of unclear origin
• ? arise from the olfactory nerve or from a meningeal branch of CN V.
• Growth into the subfrontal region and into the nasal vault is the rule.
• Often misdiagnosed for olfactory groove meningomas or olfactory neuroblastomas Due
to location and imaging
• Vestibular schwannoma (VS)
• Most common  more than 80% of skull base schwannomas.
• Commonly causes chronic progressive hearing loss.
• Trigeminal schwannoma (TS)
• 1–8% of intracranial schwannomas
• Causes facial pain and paresthesia in 91% of patients
• Occur anywhere along the course of the nerve from its cisternal segment to its main
branches.
• When protruding through its natural neural foramina they tend to enlarge and remodel
rather then erode bone

SCHWANNOMA
• Jugular foramen schwannoma (JFS)
• Approx 2.9%.
• May cause palsies  CN 9th to 11th (tolerated by their opposite nerve functions).
• Up to 50% patient  after tumors have become large and hearing loss has developed .
• Origin from nerve IX, X and XI are rare
• If large it is difficult to distinguish from which nerve it developes.
• Hypoglossal schwannoma Extremely rare.
• Destruction of pars nervosa of the foramen  glossopharyngeal (IXth) schwannoma.
• Surgery is the treatment of choice for skull base schwannomas.
• Stereotactic radiosurgery or other radiotherapy techniques may be
employed to follow incomplete resection.

SCHWANNOMA
• Hallmark  tubular or dumbbell-shaped mass along the course of the CN with
distinct margins.
• Contrast-enhanced CT or MR show variable and inhomogeneous enhancement
depending on the predominance of the cell-rich Antoni type A and the looser
Antoni type B lesions, and the presence of cyst or hemorrhage in the tumor.
• CT:
• Non Contrast: Hypodense
• Lesions expand the foramen symmetrical, the cortical bone will remain visible ( in contrast
to paragangliomas).
• MRI
• T1-weighted (Non-contrast): Iso- to hypointense
• T2-weighted: hyperintense.
• Lesions will have smooth borders and will enhance strongly,
• The enhancement is less pronounced than in paragangliomas and scattered “puddles” of
contrast medium can be seen in the mid-arterial, capillary and venous phases.

SUBFRONTAL SCHWANNOMAS
Axial CT sections in soft tissue (a) and bone windows (b) demonstrate a mass lesion centred at the left nasal vault remodelling
adjacent bone and eroding the left cribiform plate. There is bone sclerosis surrounding the lesion and intratumoural calcifications are
also noted. MRI on the same patient, coronal T2W (c) and contrast-enhanced T1W (d) images show that the lesion cannot be
separated from left olfactory nerve (note the normal nerve on the contralateral side, white arrow). The lesion is of intermediate signal
intensity on the T2W image, isointense with white matter, and shows intense and relatively homogeneous contrast-enhancement
suggesting an olfactory groove meningioma (diagnosis: SUBFRONTAL schwannoma).
2008; 66: 338 - 347

SCHWANNOMA
Radiology. 2008; 66: 348–362
(a) Axial T2-weighted and (b) coronal T1-weighted image through Meckel’s cave featuring a trigeminal Schwannoma.
Gadolinium enhanced axial T1W MR image shows a dumbbell-shaped heterogeneously enhancing mass following the course of the
trigeminal nerve with posterior and middle cranial fossa components separated by a thin waist at the level of the Porus trigeminus (black
arrow). The posterior fossa component effaces the left pre-pontine cistern and the middle cranial fossa component obliterates Meckel’s
cave. Note the fluid filled Meckel’s cave (short white arrow) and the cisternal segment of the trigeminal nerve on the contralateral side
(long white arrow). (Diagnosis: TRIGEMINAL nerve schwannoma.)

SCHWANNOMA
TRIGEMINAL schwannoma in a 38-year-old man. (A) Axial, T2-weighted image show a dumbbell-shaped, partly cystic mass (arrows) extending from the left
parasellar region to the left pterygopalatine fossa. (B) Sagittal, contrast-enhanced MR image with fat suppression shows both intra- and extracranial
components of the tumor (arrows). The third branch of the trigeminal nerve seems normal (arrow head). Schwannoma of the second branch of the trigeminal
nerve was confirmed on surgery.
JUGULAR FORAMEN schwannoma in a 66-year-old man. (A) Axial, T2-weighted image shows a mixed solid and cystic mass (arrows) extending through the
left jugular foramen. (B) Axial, post contrast, T1-weighted image shows heterogeneous enhancement of the tumor (arrows).

FIBRO-OSSEOUS CONDITIONS
• May affect the skull base
• MR imaging appearance may mimic a malignant process.
• Ossifying fibroma
• A fibro-osseous lesion
• Displays the same imaging appearance as monostotic fibrous dysplasia but more
aggressive clinical course.
• On imaging
• Presents as an expansile bone lesion, well demarcated from the adjacent bone with geographic
margins.
• On CT : A ground-glass appearance but may also contain cystic and/or sclerotic components.
• On MRI: low signal intensity on T1W, intermediate to low signal intensity on T2W images
• Enhance vividly after gadolinium administration outside the cystic areas

OSSIFYING FIBROMA
Radiology. 2008; 66: 348–362
Coronal (a) and axial CT sections on soft tissue and bone windows demonstrate a very large, expansive bony mass, centred at the orbital
plate of the right frontal bone with geographic margins. The lesion is composed of a hypodense core surrounded by a thick rimof woven
bone mostly with a ground glass appearance but containing small cystic areas, best appreciated on bone window (b). (Diagnosis: ossifying
fibroma.)

