Intracranial neoplasm by Dr. Fathmath Sudhuffa Ibrahim

1. 1
INTRACRANIAL NEOPLASM
Dr.Fathmath Shudhfa Ibrahim
MD Radiodaignosis
2nd year resident
NAMS, BIR HOSPITAL

2. Age
Location
Local tumour spread
Solitary or multifocal
Specific imaging characteristics
Tumour mimics

5.  Intra- vs. extra-axial- determine whether the mass
arises from within the brain parenchyma
(intraaxial) or from outside the brain parenchyma
(extra-axial)
 Supra- vs. infra-tentorial
 White matter vs. cortical based
 Specific anatomic sites:
 Sella/suprasellar
 Pineal region
 Intraventricular

6. EXTRAAXIAL
TUMOR
 TheT2Wimagesshowaschwannomalocatedinthecerebellopontineangle
(CPA).
 ThereisaCSFcleft(yellowarrow).
 Thesubarachnoidvesselsthatrunonthesurfaceofthebrainaredisplacedbythe
lesion(bluearrow).
 Thereisgraymatterbetweenthelesionandthewhitematter(curvedredarrow).
 Thesubarachnoidspaceiswidenedbecausegrowthofanextraaxiallesiontends
topushawaythebrain.
 IntheregionoftheCPA90%oftheextraaxialtumorsareschwannomas.

7. Intra-axial
Intra-axial is a term that
denotes lesions that are within
the brainparenchyma

8. INTRA-AXIAL EXTRA-AXIAL
Glioma
Medulloblastoma
Hemangioblastoma
Metastases
Infarction/hematoma
AVM
Abscess/inflammation
Meningioma
Pituatary adenoma
Craniopharyngioma
Schwannoma
Chordoma
Dermoid/epidermoid cyst
Lipoma
Metastases, hematoma,
infection

9. Common intra-axial CNS tumours in paediatric age group
Supratentorial:
• Astrocytoma
• Pleomorphic xanthoastrocytoma
• PNET
• DNET
• Ganglioglioma
Infratentorial:
• Juvenile pilocytic astrocytoma
• PNET (Medulloblastoma)
• Ependymoma
• Brainstem astrocytoma/glioma

10. Common intraaxial tumours
in adults
Supratentorial Infratentorial
Metastases Metastases
Gliomas Hemangioblastoma

11.  Most intra-axial tumours are white matter based
 Differential diagnosis for cortical based tumours:
neuroepithelial DNET (Dysembryoplastic
tumour)
 Ganglioglioma

12.  Glioblastomamultiforme (GBM) frequently crossesthe midline
byinfiltratingthewhitemattertractsofthecorpuscallosum.
 Radiation necrosis mimics GBM and can sometimes cross the
midline.
 Meningioma can spread along the meninges to the contralateral
side.
 Lymphomaisusuallylocatednearthemidline.
 Epidermoid cysts can cross the midlinevia the subarachnoid
space.
 MScanalsopresentasamasslesioninthecorpuscallosum.

14.  Astrocytomas spread along the white matter
tracts.
 Ependymomas of 4th ventricle in children tend to
extend through the foramen of Luschka to the CP
angle and through the foramen of Magendie to
the Cisterna Magna
 Oligodendroglioma typically show extention to
the cortex
 Medulloblastoma arising in the cerebellum tend
to extend to the upper cervical canal

15.  Primary brain tumors are derived from brain
cells and often have less mass effect for their
size than expected, due to their infiltrative
growth.
 Metastases and extra-axial tumors like
meningiomas or schwannomas, have more mass
effect due to their expansive growth

16.  Metastases and CNS lymphoma, often presenting with
multiple lesions, are rare in children
 Seeding metastases may be seen with PNET-MB
(Medulloblastoma) and ependymoma
 Multiple brain tumours may occur in phacomatoses:
 NF I: optic gliomas; astrocytomas
 NF II: meningiomas; ependymomas; choroid plexus papillomas
tubers; ependymomas; Tuberous sclerosis: subependymal
intraventricular giant cell astrocytomas
 Von Hipple Lindau: hemangioblastomas

17. Fat
Calcifi-
cation
Cystic
mass
vs. cyst
T1WI
signal
intensity
T2WI
signal
intensity
Contrast
enhance-
ment
Advanced
MRI

18.  Fat is characterised by low density on CT, high
signal on T1 and T2WI, with associated
chemical shift artefact
 Fat suppression sequences help distinguish
from other causes of high signal e.g. melanin,
hematoma and slow flow
 Masses containing fat include teratoma, lipoma
and dermoid cyst

20. Intra-axial:
• Astrocytoma-20%
• Oligodendroglioma-
90%
• Ependymoma 50%
• Choroid plexus
papilloma-25%
• Ganglioglioma-35%
Extra-axial:
• Meningioma 20-
25%
• Craniopharyngioma
-admantinomatous
90%

21. Cystic lesions that may
simulate tumours
include
• Epidermoid,
• Dermoid,
• Arachnoid,
• Neurenteric and
• Neuroglial cysts
To differentiate cystic
masses from cysts:
• Morphology
• Fluid/fluid level
• Content intensity
compared to CSF on
T1, T2 and FLAIR
sequences
• Restricted flow on
DWI

22.  Most tumors have a low or intermediate signal
intensity on T1WI.
 Exceptions to this rule can indicate a specific type
of tumor.

