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DR PRAVEEN K TRIPATHI
 1895, Wilhelm Roentgen presented his classic written
preliminary communication regarding X-rays.
 Arthur Schiiller (1874–1957), a Viennese physician,
considered as the “father of neuroradiology” studied skull X-
rays systematically with various projections
 1918, Walter Dandy described diagnostic ventriculography &
pneumoencephalography
 1927, a Portuguese neurologist, Egas Moniz, first reported the
percutaneous technique of cerebral angiography.
 Magnetic Resonance phenomenon first described
by Felix Bloch and Edward Purcell in 1946. In
1952 they were awarded the Nobel Prize.
 1971 -Raymond Damadian showed that the nuclear
magnetic relaxation times of tissues and tumors
differed, sparking interest in medical uses
 1987 –MR angiography developed by Charles
Dumoulin.
Brain tumor imaging objectives
• Tumor versus non tumoral lesion.
• Histological grade.
DIAGNOSIS
• Delineation of the tumor extent.
• Tumor versus peritumoral edema.
TREATMENT
PLAN
• Residual tumor versus treatment
necrosis.
POST
TREATMENT
FOLLOW UP
• Is this a tumor or something else?
• Is this a benign or malignant tumor?
DIAGNOSIS
• Which part should the surgeon take
out?
• Where should be irradiated?
TREATMENT
PLAN
• Recurrent/residual tumor or post
treatment effect?
POST
TREATMENT
FOLLOW UP
Available
Modalities
1)X-ray 2)CT 3)MRI
4)Nuclear
Medicine
• Primarily of historical interest since the onset of
CT in 1974.
• Rarely necessary.
• Useful in demonstrating calcification, erosion,
or hyperostosis
Skull X-rays:
• Will detect >90% of tumors, but might miss:
• Small Tumors (<0.5 cm)
• Tumors Adjacent to bone (pituitary adenomas,
clival tumors, and vestibular schwannomas)
• Brain Stem Tumors
• Low Grade Astrocytomas
• More sensitive than MRI for detecting acute
hemorrhage, calcification, and bony involvement
CT: Most widely
used for
diagnosis of
brain tumors
• More sensitive than CT scans
• Can detect small tumors
• Provides much greater anatomic detail
• Especially useful for visualizing skull base,
brain stem, & posterior fossa tumors
MRI: Preferred
for follow-up of
most brain tumors
X-ray lateral view in a patient
with craniopharyngioma showing
suprasellar calcification
•The sella is deepened; a
depth of more than 15 mm
and an AP diameter of 20
mm are definitely
abnormal.
•The floor may be so
demineralised that the
tumour actually appears to
project into the sphenoid
sinus.
•Irregular growth may
cause a step to be visible
in the floor of the sella,
“Double floor” in a “strict
lateral” view
 MRI is generally preferable to CT for evaluating
intracranial neoplasms
 CT is preferred for visualizing tumor
calcification or intratumor hemorrhage.
 Usually the preferred method of imaging
intracranial tumors due to better soft-tissue
contrast
 MRI exploits increased water content of many
neoplasms. This water content shows up as
increased signal on T2 weighted images and
decreased signal on T1 Images.
MRI has a higher sensitivity in the
demonstration of oedema and is better for
earlier detection of tumours.
Brainstem structures are better identified.
It gives a better characterisation of brain
tumours
MRI has become the most useful pre-
operative imaging tool.
Age
Location
Local tumour spread
Solitary or multifocal
Specific imaging characteristics
Tumour mimics
• Size.
• Edema.
• Location.
• Necrosis.
• Calcification.
• Hemorrhage.
• Cysts.
Unpredective
of grading
 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
 Intra-axial tumours are twice as common as extra-axial
tumours.
Signs of extra-axial location:
 Widening of the ipsilateral subarachnoid space
 Cerebrospinal fluid (CSF) cleft between the mass and the brain
parenchyma
 Deviation of pial vessels between the mass and the brain tissue
 Buckling of the grey matter (GM)/white matter (WM) junction
 Broad base along the dural or calvarial surface
 Adjacent bony changes such as hyperostosis in meningioma or
erosion in acoustic neurinoma.