CRANIAL NERVE NEUROFIBROMAS
• May occur isolated or as part of neurofibromatosis type I.
• Vidian nerve neurofibroma
• A sausage-shaped soft tissue mass expanding the vidian canal from foramen lacerum
posteriorly to the pterygopalatine fossa anteriorly.
• When large enough they displace foramen rotundum superiorly.
• Coronal sections are particularly well suited to demonstrate the exact location of the lesion.
• Plexiform neurofibromas
• Aggressive neurogenic tumours often seen in the setting of NF type I and can undergo
malignant change.
• Spread diffusely along peripheral branches of cranial nerves and have infiltrative borders.
• Tumour calcifications are sometimes seen on CT scans.
• Trigeminal nerve distribution is the most commonly affected.
• Grow peripherally as far as its terminal branches enlarging corresponding foramina and
canals

CRANIAL NERVE NEUROFIBROMAS
Radiology. 2008; 66: 348–362
Axial T1W MR image (a) shows a mass lesion following the long axis of the vidian nerve, from foramen lacerum posteriorly, to the pterygopalatine fossa
anteriorly. Coronal CT section (b) on the same patient (bone window) shows marked enlargement and remodelling of the vidian canal (white arrow) and
upward displacement of foramen rotundum (black arrow). (Diagnosis: vidian nerve neurofibroma.)

NASOPHARYNGEAL CANCER
• The midline central skull base tumour invasion
• Arising from below within the extracranial head and neck
• Presentation such as epistaxis, conductive hearing loss, nasal obstruction,
otalgia, headache, and cranial nerve involvement.
• Later  cervical nodal or distant metastasis.
• Tend to invade the central skull base, most commonly at the level of the
clivus.
• May be completely submucosal and present as nasopharyngeal bulges with
normal overlying mucosa, obscuring the diagnosis.
• A destructive central skull base mass bulges the nasopharynx should
include NPC in the differential regardless the absence of mucosal change.
• Trans-nasal deep nasopharyngeal biopsies  diagnosis.

NASOPHARYNGEAL CARCINOMA
• Contrast-enhanced CT
• An enhancing mass with aggressive behavior, bone erosion, and
opacification of mastoid cells.
• MRI
• An enhancing mass with bone infiltration.
• Diffusion tends to be restricted, with low ADCs.
• Architectural distortion, disrupted nasopharyngeal mucosa, and
enlarged lymph nodes.
• DDX  skull base osteomyelitis if findings involvement of lateral structures, soft-
tissue enhancement, high signal intensity at T2- weighted MRI (edema), and
abscess formation.

NASOPHARYNGEAL CANCER [NPC]
Sagittal (a) and axial (b) and (c) T1W MR images demonstrate a mass lesion in the roof of the nasopharynx, with extensive invasion of the
skull base. The lesion destroys the posterior wall of the clivus and bulges into the pre-pontine cistern; extends laterally into the cavernous
sinuses (left more then right), into foramen lacerum encasing the petrous (thin white arrow) and cavernous (black arrow) segments of the
left carotid artery. Also note tumour growth along the Eustachian tube (thick white arrow). (Diagnosis: undifferentiated carcinoma
nasopharyngeal type.)
Radiology. 2008; 66: 348–362
(a) (b) (c)

NPC
Nasopharyngeal carcinoma in a 63-year-old man with a
headache, diplopia, dysphagia, and hearing loss.
(a) Axial contrast-enhanced CT image shows an
enhancing mass in the nasopharynx with destruction
of the clivus and the body of the sphenoid and
erosion of the greater wings, the pterygoid process of
the sphenoid bone, and the bilateral petrous bone
(green arrows), with opacification of mastoid cells
(orange arrows).
(b) Sagittal contrast-enhanced T1-weighted MR image
shows an enhancing mass with bone infiltration
(green arrows) that extends into the prevertebral
space (blue arrows)
(c, d) Axial diffusion-weighted MR image (c) and ADC map
(d) show restricted diffusion with high- signal-intensity
foci at diffusion-weighted MRI and low signal intensity on
the ADC map (arrows). The diagnosis was keratinizing
squamous cell carcinoma.

PIGMENTED VILLONODULAR SYNOVITIS (PVNS)
• Disease of synovial joints
• Most common  large joints of the limbs.
• Characterized by the presence of hyperplasic connective tissue (villonodular
appearance of the synovial membrane) and giant foam cells (hemosiderin)
• This hyperplasic tissue leads to erosion of the articular surfaces and adjacent bone.
• Ddx  whole spectrum of spontaneously hyperdense lesions on CT
• Giant cell tumours
• Brown tumours
• Aneurismal bone cyst
• Hemorrhagic metastasis
• The clue to the diagnosis is the TMJ origin of the lesion.

