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INFRATENTORIAL BRAIN TUMORS
ANATOMY OF POSTERIOR CRANIAL FOSSA
Posterior Fossa
Medulla
Pons
Cerebellar
hemispheres
Vermis
CSF containing
spaces
Postero-
laterally
INFRATENTORIAL TUMORS
 Common in children.
 In children:
 Cerebellar astrocytoma (1/3rd) and Medulloblastoma(1/3rd) > Brain stem
gliomas(1/4th) > Ependymoma(1/8th)
 Adults:
 Mostly extra-axial.
 Schwannoma> Meningioma > Epidermoid.
 Intra-axial neoplasm: Metastasis>Hemangioblastoma>Glioma
IMAGING
 Primary imaging modality : Magnetic resonance imaging (MRI).
 Superior delineation of the extent of tumor.
 Computed tomography: Better demonstration of small or subtle calcifications within
tumors.
 Determine whether the mass is intra-axial or extra-axial in location.
 Features suggesting that the mass is extra-axial include:
Bone and meninges
• Dural tail sign.
• Erosion, invasion or
destruction of adjacent
bone.
• Hyperostosis.
Brain parenchyma
• Absence of claw sign.
• Intervening cortex
between mass and
white matter.
Subarachnoid space:
• CSF cleft sign.
• Widening of adjacent
subarachnoid space/cistern.
• Intervening pial
arteries/veins.
CLASSIFICATION OF INFRATENTORIAL TUMORS
Location Tumors
Cerebellar hemisphere and vermis Medulloblastoma
Ependymoma
Pilocytic Astrocytoma
Hemangioblastoma
Atypical teratoid/rhabdoid tumor
Metastasis
Dysplastic Cerebellar Gangliocytoma
Rare tumors (Glioblastoma multiforme,
Gliosarcoma)
Brainstem and cervicomedullary junction Brainstem Gliomas
Primitive Neuroectodermal Tumor (PNET)
Rare tumors (Ganglioglioma)
Location Tumors
Cerebellopontine angle and internal auditory canal Vestibular Schwannoma
Meningiomas
Epidermoid and dermoid
Facial nerve schwannomas
Metastatic disease
Primary exophytic parenchymal neoplasms
Arachnoid Cyst
Rare (endolymphatic sac tumor, lipoma,
chordoma, melanocytoma, paraganglioma)
Fourth Ventricle Medulloblastoma
Ependymoma
Epidermoid
Choroid plexus papillomas
Subependymoma
Posterior Fossa and skull base Paraganglioma
Meningioma
Schwannoma
CEREBELLAR HEMISPHERE AND VERMIS
MEDULLOBLASTOMA
 Malignant primitive neuroectodermal tumor.
 Midline tumors
 Most common site: Vermis and Inferior medullary velum.
 Less common: Cerebellar hemisphere(Older patients)
 Most common malignant posterior fossa tumor in children(one-thirds of childhood
pediatric tumors).
 Age group: 5-15 years.
 Clinical presentation: With features of raised intracranial pressure.
 CSF seeding and Leptomeningeal metastatic spread +.
Histologically Defined Medulloblastomas:
 Classic medulloblastoma and
 Medulloblastoma histopathologic variants:
(1) Desmoplastic/nodular medulloblastoma.
(2) Medulloblastoma with extensive nodularity.
(3) Large cell/anaplastic medulloblastoma.
Genetically Defined Medulloblastomas
• WNT-activated medulloblastoma
• SHH-activated medulloblastomas
○ TP53 mutant
○ TP53 wild-type
• Non-WNT/non-SHH medulloblastomas
○ Group 3 medulloblastoma
○ Group 4 medulloblastoma
IMAGING FEATURES
 Well-circumscribed midline mass filling the fourth ventricle.
 Midline extension through the foramen of magendie into the cisterna magna may
occur.
 Lateral extension is uncommon.
 Peritumoral edema.
 Obstructive hydrocephalus with periventricular accumulation of CSF(Best delineated
on FLAIR.)
 Calcification + (in 20%).
 Cystic and necrotic degeneration common in adult MBs.
IMAGING FEATURES
CT
• Isodense or moderately hyperdense.
• Strong but heterogeneous
enhancement on CECT.
MRI
• Isointense or hypointense on T1WIs and
T2WIs.
• Signal heterogeneity on T2-WI due to
cysts, hemorrhage, necrosis and clump-like
calcifications.
• Moderate enhancement.
• High signal intensity on DWI.
• Low ADC.
Proton MR spectroscopy: Show taurine,
detectable at short echo time, and a massive
choline peak.
EPENDYMOMA
 Age group: 1-5 years.
 Arise from differentiated ependymal cells lining the fourth ventricle and foramina of
Luschka.
 Can present within the cerebellopontine angle.
Clinical features:
 Fill and distend the fourth ventricle, resulting in hydrocephalus and symptoms of nausea and
vomiting.
 Insinuate around and within structures, encasing vessels and lower cranial nerve --> Cause
cranial neuropathies.
EPENDYMOMA
4 types:
 Ependymoma (grade 2)
 Anaplastic ependymoma (grade 3)(Greater incidence of CSF dissemination at the time
of diagnosis and a poorer prognosis)
 Subependymoma (grade 1), and
 Myxopapillary ependymoma(grade 1).
IMAGING
CT: Irregular and lobulated isodense masses with calcification (up to 45%).
MRI:
 Heterogeneous with T1 hypointensity.
 T2 iso/hyperintensity and heterogeneous enhancement.
 Demonstrate intratumoral microcysts, necrosis or hemorrhage.
 Peritumoral edema usually absent.
 Following contrast administration: Inhomogeneous enhancement +. Rarely,
ependymomas do not enhance.
 CSF seeding is found in small percentage of the cases, less frequent than PNET.
Typical feature:
 Extension through the foramina of Luschka into the cerebellopontine angle (15%)
and/or
 Inferiorly through the foramen of Magendie (60%) onto the posterior aspect of the
upper cervical cord.
 MB: More bulbous extension rather than thin tongues of tissue through the foramina
as in ependymomas.
Proton MR spectroscopy:
 Elevated choline
 Reduced N-acetylaspartate (NAA)
IMAGING
SUBEPENDYMOMA
 Biologically benign, slow-growing intraventricular tumors.
 Origin: Astrocytes and ependymal cells.
 Mean age ~ 50 years.
Location:
 Fourth ventricle(floor)- MC
 Lateral ventricle(attached to the septum pellucidum)
 Third ventricle and even in the spinal cord.(Rare)
 Rarely produce symptoms.
 Hydrocephalus is the most common presentation.
SUBEPENDYMOMA
CT:
 Fourth ventricular subependymomas:
 Variable density compared to gray matter with calcifications(50-100%) and
enhancement.
 Lateral ventricle subependymomas:
 Vary in density.
 More often hypodense.
 Do not enhance and
 Calcifications in less than 10 percent.
SUBEPENDYMOMA
MRI:
 Fourth ventricular subependymomas:
 Origin from the floor of the fourth ventricle.
 Extension through the foramina of Luschka or Magendie.
 Hypointense or isointense to gray matter on T1.
 Isointense or hyperintense to gray matter on T2.
 Heterogeneous enhancement.
 Do not demonstrate paraventricular extension, unlike other ventricular tumors.
 PET using 18F-FDG : Hypometabolic tumor (Low cellular density and slow growth.)
PILOCYTIC ASTROCYTOMA
 Benign tumors of CNS (WHO Grade 1).
 Specific histologic type.
 Present in first two decades of life.
 Sites:
 Cerebellum(vermis or hemisphere)
 Hypothalamus
 Optic nerve optic chiasm.
 Brain stem
 Cerebral hemispheres.(Less common)
IMAGING
 Cystic mass with an enhancing mural nodule or a solid-cystic mass.
MRI:
 Variable and non-specific.
 Solid portion is hypointense on T1WI (higher than CSF intensity) and hyperintense on
T2WI.
 MR with contrast shows enhancement of the solid component.
 Absent accompanying edema or intratumoral calcification.
 Proton MR spectroscopy:Lactate peak.