25.  Extra-axial tumours, pituitary, pineal and choroid
plexus tumours enhance (outside blood-brain
barrier)
 Contrast enhancement does not visualise full
extent of infiltrative tumours eg gliomas
 In gliomas, enhancement indicates higher degree
of malignancy
 Ganglioglioma and pilocytic astrocytomas are
exceptions, low grade tumours that enhance
vividly

26. No
enhancement:
• Low grade
astrocytoma
• Cystic non-
tumoral
lesions
Homogeneous
enhancement
• Germinoma
and other
pineal tumours
• Pituitary
adenoma
• Pilocytic
astrocytoma(s
olid
component)
and
haemangioblas
toma
• Ganglioglioma
• Meningioma,
schwannoma
Patchy
enhancement
• Radiation
necrosis
Ring
enhancement
• Metastasis
• Abscess
• Glioblastoma
• Infarction(su
bacute)
• Contusion
• Demyelinatin
g disease
• Radiation
necrosis/resol
ving
hematoma

28. HOMOGENOUS
ENHANCEMENT

29. PATCHY
ENHANCEMENT
 A large tumor with
limited mass effect.
 This indicates that
there is marked
infiltrative growth, a
characteristic typical
for gliomas.
 Notice the
heterogeneity on both
T2WI and FLAIR.
 There is patchy
enhancement.
 All these findings are
typical for a GBM.

30. WHO GRADING OF CNS TUMORS
WHO GRADE I : lesions with low proliferative potential, discrete nature,
possibility of cure following surgical resection
WHO GRADE II: Lesions show atypical cells that are infiltrating in nature
despite low mitotic activity, recur more frequently than grade I after local
therapy. Some tumors tends to progress to higher grades
WHO GRADE III: Lesions with histological evidence of malignancy, including
nuclear and increased mitotic activity. Lesions have anaplastic histology and
infiltrative capacity. Usually treated with adjuvant radiotherapy and/or
chemotherapy
WHO GRADE IV: Lesions that are mitotically active ,necrosis prone, associated
with neovascularity and infiltration of surrounding tissue and a propensity for
craniospinal dissemination and rapid postoperative progression and fatal
outcomes.
Lesions are treated with aggressive adjuvant therapy, typically stupp protocol
combined chemoradiotherapy.

31.  Most tumoursdo
show
of
not
significant
restriction
diffusion
 High signal on
DWI is seen with
abscesses,
epidermoid cysts
and acute
infarction

32. CT
 CT is often the first modality employed to investigate neurological signsor
symptoms, and often is the modality which detects an incidentallesion:
 non-contrast CT
70% slightly hyperdense to normal brain, the rest are moreisodense
20-30% have some calcification
 post-contrast CT
72% brightly and homogeneously contrast enhance
malignant or cystic variants demonstrate more
heterogeneity
 hyperostosis (5%)
 typical for meningiomas that abut the base of the skull
 need to distinguish reactive hyperostosis from:
 direct skull vault invasion by adjacent meningioma
 primary intraosseous meningioma
 enlargement of the paranasal sinuses (pneumosinus dilatans) has alsobeen
suggested to be associated with anterior cranial fossameningiomas

33. T2
T1
T1
isointense to grey matter (60-90%)
hypointense to grey matter (10-40%)
particularly fibrous, psammomatous variants
T1 C+ (Gd): usually intense and homogeneous
enhancement
T2
isointense to grey matter (~50%) 3,8,13
hyperintense to grey matter (35-40%)
usually correlates with soft textureand
hypervascular tumours
very hyperintense lesions may represent
the microcystic variant 12
hypointense to grey matter (10-15%): compared
to grey matter and usually correlates with harder
texture and more fibrous and calcified contents

34. A number of helpful imaging signs havebeen
described, including:
 CSF vascular cleft sign, which is not specific for
meningioma, but helps establish the mass to be extra-axial;
loss of this can be seen in grade II and grade III which may
suggest brain parenchyma invasion
 Dural tail seen in 60-72% (note that a dural tail is also seen
in other processes)
 Sunburst or spokewheel appearance of the vessels
 Arterial narrowing
 Typically seen in meningiomas which encase arteries
 Useful sign in parasellar tumours, in distinguishing a meningioma
from apituitary macroadenoma; the later typically does not narrow
vessels

35. The spoke wheel sign refers to the pattern of vessels coursing
through meningiomas, when seen in cross-section. It is the result
of the same phenomenon which results in the sunburst pattern
AXIALT1W
T1C+

36.  Epi:
 15% ofAstrocytomas
 YoungAdults
 Facts:
 Best diagnostic clue: Focal or
diffuse nonenhancing white
matter (WM) mass
 Location
 Cerebral hemispheres,
supratentorial 2/3
 Frontal lobes 1/3, temporal
lobes 1/3
 Relative sparing of occipital
lobes
 Infratentorial1/3
 Brainstem (50% of brain stem
"gliomas" are low-grade
astrocytoma)
 Occur in pons and medulla of
children/ adolescentsWidely
Infiltrate surrounding tissue
Cyst
T1 weighted T2 weighted
On Imaging:
CT: Well circumscribed, non enhancing,
hypodense or isodense lesion
MRI: MRI more sensitive than CT – useful
for identification and establishing extent
T1 image shows abnormal areas of
decreased signal
T2 image shows abnormal areas of
increased signal
Usually no enhancement