PIGMENTED VILLONODULAR SYNOVITIS
• CT Plain:
• A well defined, spontaneously hyperdense (iron content of hemosiderin laden foam cells)
soft tissue lesion
• Centred in the joint or, more medially in the lateral aspect of the sphenoid wing.
• Bone remodelling without destruction or aggressive features and no calcification or bony
matrix is seen within the lesion, a distinctive feature from synovial osteochondromatosis.
• MR
• Heterogeneous signal intensity
• T1W: increased signal intensity due to the presence of extracellular methemoglobin;
• T2W: low signal intensity reflecting the presence of fibrous tissue and punctate signal voids
due to hemossiderin.
• Contrast: serpentine enhancement of the hypervascular fibrous tissue, responsible for
repeated hemorrhages.

PVNS – TMJ
Radiology. 2008; 66: 348–362
Axial CT sections soft tissue (a) and bone window (b) show a spontaneously hyperdense, expansive mass in the medial aspect of the
TMJ, extending to the lateral aspect of the greater sphenoid wing. Bone remodelling with well corticated margins is nicely depicted on
the bone window. The mandibular condyle remains intact. There is no calcification or bony matrix within the lesion. Axial T2W (c) and
contrast-enhanced axial T1W (d) MR images on the same patient show that the lesion is markedly hypointense on T2W and shows vivid,
arborescent enhancement interspersed with areas of very low signal (Diagnosis: pigmented villonodular synovitis of the TMJ).

POSTERIOR
SKULL BASE
 Hemangioblastoma
 Medulloblastoma
 Pilocytic Astrocytoma
 Brainstem Glioma
 Subependymoma
 Ependymoma
 Choroid Plexus Tumor
 RGNT of 4th Ventricle
 Bone Metastasis

OVERVIEW POSTERIOR FOSSA TUMOR
REGION PATHOLOGY POPULATION AFFECTED SPECIAL FEATURES
CEREBELLUM HEMANGIOBLASTOMA ADULTS Association with von Hippel-Lindau syndrome
(VHL)
MEDULLOBLASTOMA CHILDREN AND YOUNGER ADULTS (age <40)
ADULTS Lateral hemispheric mass with SHH activation
PILOCYTIC ASTROCYTOMA CHILDREN AND YOUNGER ADULTS (age <40) Mixed solid-cystic tumor
DYSPLASTIC CEREBELLAR GANGLIOCYTOMA YOUNGER ADULTS (ages 20–40) Association with Cowden syndrome
CEREBELLAR LIPONEUROCYTOMA OLDER ADULTS (age >40) Appearance similar to medulloblastoma
BRAINSTEM DIFFUSE INTRINSIC BRAINSTEM GLIOMA CHILDREN AND YOUNGER ADULTS (age <40) Low grade in adults but high grade in children
MALIGNANT BRAINSTEM GLIOMA OLDER ADULTS (>40 y) a.k.a Infratentorial glioblastoma
FOCAL TECTAL GLIOMA CHILDREN AND YOUNGER ADULTS (age <40) <50% brainstem diameter
VENTRICLE SUBEPENDYMOMA OLDER ADULTS (>40 y) Hypovascular mass projecting into the ventricle
EPENDYMOMA CHILDREN AND YOUNGER ADULTS (age <40) + extraventricular or transependymal spread
CHOROID PLEXUS TUMOR INFANTS AND YOUNGER CHILDREN 4th ventricle is more frequently seen in adults
CHOROID PLEXUS MENINGIOMA OLDER ADULTS (>40 y) and WOMEN Atrium/trigone > fourth ventricle
RGNT OF THE FOURTH VENTRICLE YOUNGER ADULTS (20–40 y) May occur outside posterior fossa

HEMANGIOBLASTOMA
• a.k.a Lindau tumors  familial with von Hippel-Lindau syndrome (VHL)
• Hypervascular enhancing nodule cyst formation
• Cerebellar hemangioblastomas frequently occur at the posterior and
medial hemispheres
• WHO grade I meningeal tumor.
• Highly vascular tumors  typically intra-axial
• Located at or near the pial surface of the cerebellum and spinal cord.
• Derive from embryologic multipotent stem cells (hemangioblast)
• Become neoplastic stromal cells with the loss of both VHL tumor suppressor genes
• Retain the ability to differentiate into both hematopoietic and endothelial cells

HEMANGIOBLASTOMA
• CT or MR imaging is “a peripheral cyst in the posterior fossa with a mural nodule
supplied by enlarged vessels.”
• The nodule is the tumor nidus and enhances intensely; this may be accompanied
by hypervascular flow voids on spin-echo MR images.
• The cyst is lined by compressed brain parenchyma with occasional reactive
astrogliosis (not by tumor cells) and usually does not enhance;
• Approx 40% of hemangioblastomas  solid nodules without adjacent cysts.
• Probably all hemangioblastomas begin
• Solid nodules (Small and asymptomatic)  Vascular hyperpermeability with fluid
extravasation  to vasogenic edema  cyst formation (cause symptoms)  Surgery
• Surgery  when the diagnosis is uncertain
• Ddx  cerebellar metastasis and pilocytic astrocytoma.

HEMANGIOBLASTOMA
Shih & Smirniotopoulos. Posterior Fossa Tumors in Adult Patients. Neuroimaging Clinics of North America. 2016: 1-18 .
A 64-year-old woman with multiple falls and shuffling gait due to a cerebellar hemangioblastoma.
(A) Axial T2 image shows a circumscribed mass with hypervascular flow voids and vasogenic edema in the right cerebellar hemisphere.
(B) Axial postgadolinium T1 image shows intense enhancement.
(C) Cerebral angiography in lateral projection from left vertebral artery injection shows a hypervascular tumor blush.