ATYPICAL TERATOID/RHABDOID TUMOR
 Extremely rare.
 Highly malignant neoplasm of undetermined histogenesis.
 May arise at any site within the central nervous system.
 Non-specific features.
 Large lesions at presentation, with moderate- to- marked surrounding edema.
 CT:
 Solid(hyperdense) or mixed lesions.
 Areas of necrosis, cyst formation, hemorrhage and calcification may occur with
varying pattern of enhancement.
MR:
 Hypointense on T1WI and iso-hypo on T2WI with inhomogeneous enhancement.
 Meningeal enhancement and spinal tumor seeding common.
 Lower ADC values in MB and AT-RT compared with juvenile pilocytic astrocytomas
and ependymomas.
 Restricted diffusion + Not in the midline + CPA involvement: AT-RT > MB
HEMANGIOBLASTOMA
 Benign (WHO grade 1) tumor.
 Sporadic or manifestation of von Hipple-Lindau disease (VHL) in 25 percent.
Location
Cerebellum (83-86%)
Brain stem (2-5%)
Spinal cord (3- 13%)
Cerebrum (1.5%).
Other manifestations of VHL:
Retinal angioma
Renal cell carcinoma
Adrenal pheochromocytoma
Benign cysts in the lungs, liver, kidneys, and pancreas.
IMAGING
NCCT:
 Well marginated, cystic lesion(hypodense) with a mural nodule(isodense with the
brain parenchyma).
 Edema is usually absent.
 The mural nodule abuts the pial surface - Shows strong homogeneous contrast
enhancement.
 Solid hemangioblastomas - Hyperdense on NCCT with strong homogeneous
enhancement.
MRI:
 Cystic component of hemangioblastoma: Iso- or slightly hyperintense relative to CSF
on T1WI and hyperintense on T2WI.
 The nodule - Hypointense on T1WI and hyperintense on T2WI with intense
enhancement.
 DWI: Solid portions give low signal with increased ADC values.
 Extensive hypervascular tumor.
 Flow voids within and at the periphery of the tumor.
 Perfusion MR imaging : High rCBV ratios in these lesions (around 11)-
Significantly higher than metastases (around 5).
 Cerebral angiography: Dilated feeding arteries and a prolonged tumoral blush
corresponding to the solid portion.
 Main differential diagnosis –
 Pilocytic astrocytoma- Typically occurs in younger age group.
METASTASES
 Most common infratentorial intra-axial neoplasms in the adult population.
 Well-defined round masses.
 Nodular or ring enhancement (due to central necrosis).
 Multiple.
 Primary in adults: Lung and breast carcinoma > Melanoma > Renal cell carcinoma >
Thyroid carcinoma > Gastrointestinal malignancies.
CT: Typically hypodense.
MRI:
 Hypointense on T1WI and hyperintense on T2WI.
 Varying pattern of enhancement.
 Edema +
 Areas of hemorrhage and calcification - Variable signal on T2WI.
IMAGING
 Increased T1 signal intensity before contrast administration:
 Melanoma, kidney, lung, choriocarcinoma, and bowel (because of the presence of
mucin).
MR spectroscopy:
 Significantly elevated choline and very low NAA (may represent contamination from
adjacent tissues due to partial averaging).
 High lactate and lipids.
 The tissues surrounding the enhancing mass usually are normal by spectroscopy
(unlike high grade gliomas).
DYSPLASTIC CEREBELLAR GANGLIOCYTOMA(LHERMITTE-DUCLOS)
 Rare space occupying lesion of cerebellum.
Clinical presentation:
 Headache and hydrocephalus.
 Range in age from newborn to 74 years, with an average age of 34 years.
IMAGING
 Reflect the generally benign biologic behavior of these lesions.
NCCT:
 Hypodense
 May be isodense.
 Calcification +/-.
MRI:
 Cerebellar mass typically involving one hemisphere.
 Highly characteristic folial pattern (laminated, corduroy, lamellar, or striated).
 Do not enhance(Majority).
BRAINSTEM AND CERVICOMEDULLARY
JUNCTION
BRAINSTEM GLIOMAS
 Location: Pons(MC) and less frequently in the medulla.
 Clinical features:
 No sex predilection.
 Age group: 3-10 years.
 Multiple cranial nerve palsies, pyramidal tract signs, ataxia and nystagmus.
BRAINSTEM GLIOMAS
NCCT:
 Subtle enlargement or morphologic distortion of brainstem on CT.
 Contrast enhancement -patchy, irregular, homogeneous or absent.
 CPA cistern widening due to exophytic component producing extra-axial effect.
MR Imaging:
 Useful for diagnosis and localization of the tumor.
 Diffuse glioma: Poorly defined regions of low intensity on T1WI and high intensity
on T2WI.
 Intratumoral heterogeneity +/-.
BRAINSTEM GLIOMAS
 The basilar artery often engulfed by the anterior extension of the tumor.
 Contrast enhancement + in one-half of the cases - Often focal and nodular.
 Focal brainstem gliomas : Well circumscribed/ sometimes markedly exophytic.
 Dorsally exophytic lesions are grossly multicystic and often enhance intensely.
Other subtypes of focal gliomas :
 Tectal plate and cervicomedullary glioma.
CEREBELLOPONTINE ANGLE AND INTERNAL
AUDITORY CANAL
CPA TUMORS
 Frequent and represent 6–10 percent of all intracranial tumors.
 Most common: Vestibular schwannomas and meningiomas(~ 85–90 percent of all
CPA tumors.)
VESTIBULAR SCHWANNOMAS
 Benign and slow growing.
 NF-2 - Bilateral CN VIII schwannomas.
 Malignant degeneration – Rare- Associated with NF-1.
 Arise from the inferior vestibular nerve within the internal auditory canal (IAC).
 Clinical feature: Hearing loss or tinnitus.
Can be:
 Entirely intracanalicular
 Intracanalicular and cisternal components(‘‘Ice-cream cone’’ tumor)
 Purely intracisternal.(Rare).
 Histologically:
 Antony type A tissue(Compact)- low T2 signal relative to CSF.
 Antony type B tissue(Loose textured).
 MRI:
 Larger lesions:
 Heterogeneous appearance(internal necrosis/cyst formation).
 Higher signal intensity than CSF(Hemorrhagic byproducts, necrotic material, or
colloid-rich fluid).
 Predominance of Antoni Type B cells.
 Associated Extramural(arachnoid) cysts +.
 IAC involvement:
 Flaring of the porous acousticus.
 Expansion of the IAC.
 Acute angle with the dura.
 Low T2 signal intensity in vestibule.
 (Larger lesions)
 Small lesions - Homogeneous enhancement.
 Larger lesions:
 Heterogeneous enhancement(cystic spaces).
 Degeneration of the vestibular nucleus.
 Extent into the cochlea and “dural tails” of enhancement.
 After surgery, linear or somewhat nodular enhancement in the IAC may be seen.
MENINGIOMAS
 Second most common CPA tumor.
 Extra-axial neoplastic lesion.
 10 percent of all intracranial meningiomas arise in the posterior fossa.
 Origin: Arachnoidal cap cells.
 Arise from the posterior petrous surface or the underside of the tentorium.
 Intense enhancement is the rule.
 Relative T2 hyposignal - Characteristic of most of the lesions(especially transitional
and fibroblastic varieties)
IMAGING
NCCT:
 Hyperdense with focal areas of calcification.
 Dural tail(not pathognomonic)
 Bony reaction
 Obtuse angle with the dura.
 Center of the lesion located away from the IAC.
 Necrosis and cystic degeneration uncommon.
 May originate within the internal auditory canal, or even within the labyrinth.
Differentiate from schwannoma
EPIDERMOID AND DERMOID
 Congenital/ developmental masses.
 Arises from ectodermal heterotopia.
 Both cysts are lined with stratified squamous epithelium.
 Dermoids: Additional mesodermal elements such as hair, sebaceous and sweat glands
+.
EPIDERMOID CYST
 More common.
 Become quite large before becoming symptomatic.
 Extension into the middle cranial fossa results in a dumb-bell shape.
 Spread along the basal surfaces.
 Location: CPA > Parasellar region.