37. Lowgrade glioma
CT: Well circumscribed, non enhancing,
hypodense or isodense lesion

38. Anaplastic
astrocytoma (M)
•Hemispheric WM
lesion, usually non
enhancing
•Focal or diffuse
mass
•May be
indistinguishable
without biopsy
Ischemia
•Vascular territory
(MCA, ACA,
PCA), acute onset
•Diffusion
restriction
(acute/early
subacute)
•Often wedge-
shaped, involves
GM & WM
Cerebritis
• Edema, patchy
enhancement
characteristic
• Usually shows
restricted
diffusion
• Typically more
acute onset
Oligodendroglio
ma
• Cortically-based
mass with
variable
enhancement
• Ca++ common
• May be
indistinguishable

39. Most common of all primary intracranial neoplasms.
Location-
 Supratentorial white matter most common Frontal, temporal,
parietal lobes. Tumor may cross white matter tracts to involve
contralateral hemisphere like Corpus callosum (butterfly glioma).
May be multifocal, multicentric.
Presentation-
 Varies with location: Seizures, focal neurologic deficits common,
Increased intracranial pressure, mental changes.
Age:-
 Peak 45-70 years but may occur at any age.
 Patterns of dissemination-
 Most common: Along white matter tracts, perivascular
spaces.Less common: Ependymal/subpial spread, CSF
Metastases.

40.  On Imaging: Variable
CT
 Irregular thick margins: iso to slightly hyperattenuating
(high cellularity)
 Irregular hypodense centre representing necrosis
 Marked mass effect
 Surrounding vasogenic oedema
 Haemorrhage occasionally seen
 Calcification is uncommon
 Intense irregular, heterogeneous enhancement of the
margins is almost always present

41. Non contrast axial CT CECTAxial

42.  MRI
 T1
 hypo to isointense mass within white matter
 central heterogeneous signal (necrosis, intratumoural
haemorrhage)
 T1 C+ (Gd)
 enhancement is variable but is almost always present
 typically peripheral and irregular with nodular components
 usually surrounds necrosis
 T2/FLAIR
 hyperintense

43. •Axial T2WIMRshows
a heterogeneous hyperintense
mass with central necrosis and
surrounding signalabnormality
likely related to tumor extension
and edema. Typical imaging of
GBM.
•Axial T1C+MR
shows peripheral enhancement
with central necrosis and
extension across the splenium of
the corpus callosum,
characteristic of GBM.

44. •The �butterfly glioma� refers to a high grade astrocytoma,
usually a GBM,which crosses the midline via the corpus callosum.
•Most frequently this occurs in the frontal lobes

45. Differential diagnosis
 Abscess -Ring-enhancement typically thinner than GBM.T2
hypointense rim, diffusion restriction +typical.
 Metastasis -Typically multiple lesions at gray-white junctions.
Round> infiltrating lesion. Primary tumor often known
 Primary CNSlymphoma -Periventricular enhancing mass.Often
crosses corpus callosum. Typically isointense/hypointense on
T2W.Necrosis common in AIDSrelatedlymphoma.
 Anaplastic astrocytoma (AA)-Often nonenhancing white matter
mass. Enhancement may indicate degeneration to GBM.

46.  On Imaging:
 CT:
 Well circumscribed, hypodense lesions with
heavy calcification(70-90%)
 Cystic degeneration is common but hemorrhage
& edema are uncommon
 MRI:
 Hypointense or isointense on T1-weighted
images
 Hyperintense on T2-weighted images with
variable enhancement

48.  T2* GRE: Ca++ seen as areas of "blooming"
 DWI: No diffusion restriction is typical
 TI C+:Heterogeneous enhancement is typical. Approximately 50%enhance
Rarely, leptomeningeal enhancement is seen.
•Axial NECT shows a calcified
cortically-based frontal mass (arrow).
•Calcification is seen in the vast
majority of oligodendrogliomas,
typicallynodular or clumped..
Axial T2WI MR in the same case shows a
heterogeneously hyperintense cortically-
based mass with infiltration into the
subcortical white matter. Cystic change is
seen, but the Ca++is not visualized

49. 55 yr old male with h/o
seizures 1year and rt
sided paresis
CECT brain s/o
hetrogenously
enhancing calcified
mass with perilesional
edema in left
frontoparietal lobe s/o
oligodendroglioma

50. Ganglioglioma
•Cortically based
hemispheric mass,
solid/cystic or
solid
•Mural nodule typical,
often not adjacent to
meninges
•Variable enhancement,
no enhancing dural
"tail"
•Ca++ is common; may
Pilocytic astrocytoma
•Supratentorial location
other than
hypothalamus/chiasm
rare
• Typically solid and
cystic or solid mass
•Enhancement but no
dural "tail"
Dysembryoplastic
neuroepithelial
tumor
(DNET)
•Superficial cortical
tumor, well
demarcated
• Multicystic "bubbly"
,appearance

51.  Well differentiated, slowly growing neuroepithelial tumor
composed of neoplastic ganglion cells and neoplastic glial cells
 Most common cause of temporal lobe epilepsy (TLE).
Presentation
 Chronic temporal lobe epilepsy (approximately 90%)
 Often partial complex seizures
 Other signs/symptoms: Headache, signs of raised ICT.
Age
 Tumor of children, young adults.80% of patients < 30 yrs.
Location
 Can occur anywhere but most commonly superficial
hemispheres(temporal lobe).