MEDULLOBLASTOMA
• Derived from cerebellar granule cell precursors.
• Cerebellar granule cell precursors migrate laterally from the rhombic lip at the roof
of the fourth ventricle  external granular layer at the surface of the cerebellar
hemispheres, which may explain a more lateral preference for tumors arising later
in life.
• Most common primary cerebellar tumor in children (age <20).
• Different age predilection
• Midline vermian tumors (mean age 8 years)
• Lateral hemispheric tumors (mean age 31 years)  SHH activation
• Standard therapy is resection followed by craniospinal radiation
• Metastases at presentation or recurrence conferring a worse prognosis

MEDULLOBLASTOMA
• CT - hyperattenuating
• Due to high cellular density (small round blue cell tumor)
• MR
• T2-weighted - Low signal intensity
• Apparent diffusion coefficient (ADC): Circumscribed margins and
variable enhancement
• Spectroscopy: To differentiate  Alanine peak is increased in
meningiomas

MEDULLOBLASTOMA
A 25-year-old woman with medulloblastoma in a more lateral or hemispheric location.
(A) Head CT shows a mostly hyperattenuating mass in the right cerebellum.
(B) Axial DWI image shows corresponding restricted diffusion, which reflects high cellular density (small round blue cell tumor).
(C) Axial T2 image shows a mostly isointense mass with cystic or necrotic changes.
(D) Axial post-gadolinium T1 image shows no enhancement.
Medulloblastomas are more often lateral than midline in adults (opposite of children).

PILOCYTIC ASTROCYTOMA
• Circumscribed margins
• Solid or mixed solid-cystic tumor
• Enhancement related to leaky blood-brain barrier
• Most commonly presents in childhood as a cerebellar or suprasellar mass,
or along the optic pathways in the setting of neurofibromatosis type 1.
• Adult pilocytic astrocytoma  rare diagnosis
• < 0.1 case per 100,000 person-years in adults over age 45 years.
• Anaplastic or malignant transformation (WHO grade III) is a rare
phenomenon.

• Imaging  similar to pediatric pilocytic astrocytoma variable
enhancement and cyst formation.
• can be mistaken for a high-grade glioma or metastasis in an adult patient.
• CT/ MR imaging
• Solid component often (but not always) enhances  due to abnormal vessels with a
leaky blood-brain barrier
• Tumor margins well-defined with a lesser degree of peritumoral edema
• MRS: Elevated choline
• FDG-PET: hypermetabolism.
• Diffusion-weighted imaging (DWI), with higher ADC values in pilocytic astrocytomas.

A 27-year-old man with dizziness and who was found to have a cerebellar pilocytic astrocytoma.
(A) Head CT shows a subtle iso attenuating lesion in the right medial cerebellum.
(B) Axial T2 image shows a round circumscribed hyperintense mass.
(C) (C) Axial post-gadolinium T1 image shows no enhancement.

DYSPLASTIC CEREBELLAR GANGLIOCYTOMA
• a.k.a Lhermitte-Duclos disease, purkinjeoma, or granular cell hypertrophy of the
cerebellum
• Neuronal tumor
• A slow-growing low-grade neoplasm or hamartoma.
• Symptoms of local mass effect in young adults (mean age 34 years).
• Associated with Cowden syndrome
• A rare autosomal dominant inherited disorder characterized by multiple hamartomas of the
skin and mucosa.
• High risk of breast, thyroid, and endometrial carcinoma
• 80% have mutations  PTEN tumor suppressor gene  Lhermitte-Duclos disease.
• Considered a phakomatosis with multiple neurocutaneous hamartomas and autosomal
dominant inheritance (PTEN vs NF1, NF2, and VHL tumor suppressor genes).
Phakomatoses are a group of syndromes characterized by systemic hamartomas of the eye, brain, skin, and
sometimes the viscera and bones

• CT imaging
• PET Scan
• Hyperperfusion  increased uptake of thallium  hypermetabolism
• May mistaken for high-grade tumor (eg, medulloblastoma), or vice versa, on preoperative
imaging.
• Can have variable density on CT
• MR imaging
• Alternating bands or tiger stripes of T1 hypointensity or T2 hyperintensity
• Restricted diffusion on MR imaging  due to high cellularity.
• MR perfusion: Elevated rCBV
• Gadolinium enhancement: Rare  cortical or pial surface, due to high vascularity.
• MRS:↓ levels most metabolites (Choline)  unusual in high-grade tumor.
• ↑ lactate peaks, without increased levels of lipid (no necrosis)
rCBV: Relative cerebral blood volume

A 31-year-old woman with right-sided headaches, found to have an ipsilateral cerebellar mass.
(A) Head CT shows a heterogeneous iso attenuating mass in the right cerebellum with a few calcifications.
(B) Axial T2 image shows a round circumscribed mass with internal striations (suggestive but not specific for Lhermitte-Duclos disease).
(C) Axial post gadolinium T1 image shows a prominent vein without any tumor enhancement.
(D) Gross specimen shows thickened folia in a dysplastic gangliocytoma of the cerebellum (Lhermitte-Duclos disease).