 >80% extra-axial tumours are either meningioma or
schwannoma
 Definitive – CSF cleft
 Definitive - vessels b/n lesion &
brain
 Definitive - cortex b/n lesion & brain
Intra vs extra axial
 Suggestive –broad based towards calvarium
 Suggestive - adj bone changes
 Suggestive - enhancement of
meninges
 Invade to & through dura
EXTRA AXIAL
TUMOR
 TheT2Wimagesshowaschwannoma locatedinthecerebellopontineangle
(CPA).
 Thiscasenicelydemonstratesthetypicalsignsofanextraaxialtumor.
 ThereisaCSFcleft(yellowarrow).
 Thesubarachnoidvesselsthatrunonthesurfaceofthebrainaredisplacedbythe
lesion(bluearrow).
 Thereisgraymatterbetweenthelesionandthewhitematter(curvedredarrow).
 Thesubarachnoidspaceiswidenedbecausegrowthofanextraaxiallesiontends
topushawaythebrain.
 IntheregionoftheCPA90%oftheextraaxialtumorsareschwannomas.
Intra-axial
Intra-axial is a term that
denotes lesions that are within
the brain parenchyma
Some authors include
intraventricular lesions in the
intra-axial group as most are
lesions that arise from the
brain parenchyma and grow
exophytically into the
ventricular system.
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
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
Common intraaxial tumours in
adults
Supratentorial
Metastases
Gliomas
Infratentorial
Metastases
Hemangioblastoma
 Most intra-axial tumours are white matter based
 Differential diagnosis for cortical based tumours:
 DNET (Dysembryoplastic neuroepithelial
tumour)
 Ganglioglioma
 Glioblastoma multiforme (GBM) frequently crosses the 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 midline via the subarachnoid
space.
 MScanalsopresentasamasslesioninthecorpuscallosum.
 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
 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
 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
 Tuberous sclerosis: subependymal tubers; ependymomas;
intraventricular giant cell astrocytomas
 Von Hipple Lindau: hemangioblastomas
Fat
Calcifi-
cation
Cystic
mass
vs. cyst
T1WI
signal
intensity
T2WI
signal
intensity
Contrast
enhance-
ment
Advanced
MRI
 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
Intra-axial:
• Astrocytoma
• Ependymoma
• Choroid plexus
papilloma
• Ganglioglioma
Extra-axial:
• Meningioma
• Craniopharyngioma
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
 Most tumors have a low or intermediate signal
intensity on T1WI.
 Exceptions to this rule can indicate a specific type
of tumor.
PITUTARY
apoplexy. The high
signal is due to
hemorrhage in a
pituitary
macroadenoma.
Glioblastoma
multiforme, which
caused a
hemorrhage in the
splenium of the
corpus callosum.
Metastasis of a melanoma.
The high signal intensity is
due to the melanin
content.
 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
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
• High grade
glioma
• Metastases
• Abscess
HOMOGENOUS
ENHANCEMENT
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.
Diffusion
weighted
imaging
Diffusion
tensor
imaging
Perfusion
weighted
imaging
Magnetic
resonance
spectroscopy
 Most tumours do
not show
significant
restriction of
diffusion
 High signal on
DWI is seen with
abscesses,
epidermoid cysts
and acute
infarction
 Dynamic susceptibility perfusion imaging is
based on the premise that contrast material
remains within the intravascular compartment.
 Signal intensity depends on vascularity, not on
breakdown of blood-brain barrier
 Better correlation with grade of malignancy
than degree of contrast enhancement
Grade II astrocytoma.
Left, Fluid-attenuated inversion recovery
(FLAIR) image demonstrates an area of
increased signal intensity in the parietooccipital
region.
Right, Perfusion MRI demonstrates decreased
relative cerebral blood volume (rCBV),
consistent with a low-grade neoplasm. The final
pathologic diagnosis was a grade II astrocytoma.
Axial MRI T1 showing hypointense
mass in right frontal lobe which
appears hyperintense on T2 and shows
increased perfusion values with
elevated choline peak values
confirming a high grade glioma
CT
 CT is often the first modality employed to investigate neurological signs or
symptoms, and often is the modality which detects an incidental lesion:
 non-contrast CT
 60% slightly hyperdense to normal brain, the rest are more isodense
 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 also been
suggested to be associated with anterior cranial fossa meningiomas
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 texture and
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
T2 Contrasted T1 Perfusion-Weighted
A number of helpful imaging signs have been
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
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
AXIAL T1W
T1C+
3.1a. Pre-contrast Axial T1 Wtd MRI 3.1b. Post-contrast Axial T1 Wtd MRI
3.1c. Post-contrast Coronal T1 Wtd MRI 3.1d. Post-contrast Sagittal T1 Wtd MRI
60 year-old lady with
anosmia and short term
memory loss.