52. General Features
 Best diagnostic clue: Partially cystic, enhancing,cortically-based
mass in child/young adult with TLE.
CTFindings
isodense 40% hypodense,30% mixed hypodense (cyst),
(nodule),15% isodense or hyperdense
 Ca++common, 35-50%
 Superficial lesions may expand cortex, remodel bone
 Approximately 50% enhance
 •Varies from moderate, uniform to heterogeneous.
MRFindings
 TIWI-Mass is hypo to isointense to gray matter.
 T2WI-Hyperintense, heterogeneous.
 TlC+:Variable enhancement, usually moderate

53. Axial FLAIRMRshows a cortically-
based hyperintense mass in theright
frontal lobe. Note the lack of edema
and mass effect.
Coronal T1 C+MRshows a temporal lobe
circumscribed cystic and solid mass with
intense enhancement of the muralnodule
(arrow). Long history of temporal lobe
epilepsy. Ganglioglioma.

54. (Left)AxialT2WIMRshows a hyperintense temporallobe
mass without significant edema or mass effect. Temporal lobe is the most
common location for ganglioglioma. Patient with temporal lobe epilepsy.
(Right) Axial T1 C+MRshows a cystic and solid temporal lobe mass with
marked enhancement of the solid portion, atypical
enhancement pattern ofganglioglioma.

55. Best diagnostic clue: Well-demarcated, wedge-shaped "bubbly"
intracortical mass in young patient with longstanding partial
seizures
 Temporal lobe (often amygdala/hippocampus) mst common site
 Parietal cortex, caudate nucleus, septum pellucidum also frequent sites
 Intracortical mass scallops inner table of skull and "points" towards
ventricle
Size
 Variable: Small (involving part of a gyrus)

56.  CT Findings
NCCT
 Wedge-shaped low density area -Cortical/subcortical lesion
 Extends towards ventricle in 30%
 Scalloped inner table in 44-60+%
 Calcification in 20-36%
 May resemble stroke on initial CT BUT no temporal evolution to atrophy
CECT
 Usually non enhancing
 Faint nodular or patchy enhancement in 20%
 Slightly higher risk of recurrence if enhancement
CTA:Avascular
MR Findings
 TlWI
 Pseudocystic, multinodular ("bubbly") mass
 Hypointense on Tl
 T2WI
Very hyperintense on T2
Multinodular or septated appearance well seen on T2WI

57. (A) hypointense onT1,
(B and C) Hyperintense on T2 and
FLAIR,
(D) No significant enhancement on
contrast imaging
A B
C D

58. 106
General characteristics
Solid, cystic, or combination
Classically described as globular/ exophytic
suprasellarmass CT
Low-density to isodense
Intense enhancement with contrast
MRI
T1: Low-intensity with marked
gadolinium
enhancement- tubular or fusiform nerve in axial
T2: Hyperintense mass
Found to grow postero-superiorly with
invagination of the third ventricle
With lateral progression, may involve the Circle of
Willis

59. Sella/suprasellar:
• Optic
pathway/hypothalami
c glioma
• Craniopharyngioma
• Pitutary tumors
• Germ cell tumours
Pineal region:
• Germ cell tumours
• Pinealblastoma
(associated with
retinoblastoma)
• Astrocytoma
• Ganglioglioma
• Epidermoid
Intraventricular:
• Ependymoma
• Choroid plexus
papilloma/carcinoma
• Subependymal giant
cell astrocytoma
(associated with
tuberous sclerosis )
• Lesions arising from
suprasellar region
may involve 3rd
ventricle
• Colloid cyst (3rd
ventricle, usually
young adults)
59

60. 60

61. 61

62. 62

63. 63

64. Best diagnostic clue
 CT Finding: Partially Ca++, partially solid, cystic suprasellar mass in a child
64
 MR Finding: High signal intensity suprasellar mass on pre-contrast TlWI
CT
 cysts
 near CSF density
 typically large and a dominant feature
 present 90 % of the time
 solid component
 soft tissue density
 enhancement in 90%
 calcification
 seen in 90%
 typically stippled and often peripheral in location
MRI
 cysts: variable but ~80% are mostly or partly T2hyperintense
 T1: iso- to hyperintense to brain (due to high protein content machinery oil cysts)
 solid component
 T1 C+ (Gd): vivid enhancement
 T2: variable or mixed
 calcification
 difficult to appreciate on conventional imaging
 susceptible sequences may better demonstrate calcification
 MR angiography: may show displacement of the A1 segment of the anterior cerebral artery (ACA)