CT:
 CSF density and do not enhance.
 Calcification +
 Can have a faintly enhancing border.
EPIDERMOID CYST
MRI:
 Isointense to CSF on both T1 and T2WI.(Cholesterol in solid/crystalline state).
 The adamantinomatous craniopharyngioma typically contains cholesterol in liquid
state.
 Lamellated appearance because of surface desquamation.
 Do not enhance(Minimal rim enhancement occurs in approximately 25 percent of
cases.)
 Malignant transformation of an epidermoid (squamous cell carcinoma) is rare -
Considered if follow-up scans show significant increase in the amount of
enhancement.
 ‘‘White epidermoid’’ : Hyperintense on T1WI, and hypointense on T2WI
 High protein content, hemorrhage or the presence of saponified keratinized debris
or cholesterol in the liquid state.
 DD’s:
 Dermoid
 Lipoma.
Chemical shift artifact absent.
Fat saturation pulse sequence will not suppress the high signal in
epidermoid.
E
P
I
D
E
R
M
O
I
D
 Arachnoid cysts
Lamellate appearance.
Insinuate rather than displace.
On FLAIR: Mixed iso- to hypersignal intensities, but with poor
demarcation.
DWI: Hyperintense due to restricted diffusion (low ADC)
Useful for detecting postoperative residual epidermoid.
E
P
I
D
E
R
M
O
I
D
DERMOID CYST
 Extremely rare.
 Midline lesions.
 Locations: Parasellar, Frontobasal region or posterior fossa (vermis or fourth
ventricle).
 CT: Fat density
 Do not enhance on contrast administration.
 Associated with bone defect in nasofrontal or occipital region- Dermal sinus tract.
 MRI:
 Unruptured cysts – Hyperintense.
 Heterogeneous signal intensity on T2WI(hypo- to hyperintense.)
 Chemical shift artifact +
 DD: Lipoma
 Rupture of the cyst --> Chemical meningitis.
 Fat-like leptomeningeal and intraventricular deposits.
Less lobulated than lipomas.
Displace blood vessels and neural structures(encasement in
lipomas.)
D
E
R
M
O
I
D
ARACHNOID CYSTS
 Congenital, benign, intra-arachnoid pouchlike lesions filled with normal CSF.
 Origin : Uncertain.
 Usually supratentorial(70 percent in the temporal fossa, mostly on the left
side,anterior to the temporal poles.)
 10 percent in the posterior fossa(CPA).
Clinical presentation:
 Mostly: Asymptomatic and incidental finding.
 Compromise of cranial nerve functions.
 Spontaneous or traumatic intracystic hemorrhage.
IMAGING
 Attenuation and signal intensities of uncomplicated arachnoid cysts exactly match
those of CSF on all sequences.
 No enhancement.
 DD: Epidermoid cyst.
Complete suppression of signal intensity on FLAIR sequence.
DWI: Lack of diffusion restriction.
ARACHNOID
CYST
FACIAL NERVE SCHWANNOMAS
 Arise anywhere along the course of the nerve from the CPA to the stylomastoid
foramen.
 Arising in the IAC or CPA – Difficult to differentiate from vestibular schwannoma.
Enhancing component extending along the labyrinthine
segment of the facial nerve to the geniculate ganglion.
FACIAL NERVE
SCHWANNOMA
CEREBELLOPONTINE ANGLE/INTERNAL AUDITORY
CANAL LIPOMAS
 Rare lesions.
 Mesodermal inclusions.
 MRI: T1 hyperintense.
 DD: Hemorrhagic masses.
METASTATIC DISEASE
 Leptomeningeal(Diffuse, nodular or mass-like) OR
 Parenchymal (brainstem, cerebellum).
 Breast and lung primaries predominate.
PRIMARY PARENCHYMAL NEOPLASMS
 Infiltrative intraaxial component with an exophytic component resulting in a CPA
mass.
 Childhood neoplasms - MB, astrocytoma(MC), and ependymoma.
ENDOLYMPHATIC SAC TUMOR
 Papillary adenomatous tumors.
 Origin: Endolymphatic sac(Distal portion of the vestibular aqueduct of the petrous
bone.)
 Sporadic
 Frequent in von Hippel–Lindau disease.
 Hypervascular tumor.
CT:
 Destruction of retrolabyrinthine petrous bone.
 Geographic or moth-eaten margins.
 Intratumoral spiculated or reticulated bone.
ENDOLYMPHATIC SAC TUMOR
MRI:
 Heterogeneous on both T1 and T2WIs.
 Focal high signal intensity due to subacute hemorrhages.
 Low signal intensity due to calcification or hemosiderin.
 Blood-filled cysts and protein-filled cysts - Hyperintense on T1 and T2WIs.
 Heterogeneous enhancement.
 Flow voids within and around(> 2 cm in diameter) - Hypervascular.
PARAGANGLIOMA
Extension of paragangliomas arising at :
 Jugular foramen (glomus jugulare tumor) or
 Middle ear (glomus tympanicum tumor)
 Benign, locally aggressive tumor
CT:
 Destroy the bones of the skull base with a moth-eaten erosion pattern.
 MRI:
 Highly vascular soft tissue lesions.
 Mix of multiple punctuate and serpentine signal voids
(High-flow intratumoral vessels)
 Foci of high-signal intensity
(Intratumoral hemorrhages with methemoglobin).
 Perfusion MR imaging:
 High vascularity patterns with high rCBV.
 Conventional angiography:Intense tumoral blush with enlarged feeding arteries.
Salt-and-pepper appearance
FOURTH VENTRICLE
CHOROID PLEXUS PAPILLOMA
 Origin: Choroid plexus epithelium.
 Most frequent in first year of life.
 Hydrocephalus.
 Common site of origin : Lateral ventricles.
 Commonest site of adult CPP: Fourth Ventricle
CHOROID PLEXUS PAPILLOMA
 Well-defined lobulated masses.
 Enlargement of the involved ventricles.
 Foci of small hemorrhages and calcification may be found.
 Anaplastic papillomas, frequently invade the brain – Difficult to differentiate from
carcinomas.
 Metastasis through CSF pathways is common for both anaplastic papillomas and
carcinomas.
CHOROID PLEXUS PAPILLOMA
NCCT: Typically isodense to hyperdense with occasional foci of calcification.
 Homogenous enhancement is seen following intravenous contrast.
 Anaplastic CPP:
 Invade the ependyma and grow into the surrounding white matter, producing
vasogenic edema.
 Irregular in outline and closely resemble CPC.
 Hydrocephalus.
CHOROID PLEXUS PAPILLOMA
MRI:
 Either homogeneous or heterogeneous cauliflower-like tumors.
 Iso/hypointense on T1 and T2WI and strongly enhance after contrast injection.(Unless
highly calcified).
 Areas of low signal intensity(Calcifications).
 Foci of high signal intensity(Intratumoral hemorrhage).
 Flow voids(high flow vessels).
CHOROID PLEXUS CARCINOMA
 More aggressive than papillomas.
 Irregular in contour.
NCCT:
 Mixed density on pre-contrast study.
 Variable enhancement.
 Cysts and hemorrhage is frequent.
 Grow through the ventricular wall into the brain with associated edema.
Posterior fossa tumor
Location
Cerebellar hemispheres Brainstem Fourth ventricle Foramen of Luschka/CPA
What is
the ADC
What is
the ADC
What is
the ADC
Low ADC High ADC Low ADC High/Intermediate ADC Low ADC
Almost
extraaxial
Extra-axial +/-
multiple enhancing
nodules
Medulloblastoma
SHH
Desmoplastic
Medulloblastoma
SHH
Solid and
/or cystic
areas
Pilocytic
astrocytoma
Not
enhancing
<3 years
Multiple
enhancing
nodules
Enhancing
>3 years
Cystic/Hemorrhagic
/Calcific areas
Age < 3
years
Group 4 MB
or AT-RT
Desmoplastic
Medulloblastoma
SHH
Medulloblastoma
all the subgroups
Ependymoma AT-RT
Medulloblastoma
WNT
Yes No
REFERENCES
 AIIMS-MAMC-PGI IMAGING COURSE SERIES DIAGNOSTIC RADIOLOGY Neuroradiology Including
Head and Neck Imaging.