A well defined strikingly
enhancing (arrows) classic
meningioma is seen
involving the floor of the
anterior cranial fossa,
particularly involving the
PLANUM SPHENOIDALE
and OLFACTORY
GROOVE, finding
responsible for anosmia.
Olfactory groove
Meningioma
3.3a. Pre-contrast Axial T1 Wtd MRI 3.3b. Axial T1 Wtd MRI (C+) 3.3c. Coronal T1 Wtd MRI (C+)
A dural-based intensely enhancing (arrows) meningioma arising from the right
side of the falx.
Falcine Meningioma
MRI images of a large
sphenoidal wing
meningioma.
(A) Enplaque, (B)
Globular
MRI gadolinium. (A) Axial, (B) Coronal, (C) Sagittal images
showing a pterional meningioma
MENINGIOMA
• Alanine – Doublet at 1.47 ppm
Inverts at long TE
• Decreased NAA, Cr
• Increased Glx
• Increased mI
• Presence of Choline
• Variable Lactate
• Minimal lipids
MRI gadolinium images of rarer meningiomas: (A) Falcotentorial meningioma, (B) Torcular
meningioma, (C) Middle fossa meningioma extending through the foramen ovale, (D)
Meningioma with pituitary microadenoma, (E) Cystic meningioma with a dural tail, (F)
Multiple meningiomas
A B C
 Epi:
 15% of Astrocytomas
 Young Adults
 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
Low grade glioma
CT: Well circumscribed, non enhancing,
hypodense or isodense lesion
Low grade glioma
CT: Well circumscribed, non enhancing,
hypodense or isodense lesion
Low grade glioma
CT: Well circumscribed, non enhancing,
hypodense lesion WITH cyst S/O pilocytic
astrocytoma
TlWI
o Homogeneous hypointense
mass
o May expand white matter
and adjacent cortex
o Appears circumscribed, but
infiltrates adjacent brain
o Ca++ and cysts uncommon
o Hemorrhage or surrounding
edema (rare)
TI C+
o Usually no enhancement
o Enhancement suggests progression to higher grade
TlWI
o Homogeneous hypointense
mass
o May expand white matter
and adjacent cortex
o Appears circumscribed, but
infiltrates adjacent brain
o Ca++ and cysts uncommon
o Hemorrhage or surrounding
edema (rare)
TI C+
o Usually no enhancement
o Enhancement suggests progression to higher grade
Grade II astrocytoma in a 30-year-
old man. Nonenhanced T2-
weighted MRI shows a well-
circumscribed area of increased
signal intensity in the left temporal
lobe.
Grade II astrocytoma.
Left, Fluid-attenuated inversion recovery (FLAIR)
image demonstrates an area of increased signal
intensity in the parietooccipital region.
Right, Perfusion MRI demonstrates decreased
relative cerebral blood volume (rCBV), consistent
with a low-grade neoplasm. The final pathologic
diagnosis was a grade II astrocytoma.
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
 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.
 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
Non contrast axial CT CECT Axial
 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
•Axial T2WI MR shows
a heterogeneous hyperintense
mass with central necrosis and
surrounding signalabnormality
likely related to tumor extension
and edema. Typical imaging of
GBM.
•Axial T1 C+ MR
shows peripheral enhancement
with central necrosis and
extension across the splenium of
the corpus callosum,
characteristic of GBM.
Axial (a) and coronal (b) fluid-attenuated inversion recovery MR
images demonstrate the mass with a large amount of surrounding T2
prolongation, a finding that suggests edema.
•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
Axial CECT shows a peripherally
enhancing, centrally necrotic mass with
surrounding mass effect and midline
shift. There is uncal herniation and
early entrapment of the ventricular
system. GBM.
Single voxel MRS shows elevated Cho
and decreased NAA. Note the lactate
doublet at 1.33 (arrow), typical of high
grade tumors. Patient with a history of AA
that progressed
to GBM.
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 CNS lymphoma -Periventricular enhancing mass.Often
crosses corpus callosum. Typically isointense/hypointense on
T2W.Necrosis common in AIDS related lymphoma.