CEREBELLAR LIPONEUROCYTOMA
• Neuronal or mixed neuronal-glial tumor
• Appearance is similar to medulloblastoma (look for fat density/signal)
• Even on microscopy
• Prognosis is similar to central neurocytoma (Supratentorial)
• Older population (mean age 50 years)  Less aggressive with low mitotic
activity.
• Molecular analysis of gene expression profiles
• Similar to central neurocytoma but distinct from medulloblastoma
• Significant overexpression of fatty acid binding protein 4 (FABP4)
• Normally found in adipocytes or macrophages and not in normal cerebellum.
• Treatment is surgical resection  local recurrence (50%)  long-term follow-up.
• Adjuvant radiotherapy
• Subtotal resections
• Liponeurocytomas with unusual aggressive histology  Ki-67 proliferative index >6%

CEREBELLAR LIPONEUROCYTOMA
• CT/MR imaging
• Well-circumscribed with little peritumoral edema
• Heterogeneous or variable enhancement.
• Visualization of macroscopic fat attenuation or signal within a cerebellar
mass.
• There is propensity for exophytic growth into the adjacent
cerebellopontine angles or fourth ventricle
• Preoperative DDx  Ependymoma.

BRAINSTEM GLIOMA
• Diffuse intrinsic
• Diffuse: >50% brainstem diameter
• Low grade in adults (50%) but high grade in children (80% )
• They cause cranial nerve or long tract deficits but can rarely involve
cranial nerves on imaging
• Median survival
• 9 to 12 months in children
• 5 to 7 years in adults
• Resection is not possible for infiltrative brainstem gliomas
• Standard treatment is stereotactic biopsy to confirm the diagnosis,
followed by radiation therapy.

BRAINSTEM GLIOMA
• Malignant
• Infratentorial glioblastoma
• Present in younger adults (age < 40), a second MR imaging pattern tends to present
in older adults
• Comprises 30% of adult brainstem gliomas
• Median survival is only 11 months
• Negative prognostic factors for brainstem gliomas include
• Age greater than 40
• Duration of symptoms less than 3 months
• Karnofsky performance status less than 70,
• High-grade histology,
• Contrast enhancement, and tumoral necrosis.

BRAINSTEM GLIOMA
• Focal Tectal Glioma
• Focal: <50% brainstem diameter
• Non-enhancing mass in dorsal midbrain obstructive hydrocephalus
• Account for only 8% of brainstem gliomas in adults.
• These tumors are centered in the dorsal midbrain, occupying less than
50% of the brainstem diameter, and are well-defined without
enhancement
• They have a benign and indolent natural history
• Median survival of more than 10 years, and are usually low-grade when
biopsied.
• Treatment is directed at the hydrocephalus (eg, endoscopic third
ventriculostomy), rather than at the tumor.

BRAINSTEM GLIOMA
• Diffuse (Low Grade)
• Expansile (>50%) infiltrative T2 hyperintense lesion without significant
enhancement with poorly defined margins
• Malignant (High Grade)
• a contrast-enhancing infiltrative brainstem mass with intratumoral
necrosis and peritumoral edema
• MR spectroscopy with elevated choline.

BRAINSTEM GLIOMAS
Four examples of brainstem gliomas in adult patients.
(A) A 47-year-old man with biopsy-proved diffuse intrinsic pontine glioma (low-grade astrocytoma) on axial T2 image (non enhancing, not shown).
(B) A 41-year-old man with biopsy-proved infiltrative brainstem glioma (anaplastic oligodendroglioma) on axial 3-D FIESTA image (exophytic growth along
cranial nerves into right jugular foramen).
(C) A 71-year-old man with focal enhancing malignant brainstem glioma on axial post gadolinium T1 image (diagnosis was high-grade astrocytoma at
autopsy).
(D) A 32-year-old man with focal tectal glioma in the dorsal midbrain (not biopsied) and severe obstructive hydrocephalus on sagittal T1 image, which was
treated with shunting.

SUBEPENDYMOMA
• Fourth ventricle > lateral ventricle > spinal cord (central canal)
• Relatively hypovascular mass projecting into the ventricle
• Rare benign slow-growing neoplasm arising from glial cells in the subependymal
plate
• Anaplastic ependymoma arise from radial glial cells in the brain parenchyma.
• From the second to ninth decades but is most common in older adults (mean
age 57 years).
• Most are intracranial (supratentorial) and project into the fourth or lateral
ventricles (cerebellopontine angles); few are intramedullary (Myxopapillary
ependymoma) and arise around the central canal of the spinal cord.
• On MR imaging, intracranial subependymomas tend to be completely intra-
ventricular, with heterogeneous internal signal and often with little edema or
enhancement.

SUBEPENDYMOMA
A 52-year-old woman with incidentally discovered subependymoma. (A) Sagittal T1 image shows the mass at the inferior portion of the fourth ventricle.
(B) Sagittal postgadolinium T1 image shows mild heterogeneous enhancement at the inferior aspect of the neoplasm. (C) Axial T2 image at the foramina
of Luschka shows a solid component. (D) Axial T2 image at a slightly lower level shows a hemorrhagic or cystic component. The imaging differential
diagnosis for a heterogeneous enhancing mass in the fourth ventricle includes ependymoma. Subependymoma is more likely to be hypovascular or
nonenhancing.