65. Unenhanced CT shows the calcifications more clearly.
After intravenous contrast the total extent of the lesion and its
cystic components are much evident.
65

66. unenhanced and enhanced
T1weighted sagittal images, a
compressed pituitary gland can be
identified.
There is a large intrasellar and
suprasellar mass with cystic and
enhancing components as well as
calcifications.
These findings in a child are
virtually pathognomonic for
craniopharyngioma
66

67. Rathke cleft cyst (RCC)
 Noncalcified, usually doesn't enhance, less heterogeneous, no solid components
 Small RCC may be indistinguishable from the rare intra sellar CP
 RCCs express cytokeratin 8,20 (CPs generally don't)
Suprasellar arachnoid cyst
 No Ca++, enhancement
Hypothalamic/chiasmatic astrocytoma
 Solid, or with small cystic/necrotic components
 Ca++ rarei robust enhancement common
Pituitary adenoma
 Rare in prepubescent children
 Isointense with brain, enhancesstrongly
 When cystic and hemorrhagic can mimic CP (Epi)dermoid tumor
67

68. Imaging:
 Pituitary macroadenomas are by definition
>10 mm mass arising from the pituitary
gland, and usually extending superiorly.
Indentation at the diaphragma sellae can give
a snowman or figure eight configuration .
 Plain x-ray may show an enlarged sella
turcica;
CT
 No contrast attenuation can vary depending
on haemorrhagic, cystic and necrotic
components.
 Adenomas which are solid, without
haemorrhage, typically have attenuation
similar to brain (30-40 HU) and demonstrates
moderate contrast enhancement; less marked
than one typically sees in
meningiomas. Calcification is rare.
68

69. MRI
69
 MRI is the preferred imaging modality
 Exquisitely delineate the mass & clearly visualise the optic chiasm, anterior cerebral
vessels and cavernous sinuses.
 Overall signal characteristics can significantly vary depending on tumour components
such as haemorrhage, cystic transformation or necrosis.
 T1
 typically isointense to grey matter
 larger lesions are often heterogeneous and vary in signal due to areas of cystic
change/necrosis/haemorrhage
 T1 C+ (Gd)
 solid components demonstrates moderate to bright enhancement
 T2
 typically isointense to grey matter
 larger lesions are often heterogeneous and vary in signal due to areas of cystic
change/necrosis/haemorrhage
 T2* gradient echo
 most sensitive for detecting any haemorrhagic components, which appear as areas of
signal loss
 calcification is rare, but should be excluded by reviewing CT scans

70. PITUTARY MACROADENOMA
Pituitary macroadenoma there is suprasellar extension with elevation and compression
of the optic chiasm.
To distinguish between a pituitary macroadenoma and a meningioma.
1. Because they are soft tumors, they usually indent at the diaphragma sellae, giving
them a 'snowman' configuration
2. Enlargement of the sella turcica this generally only occurs withpituitary
macroadenomas that originate in the sella. 70

71. The lesion starts in the
sella, which is enlarged,
and extends into the
suprasellar cistern.
Note the classic
'snowman' configuration
caused by constriction by
the diaphragma sellae.
The bloodfluid level,
indicating hemorrhage.
PITUITARY ADENOMAS
71

72.  On the T2weighted images
 The leaflets are displaced upwards by
tmacroadenoma which started in the
sella and is growing upwards.
 A lesion originating above the sellaand
growing downwards would push the
leaflets in the other direction (this can
be seen with meningiomas ).
Sometimes a meningioma can
give a similar appearance.
Note there is no diaphragmatic
constriction and there is
uniform enhancement after
the administration of
intravenous gadolinium
which is typical of
meningioma.
72

73.  Another common pathway of extension is laterally into the cavernous
sinus. Look for
1. If there more than 50% encirclement of the carotid artery? Note:
meningiomas tend to constrict the carotid artery, macroadenomas do
not.
2. Is there lateral displacement of the lateral wall of the cavernous sinus
compared to the opposite side?
3. Is there an increased amount of tissue interposed between the carotid
artery and the lateral wall of the cavernous sinus?
73

74. Classification of pineal tumors
Tumors of pineal parenchymalcells
(pinealomas) (about 25%)
•Pineoblastomas
•Pineocytomas
(ganglioglioma)
Germ cell tumors
• Germinomas (about 70%)
• Embryonal carcinoma (yolk sactumor)
• Endodermal sinus tumors
• Choriocarcinomas
• Teratomas (immature and mature)
Tumors of glial cell origin
• Astrocytoma
• Glioblastoma
Miscellanous tumors and cysts
74

75. Imaging protocol
 The pineal region is best imaged with MRI although CT, angiography and ultrasound (in
infants) also play a role.
 A typical protocol would include:
 sagittal T1 and T2 (highresolution)
 pre and post contrast T1 axial andcoronal
 FLAIR
 DWI
 SWI/gradient echo (to assess for presence of calcification)
Normal appearance
 The pineal gland is a small (~7 mm AP diameter) structure located at theposterior-most
aspect of the third ventricle
Calcification
 No calcification before the age of 5 years of age.
 Calcification larger than 1 cm in any one diameter, or any calcification before the age of 4
years considered pathological.
 Pineal parenchymal tumours (e.g. pineocytoma or pineoblastoma) tend to peripherally
disperse calcification where as germ cell tumours tend to engulf the calcifications.
26