 OSBORN’S BRAIN IMAGING, PATHOLOGY, AND ANATOMY, SECOND EDITION.
THANK YOU

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IMAGING OF INFRATENTORIAL BRAIN TUMORS.pptx

  • 2. ANATOMY OF POSTERIOR CRANIAL FOSSA Posterior Fossa Medulla Pons Cerebellar hemispheres Vermis CSF containing spaces Postero- laterally
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  • 14. INFRATENTORIAL TUMORS  Common in children.  In children:  Cerebellar astrocytoma (1/3rd) and Medulloblastoma(1/3rd) > Brain stem gliomas(1/4th) > Ependymoma(1/8th)  Adults:  Mostly extra-axial.  Schwannoma> Meningioma > Epidermoid.  Intra-axial neoplasm: Metastasis>Hemangioblastoma>Glioma
  • 15. IMAGING  Primary imaging modality : Magnetic resonance imaging (MRI).  Superior delineation of the extent of tumor.  Computed tomography: Better demonstration of small or subtle calcifications within tumors.
  • 16.  Determine whether the mass is intra-axial or extra-axial in location.  Features suggesting that the mass is extra-axial include: Bone and meninges • Dural tail sign. • Erosion, invasion or destruction of adjacent bone. • Hyperostosis. Brain parenchyma • Absence of claw sign. • Intervening cortex between mass and white matter. Subarachnoid space: • CSF cleft sign. • Widening of adjacent subarachnoid space/cistern. • Intervening pial arteries/veins.
  • 17. CLASSIFICATION OF INFRATENTORIAL TUMORS Location Tumors Cerebellar hemisphere and vermis Medulloblastoma Ependymoma Pilocytic Astrocytoma Hemangioblastoma Atypical teratoid/rhabdoid tumor Metastasis Dysplastic Cerebellar Gangliocytoma Rare tumors (Glioblastoma multiforme, Gliosarcoma) Brainstem and cervicomedullary junction Brainstem Gliomas Primitive Neuroectodermal Tumor (PNET) Rare tumors (Ganglioglioma)
  • 18. Location Tumors Cerebellopontine angle and internal auditory canal Vestibular Schwannoma Meningiomas Epidermoid and dermoid Facial nerve schwannomas Metastatic disease Primary exophytic parenchymal neoplasms Arachnoid Cyst Rare (endolymphatic sac tumor, lipoma, chordoma, melanocytoma, paraganglioma) Fourth Ventricle Medulloblastoma Ependymoma Epidermoid Choroid plexus papillomas Subependymoma Posterior Fossa and skull base Paraganglioma Meningioma Schwannoma
  • 20. MEDULLOBLASTOMA  Malignant primitive neuroectodermal tumor.  Midline tumors  Most common site: Vermis and Inferior medullary velum.  Less common: Cerebellar hemisphere(Older patients)  Most common malignant posterior fossa tumor in children(one-thirds of childhood pediatric tumors).  Age group: 5-15 years.  Clinical presentation: With features of raised intracranial pressure.  CSF seeding and Leptomeningeal metastatic spread +.
  • 21. Histologically Defined Medulloblastomas:  Classic medulloblastoma and  Medulloblastoma histopathologic variants: (1) Desmoplastic/nodular medulloblastoma. (2) Medulloblastoma with extensive nodularity. (3) Large cell/anaplastic medulloblastoma. Genetically Defined Medulloblastomas • WNT-activated medulloblastoma • SHH-activated medulloblastomas ○ TP53 mutant ○ TP53 wild-type • Non-WNT/non-SHH medulloblastomas ○ Group 3 medulloblastoma ○ Group 4 medulloblastoma
  • 22. IMAGING FEATURES  Well-circumscribed midline mass filling the fourth ventricle.  Midline extension through the foramen of magendie into the cisterna magna may occur.  Lateral extension is uncommon.  Peritumoral edema.  Obstructive hydrocephalus with periventricular accumulation of CSF(Best delineated on FLAIR.)  Calcification + (in 20%).  Cystic and necrotic degeneration common in adult MBs.
  • 23. IMAGING FEATURES CT • Isodense or moderately hyperdense. • Strong but heterogeneous enhancement on CECT. MRI • Isointense or hypointense on T1WIs and T2WIs. • Signal heterogeneity on T2-WI due to cysts, hemorrhage, necrosis and clump-like calcifications. • Moderate enhancement. • High signal intensity on DWI. • Low ADC. Proton MR spectroscopy: Show taurine, detectable at short echo time, and a massive choline peak.
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  • 32. EPENDYMOMA  Age group: 1-5 years.  Arise from differentiated ependymal cells lining the fourth ventricle and foramina of Luschka.  Can present within the cerebellopontine angle. Clinical features:  Fill and distend the fourth ventricle, resulting in hydrocephalus and symptoms of nausea and vomiting.  Insinuate around and within structures, encasing vessels and lower cranial nerve --> Cause cranial neuropathies.
  • 33. EPENDYMOMA 4 types:  Ependymoma (grade 2)  Anaplastic ependymoma (grade 3)(Greater incidence of CSF dissemination at the time of diagnosis and a poorer prognosis)  Subependymoma (grade 1), and  Myxopapillary ependymoma(grade 1).
  • 34. IMAGING CT: Irregular and lobulated isodense masses with calcification (up to 45%). MRI:  Heterogeneous with T1 hypointensity.  T2 iso/hyperintensity and heterogeneous enhancement.  Demonstrate intratumoral microcysts, necrosis or hemorrhage.  Peritumoral edema usually absent.  Following contrast administration: Inhomogeneous enhancement +. Rarely, ependymomas do not enhance.  CSF seeding is found in small percentage of the cases, less frequent than PNET.
  • 35. Typical feature:  Extension through the foramina of Luschka into the cerebellopontine angle (15%) and/or  Inferiorly through the foramen of Magendie (60%) onto the posterior aspect of the upper cervical cord.  MB: More bulbous extension rather than thin tongues of tissue through the foramina as in ependymomas. Proton MR spectroscopy:  Elevated choline  Reduced N-acetylaspartate (NAA) IMAGING
  • 36.
  • 37. SUBEPENDYMOMA  Biologically benign, slow-growing intraventricular tumors.  Origin: Astrocytes and ependymal cells.  Mean age ~ 50 years. Location:  Fourth ventricle(floor)- MC  Lateral ventricle(attached to the septum pellucidum)  Third ventricle and even in the spinal cord.(Rare)  Rarely produce symptoms.  Hydrocephalus is the most common presentation.
  • 38. SUBEPENDYMOMA CT:  Fourth ventricular subependymomas:  Variable density compared to gray matter with calcifications(50-100%) and enhancement.  Lateral ventricle subependymomas:  Vary in density.  More often hypodense.  Do not enhance and  Calcifications in less than 10 percent.
  • 39. SUBEPENDYMOMA MRI:  Fourth ventricular subependymomas:  Origin from the floor of the fourth ventricle.  Extension through the foramina of Luschka or Magendie.  Hypointense or isointense to gray matter on T1.  Isointense or hyperintense to gray matter on T2.  Heterogeneous enhancement.  Do not demonstrate paraventricular extension, unlike other ventricular tumors.  PET using 18F-FDG : Hypometabolic tumor (Low cellular density and slow growth.)
  • 40. PILOCYTIC ASTROCYTOMA  Benign tumors of CNS (WHO Grade 1).  Specific histologic type.  Present in first two decades of life.  Sites:  Cerebellum(vermis or hemisphere)  Hypothalamus  Optic nerve optic chiasm.  Brain stem  Cerebral hemispheres.(Less common)
  • 41. IMAGING  Cystic mass with an enhancing mural nodule or a solid-cystic mass. MRI:  Variable and non-specific.  Solid portion is hypointense on T1WI (higher than CSF intensity) and hyperintense on T2WI.  MR with contrast shows enhancement of the solid component.  Absent accompanying edema or intratumoral calcification.  Proton MR spectroscopy:Lactate peak.