EPENDYMOMA
• MR
• Heterogeneous intraventricular mass with enhancement  secondary to intratumoral
calcifications, cysts, or hemorrhage.
• + extraventricular or transependymal spread
• Ependymoma has a propensity to “ooze out of the foramina” of Luschka or Magendie,
when located inside the fourth ventricle, and for paraventricular or transependymal
invasion into the brain parenchyma.
• Ependymoma  more vascular and frequently exhibits intense enhancement in the solid
portions.
• A non-enhancing and purely intraventricular mass  subependymoma (older
adult)
• A strongly enhancing mass with transependymal invasion  ependymoma.
• Maximal resection plus adjuvant radiotherapy has been shown to improve
progression-free survival in adults with posterior fossa ependymomas.

EPENDYMOMA
A 29-year-old man with dizziness and vertigo, due to an ependymoma in the fourth ventricle.
(A) Axial post- gadolinium T1 image shows a heterogeneous enhancing mass at the right foramen of Luschka.
(B) Coronal post gadolinium T1 image shows the mass inside the fourth ventricle.
(C) Intraoperative photo shows a posterior view of the cerebellum and tumor.

CHOROID PLEXUS TUMOR
• Arise from the neuroepithelial lining
• Papilloma (WHO grade I)
• Atypical papilloma (WHO grade II)
• Carcinoma (WHO grade III)  Approximately 20%
• More invasive and hemorrhagic than papillomas
• Rare and affect children (2%–4% of pediatric brain tumors) more frequently than
adults (0.5% of adult brain tumors).
• Location: age dependent
• Lateral ventricle (atrium or trigone) (43%)  Mostly Pediatric
• Fourth ventricle (39%)  Mostly Adult
• Third ventricle (11%)
• Cerebellopontine angle (7%), arising from small choroid tufts that normally project outside
the foramen of Luschka.
• Ddx  meningioma and metastasis.

• MR
• CPP
• Few arise from the choroid plexus within the ventricular lumen.
• Except for the occipital horns and the cerebral aqueduct
• Lobulated enhancing mass from choroid plexus
• Like ependymoma  Circumscribed intraventricular mass with internal
heterogeneity and intense enhancement BUT hydrocephalus from CSF
overproduction.
• CPC
• Arterial spin-labeling perfusion-weighted imaging  demonstrate higher CBF

A 39-year-old woman with diplopia and headaches.
(A) Coronal post gadolinium T1 image shows a
lobulated enhancing mass in the fourth ventricle
with lateral ventriculomegaly.
(B) Intraoperative photo shows a lobulated papillary
mass in the fourth ventricle, which is the most
common location for choroid plexus papilloma in
adults (atrium or trigone of the lateral ventricles in
children).

RGNT OF THE 4th VENTRICLE
• ROSETTE-FORMING GLIONEURONAL TUMOR OF THE FOURTH VENTRICLE
• Rare, slowly growing tumor (Can be solid or mixed solid-cystic)
• Fourth ventricular region
• Affects young adults (mean age 33).
• Symptoms  headaches and ataxia, with frequent obstructive hydrocephalus.
• Most are midline lesions of the posterior fossa
• Arise from pluripotential cells in the subependymal plate at the ventricular wall.
• Possible arising outside the fourth ventricle  pineal region, and around other
CSF-containing spaces from third ventricle to central canal.
• Have occurrence of satellite lesions and drop metastases through CSF
dissemination.

• MR
• Often focal contrast enhancement.
• T1W - Heterogeneous hypointensity
• T2W - Hyperintensity
• T2* W - hypointense foci related to intratumoral calcification or hemorrhage.
T2* or "T2-star (gradient-recalled echo/ susceptibility-weighted imaging)  hemorrhages and hemosiderin deposits become hypointense.

A 22-year-old woman with possible seizure, found to have a lesion in the midline posterior fossa.
(A) Sagittal T1 image shows a multicystic lesion involving the cerebellar vermis.
(B) Axial T2 image shows a multicystic lesion at the posterior aspect of the fourth ventricle.
(C) Axial post-gadolinium T1 image shows no enhancement, in this particular RGNT.

PARAGANGLIOMAS
• In women 3x
• Multiple lesions are found in up to 10% of the patients.
• Jugulotympanic paragangliomas  from the paraganglia along the
• Nerve of Jacobson (tympanic branch of the IXth nerve)
• Nerve of Arnold (auricular branch of the Xth nerve).

PARAGANGLIOMAS
• On CT
• Diffuse infiltration and destruction of the walls of the jugular foramen, giving it a so
called “moth-eaten” appearance.
• On MR
• T1 and T2W: A typical “salt-and-pepper” pattern  reflects the hypervascularity of
tumors.
• Become difficult to distinguish in smaller lesions.
• Unenhanced high-resolution TOF-MRA : More sensitive
• To make high quality multiplanar reconstructions  needed to detect extension of the tumor in
the middle ear, hypoglossal canal and especially in the cerebellopontine angle (CPA).
• Show the feeding vessels inside the tumor (even in smaller tumor)
• Conventional angiography (only)  visualize all feeding vessels and
connections
• Needed when surgery and/or embolization is planned.
TOF-MRA : time-of-flight (TOF) MRA was the dominant non-contrast bright-blood method for imaging the human vascular system

ANYWHERE
SKULL BASE
 Skull base Meningiomas
 Metastasis
 Bone Metastasis
 Multiple Myeloma

SKULL BASE MENINGIOMAS
• 36–50% of all meningiomas.
• Their common locations include the:
• Intraventricular Meningiomas
• Less than 1% of cases
• Arising from meningothelial or arachnoidal cap
cells in the choroid plexus stroma
• In the atrium or trigone of the lateral ventricle
• Rarely in the posterior fossa.