76. Solid component
 Cystic lesion, identification of a significant nodular component or of a thickened
(>2 mm) wall makes a pineal cyst unlikely and essentially excludes an arachnoid
cyst of cavum velum interpositum.
 DWI is also helpful as densely cellular tumours
(e.g.pineoblastoma, meningioma and lymphoma) tend to demonstrate increased
restricted diffusion compared to normal brain parenchyma.
Local invasion
 well circumscribed mass - pineal cyst, pineocytoma whereas more aggressive
masses can extend extensively into the adjacent brain and brainstem
e.g. pineoblastoma, some germ cell tumours.
CSF seeding
 Some aggressive pineal region masses tend to seed the ventricular and
subarachnoid space (e.g.pineoblastoma).
 Germinomas- multifocal disease involving not only the pineal gland but alsothe
floor of the third ventricle is relatively common
27

77.  Facts:
T1 Images
 Germ Cell Tumors
 Causes Parinaud’s Syndrome
 disorder characterized by fixed upward gaze
 Location:
 Commonly in Pineal Region (>50%)
 Overlies tectum of midbrain
 Presentation:
 Obstructive Hydrocephalus due to aqueductal
stenosis
 On Imaging:
 CT
 Isodense or hyperdense
 Enhances with contrast
 MRI
 Isointense or Hypointense on T1-weighted
images
& enhance with gadolinium
Hyperintense on T2 images 28

78. MRI of an asymptomatic pineal cyst in a 17-year-old girl
78

79. Ependymoma
Subependymoma
Choroid plexus papilloma
Colloid cyst
Central neurocytoma
Meningioma
Gaint cell astrocytoma
79

80. General Features
 Best diagnostic clue-Heterogeneous signal, Soft or "plastic"
tumor: Squeezes out through 4th ventricle foramina into
cisterns.Indistinct interface with floor of 4th ventricle.
Radiographic Findings
 Myelography: May be helpful in showing "drop"metastases
CT Findings
 Infratentorial- 4th ventricle tumor, extends into CPA/cisterna
magna.Ca++ common (50%); +/- cysts, hemorrhage.
Hydrocephalus common.
 Supratentorial-Large heterogeneous periventricular mass. Ca++
common (50%).Variable heterogeneous enhancement.
80

81. MR Findings
 T1WI-Heterogeneous, usually iso- to hypointense. Cystic foci
slightly hyperintense to CSF.
 T2WI-Heterogeneous, usually iso-to hyperintense
Hyperintense cystic foci, Hypointense Ca++, blood products
 T1C+: Mild to moderate, heterogeneous enhancement.
Axial NECTshows irregularly shaped 4th ventricular tumor with Ca++and cyst
(open arrow) extending laterally into right CPA(curved arrow).Classic
ependymomaextending from 4th V into CPAcistern. 33

82. On MRI, heterogeneous secondary to necrosis,
hemorrhage and calcification.
Heterogenous contrast enhancement
Plasticity
Extension to the cerebellopontine angle is
characteristic of ependymomas
82

83. MRI gadolinium (A) sagittal, (B) axial images showing fourth ventricular ependymoma
83

84. well-differentiated
84
intraventricular ependymal Rare, benign
tumor
Presentation
 Most asymptomatic. 40% become symptomatic
 symptoms: Related to increased intracranial pressure,
hydrocephalus,Headache, gait ataxia, visual disturbance,
cranial neuropathy, nystagmus, vertigo, nausea, vomiting.
Age
 Middle-aged/elderly adult, (typically 5th-6th decades)
 Asymptomatic patients: Mean age = 60 years
 Symptomatic patients: Mean age = 40 years
Location
 Inferior fourth ventricle, frontal horns of lateral ventricle.

85. General Features
 Best diagnostic clue: T2 hyperintense lobular,nonenhancing
intraventricular mass.
CT Findings
 Iso to hypodense intraventricular mass.Cysts or Ca++ may be
seen in larger lesions.Rarely hemorrhage
 No enhancement, mild enhancement (heterogenous)typical.
MR Findings
 TlWI-Intraventricular mass, hypointense or isointense.
 Typically homogeneous solid mass.
 T2WI-Hyperintense intraventricular mass
 Heterogeneity related to cystic changes, blood products or Ca++
may be seen in larger lesions
 No edema seen in adjacent brain parenchyma
85

86. Axial NECTshows acalcified 4th
ventricular mass in this 52 yearold
female. Calcification is more
commonly seen in 4th Ventricular
subependymomas.
86
Sagittal T1 C+M Rshows aclassic
nonenhancing 4th ventricular
subependymoma (arrow). 4th
ventricular floor origin istypical.