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  • 44. ATYPICAL TERATOID/RHABDOID TUMOR  Extremely rare.  Highly malignant neoplasm of undetermined histogenesis.  May arise at any site within the central nervous system.  Non-specific features.  Large lesions at presentation, with moderate- to- marked surrounding edema.  CT:  Solid(hyperdense) or mixed lesions.  Areas of necrosis, cyst formation, hemorrhage and calcification may occur with varying pattern of enhancement.
  • 45.
  • 46. MR:  Hypointense on T1WI and iso-hypo on T2WI with inhomogeneous enhancement.  Meningeal enhancement and spinal tumor seeding common.  Lower ADC values in MB and AT-RT compared with juvenile pilocytic astrocytomas and ependymomas.  Restricted diffusion + Not in the midline + CPA involvement: AT-RT > MB
  • 47. HEMANGIOBLASTOMA  Benign (WHO grade 1) tumor.  Sporadic or manifestation of von Hipple-Lindau disease (VHL) in 25 percent. Location Cerebellum (83-86%) Brain stem (2-5%) Spinal cord (3- 13%) Cerebrum (1.5%). Other manifestations of VHL: Retinal angioma Renal cell carcinoma Adrenal pheochromocytoma Benign cysts in the lungs, liver, kidneys, and pancreas.
  • 48. IMAGING NCCT:  Well marginated, cystic lesion(hypodense) with a mural nodule(isodense with the brain parenchyma).  Edema is usually absent.  The mural nodule abuts the pial surface - Shows strong homogeneous contrast enhancement.  Solid hemangioblastomas - Hyperdense on NCCT with strong homogeneous enhancement.
  • 49. MRI:  Cystic component of hemangioblastoma: Iso- or slightly hyperintense relative to CSF on T1WI and hyperintense on T2WI.  The nodule - Hypointense on T1WI and hyperintense on T2WI with intense enhancement.  DWI: Solid portions give low signal with increased ADC values.  Extensive hypervascular tumor.  Flow voids within and at the periphery of the tumor.
  • 50.  Perfusion MR imaging : High rCBV ratios in these lesions (around 11)- Significantly higher than metastases (around 5).  Cerebral angiography: Dilated feeding arteries and a prolonged tumoral blush corresponding to the solid portion.  Main differential diagnosis –  Pilocytic astrocytoma- Typically occurs in younger age group.
  • 51.
  • 52. METASTASES  Most common infratentorial intra-axial neoplasms in the adult population.  Well-defined round masses.  Nodular or ring enhancement (due to central necrosis).  Multiple.  Primary in adults: Lung and breast carcinoma > Melanoma > Renal cell carcinoma > Thyroid carcinoma > Gastrointestinal malignancies.
  • 53. CT: Typically hypodense. MRI:  Hypointense on T1WI and hyperintense on T2WI.  Varying pattern of enhancement.  Edema +  Areas of hemorrhage and calcification - Variable signal on T2WI.
  • 54.
  • 55. IMAGING  Increased T1 signal intensity before contrast administration:  Melanoma, kidney, lung, choriocarcinoma, and bowel (because of the presence of mucin). MR spectroscopy:  Significantly elevated choline and very low NAA (may represent contamination from adjacent tissues due to partial averaging).  High lactate and lipids.  The tissues surrounding the enhancing mass usually are normal by spectroscopy (unlike high grade gliomas).
  • 56. DYSPLASTIC CEREBELLAR GANGLIOCYTOMA(LHERMITTE-DUCLOS)  Rare space occupying lesion of cerebellum. Clinical presentation:  Headache and hydrocephalus.  Range in age from newborn to 74 years, with an average age of 34 years.
  • 57. IMAGING  Reflect the generally benign biologic behavior of these lesions. NCCT:  Hypodense  May be isodense.  Calcification +/-. MRI:  Cerebellar mass typically involving one hemisphere.  Highly characteristic folial pattern (laminated, corduroy, lamellar, or striated).  Do not enhance(Majority).
  • 58.
  • 60. BRAINSTEM GLIOMAS  Location: Pons(MC) and less frequently in the medulla.  Clinical features:  No sex predilection.  Age group: 3-10 years.  Multiple cranial nerve palsies, pyramidal tract signs, ataxia and nystagmus.
  • 61. BRAINSTEM GLIOMAS NCCT:  Subtle enlargement or morphologic distortion of brainstem on CT.  Contrast enhancement -patchy, irregular, homogeneous or absent.  CPA cistern widening due to exophytic component producing extra-axial effect. MR Imaging:  Useful for diagnosis and localization of the tumor.  Diffuse glioma: Poorly defined regions of low intensity on T1WI and high intensity on T2WI.  Intratumoral heterogeneity +/-.
  • 62. BRAINSTEM GLIOMAS  The basilar artery often engulfed by the anterior extension of the tumor.  Contrast enhancement + in one-half of the cases - Often focal and nodular.  Focal brainstem gliomas : Well circumscribed/ sometimes markedly exophytic.  Dorsally exophytic lesions are grossly multicystic and often enhance intensely. Other subtypes of focal gliomas :  Tectal plate and cervicomedullary glioma.
  • 63.
  • 64.
  • 65.
  • 66.
  • 67. CEREBELLOPONTINE ANGLE AND INTERNAL AUDITORY CANAL
  • 68. CPA TUMORS  Frequent and represent 6–10 percent of all intracranial tumors.  Most common: Vestibular schwannomas and meningiomas(~ 85–90 percent of all CPA tumors.)
  • 69. VESTIBULAR SCHWANNOMAS  Benign and slow growing.  NF-2 - Bilateral CN VIII schwannomas.  Malignant degeneration – Rare- Associated with NF-1.  Arise from the inferior vestibular nerve within the internal auditory canal (IAC).  Clinical feature: Hearing loss or tinnitus. Can be:  Entirely intracanalicular  Intracanalicular and cisternal components(‘‘Ice-cream cone’’ tumor)  Purely intracisternal.(Rare).
  • 70.  Histologically:  Antony type A tissue(Compact)- low T2 signal relative to CSF.  Antony type B tissue(Loose textured).  MRI:  Larger lesions:  Heterogeneous appearance(internal necrosis/cyst formation).  Higher signal intensity than CSF(Hemorrhagic byproducts, necrotic material, or colloid-rich fluid).  Predominance of Antoni Type B cells.  Associated Extramural(arachnoid) cysts +.
  • 71.
  • 72.
  • 73.
  • 74.
  • 75.
  • 76.  IAC involvement:  Flaring of the porous acousticus.  Expansion of the IAC.  Acute angle with the dura.
  • 77.  Low T2 signal intensity in vestibule.  (Larger lesions)  Small lesions - Homogeneous enhancement.  Larger lesions:  Heterogeneous enhancement(cystic spaces).  Degeneration of the vestibular nucleus.  Extent into the cochlea and “dural tails” of enhancement.  After surgery, linear or somewhat nodular enhancement in the IAC may be seen.
  • 78. MENINGIOMAS  Second most common CPA tumor.  Extra-axial neoplastic lesion.  10 percent of all intracranial meningiomas arise in the posterior fossa.  Origin: Arachnoidal cap cells.  Arise from the posterior petrous surface or the underside of the tentorium.  Intense enhancement is the rule.  Relative T2 hyposignal - Characteristic of most of the lesions(especially transitional and fibroblastic varieties)
  • 79. IMAGING NCCT:  Hyperdense with focal areas of calcification.  Dural tail(not pathognomonic)  Bony reaction  Obtuse angle with the dura.  Center of the lesion located away from the IAC.  Necrosis and cystic degeneration uncommon.  May originate within the internal auditory canal, or even within the labyrinth. Differentiate from schwannoma
  • 80.
  • 81.
  • 82.
  • 83. EPIDERMOID AND DERMOID  Congenital/ developmental masses.  Arises from ectodermal heterotopia.  Both cysts are lined with stratified squamous epithelium.  Dermoids: Additional mesodermal elements such as hair, sebaceous and sweat glands +.
  • 84. EPIDERMOID CYST  More common.  Become quite large before becoming symptomatic.  Extension into the middle cranial fossa results in a dumb-bell shape.  Spread along the basal surfaces.  Location: CPA > Parasellar region. CT:  CSF density and do not enhance.  Calcification +  Can have a faintly enhancing border.