SKULL BASE MENINGIOMAS - CLASSICAL
• MR
• Isointense to brain on both T1W and T2W images, well- circumscribed
• and show intense and homogeneous gadolinium enhancement.
• Adjacent linear dural enhancement, known as dural tail, is commonly seen.

• Olfactory groove meningioma
• Most common intracranial lesion affecting the anterior skull base from above.
• Meningiomas in this particular location may extend through the cribiform plate into
the ethmoid sinuses and nasal cavity.
• Associated bone changes include bone remodelling or bone sclerosis.
• Intra-tumoural calcifications are seldom seen.
• En plaque meningiomas
• The greater sphenoid wing is commonly affected
• On imaging, by slight bone expansion and extensive hyperostosis.
• Classic globular meningiomas are also seen in this location and arising from the
lateral sphenoid ridge, displacing the temporal pole posteriorly.

SKULL BASE MENINGIOMAS - OLFACTORY GROOVE
Radiology. 2008; 66: 348–362
MR sagittal contrast enhanced T1W images (a) and (b) show a large hemispheric extra-axial lesion based on the roof of the ethmoid sinuses, planum
sphenoidale and nasal vault. The lesion enhances vividly, although to a lesser extent than the adjacent sinonasal mucosa. There is a small exocranial tumour
component protruding into the nasal vault through the cribiform plate (short black arrow). Also note blistering and sclerosis of the planum (long black
arrow) and the apparent expansion of the sphenoid sinus, a condition known as pneumosinus dilatans (white arrow) (diagnosis: olfactory groove
meningioma).

SKULL BASE MENINGIOMAS - EN PLAQUE
Radiology. 2008; 66: 348–362
Axial CT section (a) in bone window shows a markedly sclerotic bone lesion of the sphenoid triangle with a slightly spiculated outer margin.
On MR the lesion shows void of signal on T2W (b) and, on post-contrast T1W image (c), thick dural enhancement is noted along the medial
cranial fossa.
Also note slight postero-medial displacement of the temporal lobe. The orbital apex is free of tumour (white arrows).
(Diagnosis: En plaque meningioma of the sphenoid triangle.)

• Cavernous sinus or sphenocavernous meningiomas
• Most common parasagittal tumours
• Originating from above are petroclival and cavernous sinus
meningiomas.
• Difficult to manage surgically due to involvement of critical
neurovascular structures travelling through the cavernous sinus.
• Lesions in this location may extend
• Anteriorly into the orbital apex,
• Medially into the sphenoid sinus and suprasellar cistern,
• Posteriorly into Meckel’s cave and
• Inferior and laterally into the masticator space, through foramen ovale.

SKULL BASE MENINGIOMAS - SPHENOCAVERNOUS
(a) (b) (c)
Axial T1W (a), T2W (b) and gadolinium enhanced T1W MR images show a large sphenocavernous lesion, which follows the signal intensity of grey matter
on both T1 and T2W images and shows vivid, homogeneous contrast enhancement and a dural tail along the superior petrous ridge (white arrow). The
lesion encases the cavernous carotid, narrowing its lumen (black arrow). Also note tumour bulge into the posterior fossa effacing the left lateral aspect of
pre-pontine cistern at the expected course of the trigeminal nerve. (Diagnosis: sphenocavernous/petroclival meningioma.)
Radiology. 2008; 66: 348–362

• Sellar and parasellar meningiomas
• Common tumours arising from above.
• Comprise 20–25% of all meningiomas
• May originate from the tuberculum sella, planum sphenoidale, anterior
and posterior clinoid processes and diaphragm sella.
• Features:
• Broad dural-based lesions, along the planum sphenoidale, filling in the sella.
• Usually the pituitary gland is compressed against the sellar floor, an important
diagnostic.
• Increased pneumatization of the sphenoid sinus (pneumosinus dilatans)
• Hyperostosis of the planum sphenoidale with upward blistering  CT scans.
• Bone sclerosis, remodelling or demineralization (bone washout).

82: 398-409
Skull base meningioma in a 29-year-old woman. (A) Coronal-reformatted, post contrast, T1-weighted image shows a
meningioma with typical dural tail sign (arrows). (B) Coronal-reformatted, bone window CT image demonstrates
hyperostosis of the underlying bones (arrows).

METASTASES
• Skull base metastases are rare.
• Asymptomatic or experience cranial neuropathy or craniofacial pain.
• Metastasis of several primary cancers including breast cancer, prostate
cancer, lung cancer, renal cell carcinoma, thyroid cancer, melanoma, and
hepatocarcinoma.
• Medical Hx of a known primary tumor supports the diagnosis.
• 6% of intraventricular neoplasms a/w  most commonly with renal and
lung carcinoma.
• CT  bone erosion or destruction, with a soft-tissue mass.
• MRI  detection of infiltration of the dura or cranial nerves.