 Anaplastic astrocytoma (AA) -Often nonenhancing white matter
mass. Enhancement may indicate degeneration to GBM.
 On Imaging:
 CT:
 Well circumscribed, hypodense lesions with
heavy calcification
 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
 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
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
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
 Distinct type of (usually) benign supratentorial astrocytoma
found almost exclusively in young adults.
Presentation
 Majority with long-standing epilepsy, often partial complex
seizures (temporal lobe)
 Other signs/symptoms: Headache, focal neurologic deficits
Age
 Tumor of children/young adults
 2/3 < 18 years.
Location
 Peripherally located hemispheric mass, often involves cortex
and meninges.
 98% supratentorial-Temporal lobe most common.
General Features
 Best diagnostic clue- Supratentorial cortical mass with adjacent
enhancing dural "tail“.
 Cyst and enhancing mural nodule typical.
CT Findings
 Cystic/solid mass: Hypodense with mixed density nodule
 Solid mass: Variable; hypodense, hyperdense or mixed.
Minimal or no edema is typical. Ca++, hemorrhage, frank skull
erosion rare.
 Strong, sometimes heterogeneous enhancement of tumor
nodule.
MR Findings
 TlWI-Mass is hypointense or isointense to gray matter.
 T2WI-Hyperintense or mixed signal intensity mass
 Cystic portion isointense to CSF. Surrounding edema rare
 T1 C+- Enhancement usually moderate/strong, well-delineated
 Enhancement of adjacent meninges, dural"tail"common
(approximately 70%)
 Enhancing nodule often abuts pial surface.
Axial and coronal FLAIR, T2W and T1C+ scans showing solid cystic mass with
ehhancing mural nodule.
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
remodel calvarium
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
 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).
General Features
 Best diagnostic clue: Partially cystic, enhancing,cortically-based
mass in child/young adult with TLE.
CT Findings
 40% hypodense,30% mixed hypodense (cyst), isodense
(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.
MR Findings
 TIWI-Mass is hypo to isointense to gray matter.
 T2WI-Hyperintense, heterogeneous.
 Tl C+:Variable enhancement, usually moderate
Axial FLAIR MR shows a cortically-
based hyperintense mass in the right
frontal lobe. Note the lack of edema
and mass effect.
Coronal T1 C+ MR shows a temporal lobe
circumscribed cystic and solid mass with
intense enhancement of the mural nodule
(arrow). Long history of temporal lobe
epilepsy. Ganglioglioma.
(Left) Axial T2WI MR shows a hyperintense temporal lobe
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+ MR shows a cystic and solid temporal lobe mass with
marked enhancement of the solid portion, a typical
enhancement pattern of ganglioglioma.
Best diagnostic clue: Well-demarcated, wedge-shaped "bubbly"
intracortical mass in young patient with longstanding partial
seizures
Location
 Temporal lobe (often amygdala/hippocampus) most 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)
 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
Non-enhanced CT scan
reveals a parietal lesion with
calcific hyperdensity.
Calvarial remodeling is evident on
bone window CT scan.
MRI axial images showing
multicystic lesion in the right
temporal lobe which appears
(A)hypointense on T1,
(B and C) Hyperintense on T2 and
FLAIR,
(D) No significant enhancement on
contrast imaging
A B
C D
DNET
Axial T2WI MR in a 5 year old
with seizures shows
multicentric, "bubbly", DNET
with involvement of the body of
the caudate nucleus (arrow).
Axial T2WI MR shows bubbly
temporal lobe DNET
expanding involved gyri and
remodeling the inner calvarial
table (arrow).
23 May 2016 106
■ General characteristics
– Solid, cystic, or combination
– Classically described as globular/ exophytic
suprasellar mass
■ 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
Radiology Vol. 243, No. 2: 539-550
©RSNA, 2007
 Age and clinical feature should always considered.
 Neuroradiology provides details of the structural
pathology, the functional and physiological data.
 MRI is the choice of neuroimaging; CT still has a role.
 MRI (FLAIR) increases the conspicuity of lesions at brain-
CSF interfaces.
 MRI (STIR) suppresses fat, which is useful for skull base
and orbital imaging.
 fMRI and DTI decide the surgical approach.
 Advanced imaging helps in narrowing the D/Ds
 Good preoperative work up & team approach is key to
success.