87. On Imaging:
CT:
Smooth, round lesions
lesion hyperdense to brain
tissue
Thin rim of enhancement
after IV contrast
MRI:
T1-weighted hyperintense
lesion due to proteinaceous
nature.
T2-weighted shows
hypointense lesion
87

88.  Ant 3rd ventricle
 Neuroepithelial
cyst
 Hypo to hyperI
on T1 & T2WI
88

89. General Features
 Best diagnostic clue: Child with strongly enhancing, lobulated
intraventricular mass.
Radiographic Findings
 Increased cranial-to-facial ratio
 Sutural diastasis due to hydrocephalus
CT Findings
 Intraventricular bosselated mass
 75% iso- or hyperattenuating. Ca++ in 25%, hydrocephalus
 Intense, homogeneous enhancement
 Heterogeneous enhancement suggests choroid plexus carcinoma
(CPCA).
89

90. MR Findings
 TlWI-Well delineated, lobulated mass. Iso- to hypointense
 CSF trapped between papillae :-a mottled appearance
 T2WI-Iso- to hyperintense. ± Internal linear and branching
vascular flow voids. Hydrocephalus
 Foci of diminished signal representing Ca++
 ±Intratumoral hemorrhage.
 T1 C+ :Robust homogeneous enhancement.
90

91. Axial CECT showsavividly enhancing
lobulated CPP arising from thetrigone of
left lateral ventricle. Notenormal
contralateral choroid plexus(arrow),
Axial CECT showsan obstructing, robustly
enhancing choroid plexuspapilloma
arising from roof ofthird ventricle. Note
papillary surface projections
45

92. 92

93. Neurocytoma
Magnetic resonance
image of central
neurocytoma. FLAIR
(A) and postcontrast T1-
weighted (B) axial
images of a central
neurocytoma projecting
from the septum
pellucidum into the
anterior body of the left
lateral ventricle.
93

94. tumor location T2WI contrast
Central
neurocytoma
Lat, septum
pellucidum
Iso to GM dense
ependymoma lateral Heterogeneous heterogeneous
meningioma lateral Iso to GM dense
Choroid
plexus tumor
fourth heterogeneous dense
Colloid cyst third Hyper to GM none
94

95. Cerebellar
liponeuroc
ytoma
Metastasis
16%
Hemangiobl
astoma 7-
12%
Choroid
plexus
tumor
(<1%)
Brain stem
glioma (1%
of adult
tumor)
Pilocytic
astrocytoma
(2nd
decade)
95

96. Axial CT contrast image
showing multiple metastases
Axial T2 image showing SINGLE
metastases
96

97. General Features
 Best diagnostic clue-Cystic cerebellar mass with
enhancing mural nodule
 Enlarged optic nerve/chiasm/tractwith variable enhancement.
CTFindings
 Discrete cystic/solid mass. May have little or no surrounding
edema.Solid componenthypo-to isodense.
 Ca++20%, hemorrhage rare
 Often causeobstructive hydrocephalus.
 > 95% enhance (patterns vary).50% non enhancing cyst.
strongly enhancing mural nodule. 40% solid with necrotic
center, heterogeneous enhancement
97

98. MRFindings
 T1WI- Solid portions iso/hypointense to GM.
Cyst contentsiso-toslightly hyperintense to
CSF
 T2WI-Solid portions hyperintense to GM.
Cyst contentshyperintense to CSF.
 T1C+:Intense butheterogeneousenhancementof solid
portion or mural nodule. Cyst wall occasionally
enhances.
Ultrasonographic Findings
 Real Time-Solid componentsare hyperechoic relative
tobrain parenchyma. Cystsmaycontain debris.
98

99. •A large partially cystic mass in the right cerebellarhemisphere.
•The solid component only minimally enhances with a focal region demonstrating
more prominent ring enhancement.
•The fourth ventricle is effaced, and the lateral ventricles are enlarged.
•There is also marked effect on the brainstem with the
Perimesencephaliccisternsobliterated.
prepontine and
55

100. (A)MRI T1,
(B) MRI gadolinium
images showing
sellar pilocytic
astrocytoma,
(C) MRI T1,
(D) MRI gadolinium
images showing
cerebellar
pilocytic
astrocytoma
10

101. CT
 The mural nodule is isodense to brain on non-contrast scans with fluid density surrounding cyst
 Bright enhancement of the nodule is demonstrated with contrast
 The cyst walls do not usually enhance & calcification is not a feature
MRI T1
 Hypointense to isointense mural nodule,
 CSF signal cyst content
 T1 C+ (Gd)
 mural nodule vividly enhances BUT cyst wall does not enhance
T2
 Hyperintense mural nodule
 Flow voids due to enlarged vessels may be evident especially at the periphery of the cyst, seen in 60-
70% of cases
 Fluid filled cyst, similar to CSF
MR perfusion imaging: high rCBVratios
Angiography (DSA)
 Enlarged feeding arteries and often dilated draining veins are demonstrated, with a dense tumour
blush centrally
10

102. Coronal MRI gadolinium image
showing cystic hemangioblastoma with
a mural nodule
CT showing cystic hemangioblastoma
with a mural nodule
10

103. CT
•mass arising from the vermis, resulting in effacement of the fourth ventricle /basal
cisterns and obstructive hydrocephalus.
•Usually hyperdense (90%) and cysts formation/necrosis is common (40-50%)
•Calcification is seen in 10-20% of cases .
•Enhancement is present in over 90% of cases and is usuallyprominent
MRI
T1
hypointense to grey matter
T1 C+ (Gd)
overall 90% enhance, often heterogeneously
T2/FLAIR
overall are iso to hyperintense to grey matter
heterogeneous due to calcification, necrosis and cystformation
surrounding oedema is common
DWI/ADC- restricted diffusion (low ADCvalues)
MR spectroscopy
elevated choline
decreased NAA
61
Medulloblastoma
2
mayshowa taurine peak