BONE METASTASIS
• Most cases of advanced malignancies.
• The skull and the skull base  frequent sites for bone metastasis.
• Bone metastasis can be either osteolytic or osteoblastic,
depending on the activities of osteoblasts, osteoclasts and
relevant cytokines.
• Clinical symptoms include headache, nausea and local
neurological deficits.
• Treatment  depends on tumor volume, lesion location, tumor
pathology and the general condition of the patient.
• Radiotherapy and/or systemic chemotherapy  frequent

BONE METASTASIS
• CT
• Forms a destructive mass centered in the bone with no sclerotic rim.
• Osteolytic metastasis is more common.
• MRI
• Non Contrast T1-weighted: Hypointense to normal bone marrow.
• Diffusion-weighted: Improve detection of skull metastasis  breast ca and lung ca
• Insensitive to Prostate Ca.
• T2-weighted: Signal intensity variable.
• Contrast-enhanced T1-weighted: Sometimes enhances to normal bone marrow
signal
• Addition of a fat suppression technique is desirable.

MULTIPLE MYELOMA
• A low grade hematologic malignancy characterized by monoclonal proliferation
of B lymphocytes in the plasma cell lineage.
• Deceiving benign appearance on imaging grounds
• Presenting as a polypoid nasal mass associated with bone remodelling.
• It accounts for 10% of all hematologic tumors
• Most commonly occurs in the elderly, with a slight male predominance.
• Anemia and bone pain are typical symptoms
• MM  multiple lesions or diffuse marrow abnormality on MR images.
• A single lesion may suggest plasmacytoma.
• Treatment depends on the disease status, ranging from observation with
supportive care to chemotherapy.

MULTIPLE MYELOMA
• CT
• Multiple, punched-out, lytic bone lesions, and solitary bone plasmacytoma as a single lytic
bone lesion without sclerotic borders.
• Skull base extramedullary plasmacytoma may erode adjacent bones.
• MR
• T1-weighted: Hypointensity
• T2-weighted: Hyperintensity.
• Diffusion-weighted: Can detect smaller myeloma lesions.
• Diffuse infiltration is less common and shows a diffuse decrease in the signal of the marrow
on T1-weighted MR images and a variable increase in the signal of the marrow on T2-
weighted MR images.
• Up to 30% of myeloma patients have normal-looking bone marrow signals on MR images.
• Contrast-enhanced: Marked enhancement.

MULTIPLE MYELOMA
Multiple myeloma in a 76-year-old man. (A) Axial, non-contrast T1-weighted MR image shows a hypointense mass (arrow) destroying
the left petrous bone and the left lower clivus, in contrast to normal hyperintense fatty bone marrow. (B) On an axial, diffusion-
weighted image, the mass is hyperintense, equivalent to the brain tissue
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EOSINOPHILIC GRANULOMA
• A benign tumour  affect bones
• Characteristic  punched out or bevelled margins, with or without surrounding
sclerosis
• Part of Langerhans cell histiocytosis (LCH)
• A rare histiocytic disorder
• Characterized by the presence of a typical histiocyte-like cell, containing a large “coffee bean”-
shaped nucleus.
• Present single or multiple osteolytic bone lesions  histiocytic infiltration with or without invasion
of the extraskeletal organs.
• Commonly occurs in children
• Bone pain and palpable mass are typical clinical symptoms
• Peripheral blood eosinophilia
• Treatment whether LCH affects a single system or many systems, and on the number
and location of LCH lesions.
• Bone involvement  skull base are at increased risk of developing CNS involvement by
LCH and endocrine abnormalities.

EOSINOPHILIC GRANULOMA
• CT
• Appears as a soft tissue mass replacing bones of the skull base.
• MRI
• Non-contrast T1-weighted: non-specific hypointensity
• T2-weighted: Mild hyperintensity .
• Contrast: Uniform and strong enhancement

SUMMARY
SKULL BASE TUMOR AND ITS DIFFERENTIAL DIAGNOSIS

ANTERIOR SKULL BASE
• Olfactory groove
• Meningioma
• Olfactory neuroblastoma
• Sinonasal region
• Benign sinonasal masses
• Benign sinonasal masses.
• Juvenile angiofibroma.
• Sinonasal malignancy
• Adenoid cystic carcinoma
• Adenocarcinoma
• Sinonasal undifferentiated carcinoma.
• Mucoepidermoid carcinoma
• Sarcoma
• Sinonasal melanoma
• Non-hodgkins lymphomas
• Orbital region
• Skull base lesions with orbital invasion
• Orbital tumours with spread to the
skull base

CENTRAL SKULL BASE
• Sella turcica
• Pituitary microadenoma
• Pituitary macroadenoma.
• Craniopharyngioma
• Other suprasellar tumours.
• Parasellar tissues and neural foramina
• Perineural spread.
• Meningioma
• Schwannoma
• Clivus and osseous central skull base
• Chordoma
• Chondrosarcomas.
• Metastases
• Osteosarcoma
• Fibrous dysplasia

POSTERIOR SKULL BASE
• Petrous temporal region
• Glomus tympanicum
• Glomus jugulare
• Vestibular aqueduct
• Endolymphatic sac tumour.
• Cerebellopontine angle
• Vestibular schwannoma
• Meningioma
• Other differentials.
• Foramen magnum
• Foramen magnum tumours

Skull Base Radiology and Ddx.pptx

Skull Base Radiology and Ddx.pptx

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