  • 85. EPIDERMOID CYST MRI:  Isointense to CSF on both T1 and T2WI.(Cholesterol in solid/crystalline state).  The adamantinomatous craniopharyngioma typically contains cholesterol in liquid state.  Lamellated appearance because of surface desquamation.  Do not enhance(Minimal rim enhancement occurs in approximately 25 percent of cases.)  Malignant transformation of an epidermoid (squamous cell carcinoma) is rare - Considered if follow-up scans show significant increase in the amount of enhancement.
  • 86.
  • 87.  ‘‘White epidermoid’’ : Hyperintense on T1WI, and hypointense on T2WI  High protein content, hemorrhage or the presence of saponified keratinized debris or cholesterol in the liquid state.  DD’s:  Dermoid  Lipoma. Chemical shift artifact absent. Fat saturation pulse sequence will not suppress the high signal in epidermoid. E P I D E R M O I D
  • 88.  Arachnoid cysts Lamellate appearance. Insinuate rather than displace. On FLAIR: Mixed iso- to hypersignal intensities, but with poor demarcation. DWI: Hyperintense due to restricted diffusion (low ADC) Useful for detecting postoperative residual epidermoid. E P I D E R M O I D
  • 89. DERMOID CYST  Extremely rare.  Midline lesions.  Locations: Parasellar, Frontobasal region or posterior fossa (vermis or fourth ventricle).  CT: Fat density  Do not enhance on contrast administration.  Associated with bone defect in nasofrontal or occipital region- Dermal sinus tract.
  • 90.  MRI:  Unruptured cysts – Hyperintense.  Heterogeneous signal intensity on T2WI(hypo- to hyperintense.)  Chemical shift artifact +  DD: Lipoma  Rupture of the cyst --> Chemical meningitis.  Fat-like leptomeningeal and intraventricular deposits. Less lobulated than lipomas. Displace blood vessels and neural structures(encasement in lipomas.) D E R M O I D
  • 91. ARACHNOID CYSTS  Congenital, benign, intra-arachnoid pouchlike lesions filled with normal CSF.  Origin : Uncertain.  Usually supratentorial(70 percent in the temporal fossa, mostly on the left side,anterior to the temporal poles.)  10 percent in the posterior fossa(CPA). Clinical presentation:  Mostly: Asymptomatic and incidental finding.  Compromise of cranial nerve functions.  Spontaneous or traumatic intracystic hemorrhage.
  • 92. IMAGING  Attenuation and signal intensities of uncomplicated arachnoid cysts exactly match those of CSF on all sequences.  No enhancement.  DD: Epidermoid cyst. Complete suppression of signal intensity on FLAIR sequence. DWI: Lack of diffusion restriction. ARACHNOID CYST
  • 93.
  • 94. FACIAL NERVE SCHWANNOMAS  Arise anywhere along the course of the nerve from the CPA to the stylomastoid foramen.  Arising in the IAC or CPA – Difficult to differentiate from vestibular schwannoma. Enhancing component extending along the labyrinthine segment of the facial nerve to the geniculate ganglion. FACIAL NERVE SCHWANNOMA
  • 95. CEREBELLOPONTINE ANGLE/INTERNAL AUDITORY CANAL LIPOMAS  Rare lesions.  Mesodermal inclusions.  MRI: T1 hyperintense.  DD: Hemorrhagic masses.
  • 96. METASTATIC DISEASE  Leptomeningeal(Diffuse, nodular or mass-like) OR  Parenchymal (brainstem, cerebellum).  Breast and lung primaries predominate.
  • 97. PRIMARY PARENCHYMAL NEOPLASMS  Infiltrative intraaxial component with an exophytic component resulting in a CPA mass.  Childhood neoplasms - MB, astrocytoma(MC), and ependymoma.
  • 98. ENDOLYMPHATIC SAC TUMOR  Papillary adenomatous tumors.  Origin: Endolymphatic sac(Distal portion of the vestibular aqueduct of the petrous bone.)  Sporadic  Frequent in von Hippel–Lindau disease.  Hypervascular tumor. CT:  Destruction of retrolabyrinthine petrous bone.  Geographic or moth-eaten margins.  Intratumoral spiculated or reticulated bone.
  • 99. ENDOLYMPHATIC SAC TUMOR MRI:  Heterogeneous on both T1 and T2WIs.  Focal high signal intensity due to subacute hemorrhages.  Low signal intensity due to calcification or hemosiderin.  Blood-filled cysts and protein-filled cysts - Hyperintense on T1 and T2WIs.  Heterogeneous enhancement.  Flow voids within and around(> 2 cm in diameter) - Hypervascular.
  • 100.
  • 101. PARAGANGLIOMA Extension of paragangliomas arising at :  Jugular foramen (glomus jugulare tumor) or  Middle ear (glomus tympanicum tumor)  Benign, locally aggressive tumor CT:  Destroy the bones of the skull base with a moth-eaten erosion pattern.
  • 102.  MRI:  Highly vascular soft tissue lesions.  Mix of multiple punctuate and serpentine signal voids (High-flow intratumoral vessels)  Foci of high-signal intensity (Intratumoral hemorrhages with methemoglobin).  Perfusion MR imaging:  High vascularity patterns with high rCBV.  Conventional angiography:Intense tumoral blush with enlarged feeding arteries. Salt-and-pepper appearance
  • 103.
  • 105. CHOROID PLEXUS PAPILLOMA  Origin: Choroid plexus epithelium.  Most frequent in first year of life.  Hydrocephalus.  Common site of origin : Lateral ventricles.  Commonest site of adult CPP: Fourth Ventricle
  • 106. CHOROID PLEXUS PAPILLOMA  Well-defined lobulated masses.  Enlargement of the involved ventricles.  Foci of small hemorrhages and calcification may be found.  Anaplastic papillomas, frequently invade the brain – Difficult to differentiate from carcinomas.  Metastasis through CSF pathways is common for both anaplastic papillomas and carcinomas.
  • 107. CHOROID PLEXUS PAPILLOMA NCCT: Typically isodense to hyperdense with occasional foci of calcification.  Homogenous enhancement is seen following intravenous contrast.  Anaplastic CPP:  Invade the ependyma and grow into the surrounding white matter, producing vasogenic edema.  Irregular in outline and closely resemble CPC.  Hydrocephalus.
  • 108. CHOROID PLEXUS PAPILLOMA MRI:  Either homogeneous or heterogeneous cauliflower-like tumors.  Iso/hypointense on T1 and T2WI and strongly enhance after contrast injection.(Unless highly calcified).  Areas of low signal intensity(Calcifications).  Foci of high signal intensity(Intratumoral hemorrhage).  Flow voids(high flow vessels).
  • 109.
  • 110. CHOROID PLEXUS CARCINOMA  More aggressive than papillomas.  Irregular in contour. NCCT:  Mixed density on pre-contrast study.  Variable enhancement.  Cysts and hemorrhage is frequent.  Grow through the ventricular wall into the brain with associated edema.
  • 111. Posterior fossa tumor Location Cerebellar hemispheres Brainstem Fourth ventricle Foramen of Luschka/CPA What is the ADC What is the ADC What is the ADC Low ADC High ADC Low ADC High/Intermediate ADC Low ADC Almost extraaxial Extra-axial +/- multiple enhancing nodules Medulloblastoma SHH Desmoplastic Medulloblastoma SHH Solid and /or cystic areas Pilocytic astrocytoma Not enhancing <3 years Multiple enhancing nodules Enhancing >3 years Cystic/Hemorrhagic /Calcific areas Age < 3 years Group 4 MB or AT-RT Desmoplastic Medulloblastoma SHH Medulloblastoma all the subgroups Ependymoma AT-RT Medulloblastoma WNT Yes No
  • 112. REFERENCES  AIIMS-MAMC-PGI IMAGING COURSE SERIES DIAGNOSTIC RADIOLOGY Neuroradiology Including Head and Neck Imaging.  OSBORN’S BRAIN IMAGING, PATHOLOGY, AND ANATOMY, SECOND EDITION.