104. (A) Contrast CT, (B) MRI T1, (C) MRI gadolinium images showing medulloblastoma
10

105. • Imaging
– MRI is the method of
choice to image these
tumors (brainstem
glioma appears isodense
on CT and can be
missed);
– Appear isointense or
hypointense on T1
images, hyperintense on
T2, and enhance
uniformly and brightly
with IV contrast;
10

106. Classification
1. Diffuse brain stem glioma
most are diffuse midline glioma H3 K27M–mutant
2. Focal brain stem glioma
tectal plate glioma
other focal gliomas
3.(dorsally) exophytic
4.Cervicomedullary
probably an artificial group made up of the downward extension of
true brainstem gliomas or upward extension of upper cervical cord
intramedullary spinal cord tumours

107. Magnetic resonance imaging axial sections showing: (A) “Diffuseinfiltrating
type” as compared to. (B) “Expanding type” of brainstem glioma.
10

108. Schwannoma
10
Meningioma Arachnoid cyst
Epidermoid Paraganglioma Metastasis

109. CT
 May show erosion and widening of the internal acoustic
canal.
 The density of these tumours on non-contrast imaging is
variable, and often they are hard to see, especially on
account of beam hardening and streak artefact form the
adjacent petrous temporal bone.
 Contrast enhancement is present, but can be
underwhelming, especially in larger lesions with cystic
components.
MRI
 T1
 slightly hypointense cf. adjacent brain (63%)
 isointense cf. adjacent brain (37%)
 may contain hypointense cystic areas
 T2
 heterogeneously hyperintense cf. to adjacent brain
 cystic areas fluid intensity
 may have associated peritumoural arachnoid cysts
 T1 C+ (Gd)
 contrast enhancement is vivid
 but heterogeneous in larger tumours
10

110. 11

111. 11

112. 11

113. 11

114. 11

115.  Epidermoid. A, Contrast-enhancedaxial
T1-weighted image demonstrates right
cerebellopontine angle mass (arrow),
showing close to cerebrospinal fluid
(CSF) intensity signal on this sequence,
and no postcontrast enhancement.
 B, Fluid-attenuated inversion recovery
(FLAIR) image, showing the same lesion
demonstrating signal intensity somewhat
higher than CSF.
 C, On diffusion-weighted image, the
lesion is hyperintense, whereas on the
apparent diffusion coefficient map
calculated from the diffusion data
 (D), the lesion (short arrow) is
significantly lower in intensity than is the
CSF in the fourth ventricle (long arrow).
11

116. meningioma
11
• usually more
homogeneous in
appearance:
significant signal
heterogeneity with
cystic or
haemorrhagic areas
is more typical of
vestibular
schwannoma than
meningiomas
(although cystic
meningiomas do
occur)
• meningiomas tend to
have a broad dural
base
• usually lack trumpet
IAM sign
• calcification more
common
epidermoid
• no enhancing
component
• very high signal on
DWI
• does not widen the
IAC
metastasis
• uncommon
• usually does not
remodel the IAC as
metastases are
usually present for
only a short time
ependymoma
• centered on the
fourth ventricle
• does not extend into
the IAC
• usually younger
patients
Differential diagnosis
The most frequent differential to be considered are:

117. Chordoma
Chondrosarco
ma
Esthesioneuro
blastoma
Sinonasal
carcinoma
Myeloma
11

118. (A) Lateral radiograph; (B) Coronal MRI; (C) CT bone window images showing a
giant osteoma of anterior skull base
11

119.  On CT image- isointense on the non-contrast studies. There is irregular bone
destruction at its site of origin, which may be in the midline of the clivus or
eccentrically located.
 The tumour may also show areas of calcification.
MRI
 Lobulated masses arising from the clivus. They manifest low signal intensity
on T1-weighted images and have high signal intensity on T2-weightedimages.
 They do enhance with the administration of gadolinium, but this occurs to a
variable degree.
 They can vary greatly in size and distribution.
 They often extend intracranially as well as extracranially into adjacent
anatomical areas
 Differentiating chordomas from chondrosarcomas is often difficult due to the
identical imaging appearance.
 Chondrosarcomas usually arise eccentrically at the petroclivalsynchondrosis.
11

120. MRI scan of 43-year-old man showing a enhancing large clival
chordoma at the skull base
12

121. 12

122. Age distribution
Tumor spread
• Intra-versus
Extraaxial
• Midline crossing
• Multifocal disease
• Cortical based tumors
CT and MR
Characteristics
• Fat - Calcification -
Cyst - High density
• High onT1
• Low onT2
• Diffusion weighted
imaging
• Perfusion Imaging
Enhancement
Differential
diagnosis for
specific
anatomic area
• Skull base
• Sella/suprasellar
• Cerebello-pontine
angle
• Pineal region
• Intraventricular
• 4th ventricle
TumorMimics
12

123. Thank you
12