Editor's Notes

  1. Largest and deepest of all the cranial fossae. Bowl-shaped, relatively protected space that lies below the tentorium Part of the cerebral aqueduct, the fourth ventricle, and CSF cisterns that surround the brainstem and cerebellum.
  2. Anterior wall: Dorsum sellae of the sphenoid body and clivus of the basioccipital bone. Lateral wall: Petrous temporal bone. Floor: Occipital squamae. Superiorly: Tentorium cerebelli. Communicates with : Supratentorial compartment via tentorial incisura. Cervical subarachnoid space through the ovoid foramen magnum.
  3. Anteriorly clivus Nuleus gracilis Cerebellar tonsil. Primary fissure of vermis lies along tentorial surface.
  4. Axial T2WI shows normal superior cerebellar peduncles,vermis, and horizontal fissures of the cerebellum.
  5. Three surfaces: Superior (tentorial). Inferior (suboccipital) Anterior (petrosal). Fissures: Horizontal fissure. Primary fissure. Prominent superficial landmarks: Cerebellar tonsils. The flocculus.
  6. Images through the upper PF show the vermis and superior surfaces of the cerebellar hemispheres lying behind the pons and midbrain, just inside the tentorial incisura. Slightly farther down, the superior cerebellar peduncles are seen as thin white matter bands lying along either side of the upper fourth ventricle. Axial T2WI shows normal superior cerebellar peduncles,vermis, and horizontal fissures of the cerebellum. Axial scan through the body of the fourth ventricle shows CSF-filled posterior superior recesses capping the tops of the cerebellar Tonsils. Dentate nuclei are mineralized an hypointense.
  7. More inferior scan through the bottom of the fourth ventricle shows the midline foramen of Magendie, latera recesses,tonsils , and floccular lobes of the cerebellum projecting into cerebellopontine angle cisterns. T2WI through the foramen magnum shows the medulla, cerebellar tonsils , and vallecula lying between the tonsils at the bottom of the cisterna magna.
  8. Coronal graphic shows brachium pontis (middle cerebellar peduncles) , vermis , flocculi, and tonsils projecting inferiorly from the biventral lobules. Coronal T2WI shows tonsils , foramina of Luschka , and horizontal fissures.The flocculi lie just in front of the horizontal fissure. Moving posteriorly, the rhomboid or diamond shape of the fourth ventricle can be appreciated. Thin caps of CSF, the posterior superior recesses, cover the tops of the cerebellar tonsils. Inferiorly, the fourth ventricle opens into the cisterna magna via the foramen of Magendie. The large middle cerebellar peduncles are seen along the sides of the fourth ventricle. More posteriorly, the vermis can be seen lying between the two hemispheres.
  9. More posterior coronal image shows foramen of Magendie, vermis, superior cerebellar peduncles and posterior superior recesses capping tonsils. More posterior T2WI shows the primary fissures, horizontal fissures, and midline vermis.
  10. Complex diamond-shaped space that runs along the dorsal pons and upper medulla. Anatomic landmarks: Fastigium. Foramen of Magendie.(Fourth ventricle to cisterna magna) Paired lateral recesses. Foramina of Luschka. Choroid plexus. Bulbous tufts of choroid plexus in the CPA cistern - "Bochdalek’s flower basket" Posterior superior recesses. Obex PF cisterns: Prepontine cistern. Cerebellopontine angle cistern Cisterna magna. The vallecula- Extends superiorly between the two cerebellar tonsils and is connected to the fourth ventricle via the foramen of Magendie.
  11. Thin rim of CSF between a tumor and brain parenchyma.  Buckling: White Matter projecting into gyri being compressed and displaced by the mass, even in the presence of edema. 
  12. Tumors can arise from the brain tissue itself, the cranial nerves, the meninges, or the skull or can be invaded by neoplasms and infections from the head and neck regions.
  13. Although much less common, the disease may also occur in adults, usually in the 3rd and 4th decades of life. Evaluate with contrast-enhanced MR imaging of the brain and the spine.
  14. All four MB subtypes have different origins, preferred anatomic locations, and demographics, as well as dramatically different prognosis and therapeutic implications. Classic medulloblastoma in the midline fourth ventricle with CSF spread. Medulloblastoma in the cerebellar peduncle/CPA cistern. This location is classic for WNT medulloblastoma. Medulloblastoma in the lateral cerebellar hemisphere. This is the classic location for desmoplastic medulloblastoma, SHH molecular subtype. Nonfocal, diffusely infiltrating medulloblastoma.Groups 3 and 4 can be diffusely infiltrating with no dominant mass. Group 4 MBs are sometimes characterized by exhibiting minimal or no enhancement on T1 C+ FS.
  15. Combination of high density on NCCT and low signal intensity on T2-WI is believed to be highly suggestive of MB and this may help to differentiate it from other posterior fossa tumors. If dense tentorial or falcine calcifications are present, the patient should be evaluated for basal cell nevus (Gorlin) syndrome.
  16. NCCT Brain showing ill defined iso to hypodense lesion near completely filling the fourth ventricle with a calcific foci within.
  17. Axial T1W image showing relatively well defined lesion almost completely filling the fourth ventricle, hypointense on T1WI and heterointense on T2 WI with few hyperintense areas within
  18. Hyperintense on T2-FLAIR with few flow voids within.
  19. DWI shows areas of diffusion restriction
  20. Postcontrast- Shows enhancement of the mass
  21. Midline vermian mass : Iso-hyperintense on T2WI (A) Iso-hypointense on T1WI (B). Hyperintense on DWI (C) and hypointense on ADC maps (D), suggesting restricted diffusion. Post gadolinium axial (E) and sagittal (F) T1WI show intense enhancement of the mass
  22. Medulloblastoma with leptomeningeal spread. Axial (A) and sagittal (B) T1WIs of brain reveal patchy enhancement within the mass and enhancement of the leptomeningeal deposits in bilateral CPA cistern and cerebellar sulci. Sagittal T1WI (C) of spine show diffuse leptomeningeal deposits in the spinal subarachnoid spaces
  23. Desmoplastic Medulloblastoma. Axial (A) and coronal T2WI (B) image show a iso-hyperintense cerebellar hemispheric mass with nodular morphology. The mass show mild enhancement following gadolinium administration (C)
  24. Common tumors in children. 60% of ependymomas are infratentorial. Can present within the cerebellopontine angle, presumably arising from the rests of ependymal cells.
  25. Ependymoma. Axial T1WI (A) and T2WI (B) show a heterogeneous mass filling the fourth ventricle. Post-gadolinium sagittal (C) and axial (D) T1WI demonstrate heterogeneous enhancement. The tumor is creeping anteriorly through foramen of Luschka into CPA cisterns and posteriorly through foramen of Magendie into upper cervical canal
  26. Clinical presentation: Waxing and waning headache. Cerebellar signs: Truncal ataxia, dysdidochokinesia. Excellent prognosis
  27. Hemorrhage is rare in the lesion.
  28. Pilocytic astrocytoma. NCCT (A) shows a cystic lesion in the vermis. A solid nodule of the tumor that is of lower attenuation than surrounding cerebellum is located within right lateral aspect of tumor. The cyst is hypointense on T1WI (B) and hyperintense on T2WI (C) and nodule shows intense enhancement after gadolinium administration (D)
  29. Welldefined left cerebellar mass, hypointense on T1WI (A), hyperintense on T2WI (B), compressing the fourth ventricle and without any associated edema. On gadolinium administration, mass shows heterogeneous enhancement (C, D).
  30. AT-RT. CECT demonstrate a mixed density lesion in the vermis. The solid part of the tumor is densely enhancing.
  31. Compared with sporadic cases of hemangioblastomas, the tumors in VHL disease develop at an earlier age and are often multifocal. Multiple hemangioblastomas occur in up to 20 percent of patients with VHL disease.
  32. Super-selective catheterization of the feeding vessels allows preoperative embolization of the tumor and can potentially decrease the morbidity and mortality of surgical resection.
  33. Hemangioblastoma. CECT at level of medulla (A) and pons (B) show a solid enhancing tumor in dorsal medulla and cyst with a mural nodule in the right cerebellar hemisphere
  34. However, even if solitary, the lesion is still more commonly metastasis than a primary intracranial neoplasm.
  35. Mid-brain metastasis. A 35-year-female with a known carcinoma breast. Sagittal T1WI reveals a heterogeneously enhancing lesion in the region of tectal plate
  36. Coexisting conditions: Holoprosencephaly Neurofibromatosis Cowden’s disease Multiple hamartoma syndrome.
  37. When the rare enhancing dysplastic cerebellar gangliocytoma is encountered, it is believed to be secondary to vascular proliferation or the presence of anomalous veins Alternating bands of high signal intensity and normal signal intensity relative to gray matter on T2WIs.
  38. Dysplastic cerebellar gangliocytoma. (A) Axial T2WI shows a cerebellar mass with a striped appearance, composed of alternating hyperintense and isointense bands associated with compression on the 4th ventricle (B) Contrast-enhanced axial T1WI shows no enhancement of the mass
  39. 10-20 percent of pediatric CNS tumors. 75 percent occur before the age of 20 years. Majority (85%) composed of high-grade fibrillary gliomas. Diffuse pontine gliomas have the worst prognosis
  40. Flattening of ventral aspect of fourth ventricle or reduction of the diameter of prepontine cistern.
  41. An undulating ventral border of the brainstem on sagittal image – Indirect clue to the presence of the mass lesion.
  42. Diffuse pontine glioma. Diffuse pontine glioma expands the pons, compresses the fourth ventricle, envelops basilar artery; and extends into right brachium pontis. The mass is hypodense on CECT (A), predominantly hyperintense on sagittal T2WI (B) except an isointense dorsal component and predominantly hypointense on axial T1WI (C). Post-contrast axial T1WI shows patchy enhancement in dorsal part of the mass.
  43. Dorsally exophytic brainstem glioma. Axial T1WI (A) shows a large tumor originating from posterolateral pons. The tumor is heterogeneous with cystic areas and shows heterogeneous enhancement (B)
  44. Tectal plate glioma. Axial flair (A) images show thickening and hyperintensity in the region of tectal plate, compressing the aqueduct and causing proximal hydrocephalus. No enhancement is seen following gadolinium administration (B)
  45. Cervicomedullary glioma. Axial (A) and sagittal T2WI (B) images show an expansile well-defined mass lesion involving medulla and upper cervical spinal cord
  46. Intracisternal - Reach a larger size before presenting with mass effect on the cerebellar hemispheres and fourth ventricle rather than hearing loss
  47. Associated Extramural(arachnoid) cysts - secondary to elevation and deformation of the leptomeninges, which results in the formation of peritumoral adhesions, thereby creating a pseudoduplication of the arachnoid, trapping fluid between the leptomeninges and the mass.
  48. A T1 hypointense, T2 heterogeneously hyperintense lesion noted in the left cerebellopontine angle and internal auditory canal, not showing diffusion restriction. Few blooming foci noted within the lesion on gradient sequence. On post contrast study the lesion shows moderate heterogenous enhancement.
  49. A T1 hypointense, T2 heterogeneously hyperintense lesion noted in the left cerebellopontine angle and internal auditory canal, not showing diffusion restriction. Few blooming foci noted within the lesion on gradient sequence. On post contrast study the lesion shows moderate heterogenous enhancement.
  50. A T1 hypointense, T2 heterogeneously hyperintense lesion noted in the left cerebellopontine angle and internal auditory canal, not showing diffusion restriction. Few blooming foci noted within the lesion on gradient sequence. On post contrast study the lesion shows moderate heterogenous enhancement.
  51. Schwannomas. A patient of neurofibromatosis 2 with bilateral acoustic schwannomas and right facial nerve schwannoma in region of geniculate ganglion. These lesions are isointense on T2WI (A) and show homogenous enhancement on contrast administration (B)
  52. Vestibular Schwannoma. MR imaging shows a well-defined extra-axial mass in right CPA with extension into right IAC. The mass is iso-hypointense on T1WI (A), iso-hyperintense on T2WI (B, D) and have foci of magnetic susceptibility on SWI images (C) suggesting hemorrhagic products. Following contrast administration, heterogenous enhancement is seen (E, F)
  53. Low T2 signal intensity in vestibule , presumably due to increased protein concentration in the perilymph (but not in patients who have CPA meningioma). - Tiny area of hyperintensity in the dorsal brain stem on T2WIs at the lateral angle of the fourth ventricle floor. Linear enhancement does not indicate tumor. Nodular enhancement - Suspect for tumor.(Needs to be followed with MRI(yearly)- disappear in most patients.) Degen of vest nucleus shud not be confused with infarction. Post stereotactic radiation- shrink very slowly - Enhance less and develop central areas of presumed necrosis or cystic changes. The retrosigmoid approach has the greatest risk of unintentional residual tumor in the lateral (fundal) aspect of the IAC, and this area should be searched carefully with postoperative scans.
  54. A well defined T1 hypointense and T2/FLAIR hetero-intense dural based extra axial lesion showing few blooming foci ( likely representing calcifications) and no significant diffusion restriction noted in right cerebello-pontine angle, the lesion is seen causing compression of right middle cerebellar peduncle, medially abutting right trigeminal nerve at its origin however no signal intensity changes seen, laterally it is seen extending upto porus acusticus with signal intensity changes involving right facial and vestibulocochlear nerve –Likely due to mass effect.
  55. moderate homogenous enhancement
  56. No significant diffusion restriction
  57. Strong tendency to grow along paths of least resistanceand, as such, conform to the surface of the brain
  58. Grow very slowly via desquamation and therefore often do not present until adulthood. Tend to surround (encase) normal vascular structures rather than displace or invade them.
  59. Epidermoid. MR scans show an extra-axial right CPA mass which is hypointense on T1WI (A) and hyperintense on T2WI (B). The mass has little internal heterogeneity on FLAIR images (C); bright on DWI (D) and dark on ADC images (E). No enhancement is seen following gad administration (F)
  60. On FLAIR: Mixed iso- to hypersignal intensities, but with poor demarcation, while the signal of the arachnoid cyst is suppressed, like the signal of CSF.
  61. CT is essential for detection of the calvarial defect, while MR delineates the tumor better. Unruptured cysts - Hyperintense, similar to fat on T1WIs.
  62. They could result from a splitting of the embryonic meninges. Can compromise cranial nerve functions in the posterior fossa by stretching them.
  63. Arachnoid cyst. Axial T2WI show a well-defined extra-axial cyst in superior cerebellar cistern which is isointense to the CSF on T1WI (A), T2WI (B) and Flair (C). The lesion is dark on DWI (D) suggesting increased diffusion
  64. T1 hypersignal is characteristic as it is for fatty structures elsewhere.
  65. Endolymphatic sac tumor. Axial CT scan (A) shows a well-defined retrolabyrinthine mass in right petrous bone with intratumoral bony spicules. The mass is heterogeneously hyperintense in fat-saturated T1WI (B) and T2WI (C) and show heterogeneous enhancement (D)
  66. Conventional angiography:Intense tumoral blush with enlarged feeding arteries, which may allow hemostatic embolization prior to surgical resection, though it is rarely used as a primary diagnostic modality
  67. Paraganglioma. Large posterior fossa skull base mass lesion destroying the right petrous apex and extending into right CPA cistern. The mass is heterogeneously hypointense on T1WI (A), hyperintense on T2WI with intratumoral flow-voids. Following gadolinium administration, intense enhancement is seen within the mass (C, D)
  68. Rare in third and fourth ventricles are rarely involved in children.
  69. Bilateral papillomas are rare. Hydrocephalus: CSF hypersecretion by the tumor, but also by fourth ventricle obstruction when the tumor is located in the posterior fossa
  70. Choroid plexus papilloma. Axial (A) and reformatted sagittal (B) NCCT scan images show a partially calcified mass in the inferior fourth ventricle
  71. 30 percent to 40 percent of choroid plexus tumors First 5 years of life. Clinical presentation: Focal neurologic deficit from adjacent brain invasion. Male predominance.