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Brain Tumor Imaging Modalities

  • 1. DR PRAVEEN K TRIPATHI
  • 2.  1895, Wilhelm Roentgen presented his classic written preliminary communication regarding X-rays.  Arthur Schiiller (1874–1957), a Viennese physician, considered as the “father of neuroradiology” studied skull X- rays systematically with various projections  1918, Walter Dandy described diagnostic ventriculography & pneumoencephalography  1927, a Portuguese neurologist, Egas Moniz, first reported the percutaneous technique of cerebral angiography.
  • 3.  Magnetic Resonance phenomenon first described by Felix Bloch and Edward Purcell in 1946. In 1952 they were awarded the Nobel Prize.  1971 -Raymond Damadian showed that the nuclear magnetic relaxation times of tissues and tumors differed, sparking interest in medical uses  1987 –MR angiography developed by Charles Dumoulin.
  • 4. Brain tumor imaging objectives • Tumor versus non tumoral lesion. • Histological grade. DIAGNOSIS • Delineation of the tumor extent. • Tumor versus peritumoral edema. TREATMENT PLAN • Residual tumor versus treatment necrosis. POST TREATMENT FOLLOW UP
  • 5. • Is this a tumor or something else? • Is this a benign or malignant tumor? DIAGNOSIS • Which part should the surgeon take out? • Where should be irradiated? TREATMENT PLAN • Recurrent/residual tumor or post treatment effect? POST TREATMENT FOLLOW UP
  • 7. • Primarily of historical interest since the onset of CT in 1974. • Rarely necessary. • Useful in demonstrating calcification, erosion, or hyperostosis Skull X-rays: • Will detect >90% of tumors, but might miss: • Small Tumors (<0.5 cm) • Tumors Adjacent to bone (pituitary adenomas, clival tumors, and vestibular schwannomas) • Brain Stem Tumors • Low Grade Astrocytomas • More sensitive than MRI for detecting acute hemorrhage, calcification, and bony involvement CT: Most widely used for diagnosis of brain tumors • More sensitive than CT scans • Can detect small tumors • Provides much greater anatomic detail • Especially useful for visualizing skull base, brain stem, & posterior fossa tumors MRI: Preferred for follow-up of most brain tumors
  • 8. X-ray lateral view in a patient with craniopharyngioma showing suprasellar calcification
  • 9.
  • 10.
  • 11. •The sella is deepened; a depth of more than 15 mm and an AP diameter of 20 mm are definitely abnormal. •The floor may be so demineralised that the tumour actually appears to project into the sphenoid sinus. •Irregular growth may cause a step to be visible in the floor of the sella, “Double floor” in a “strict lateral” view
  • 12.  MRI is generally preferable to CT for evaluating intracranial neoplasms  CT is preferred for visualizing tumor calcification or intratumor hemorrhage.  Usually the preferred method of imaging intracranial tumors due to better soft-tissue contrast  MRI exploits increased water content of many neoplasms. This water content shows up as increased signal on T2 weighted images and decreased signal on T1 Images.
  • 13. MRI has a higher sensitivity in the demonstration of oedema and is better for earlier detection of tumours. Brainstem structures are better identified. It gives a better characterisation of brain tumours MRI has become the most useful pre- operative imaging tool.
  • 14. Age Location Local tumour spread Solitary or multifocal Specific imaging characteristics Tumour mimics
  • 15. • Size. • Edema. • Location. • Necrosis. • Calcification. • Hemorrhage. • Cysts. Unpredective of grading
  • 16.
  • 17.
  • 18.  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
  • 19.  Intra-axial tumours are twice as common as extra-axial tumours. Signs of extra-axial location:  Widening of the ipsilateral subarachnoid space  Cerebrospinal fluid (CSF) cleft between the mass and the brain parenchyma  Deviation of pial vessels between the mass and the brain tissue  Buckling of the grey matter (GM)/white matter (WM) junction  Broad base along the dural or calvarial surface  Adjacent bony changes such as hyperostosis in meningioma or erosion in acoustic neurinoma.  >80% extra-axial tumours are either meningioma or schwannoma
  • 20.  Definitive – CSF cleft
  • 21.  Definitive - vessels b/n lesion & brain
  • 22.  Definitive - cortex b/n lesion & brain Intra vs extra axial
  • 23.  Suggestive –broad based towards calvarium
  • 24.  Suggestive - adj bone changes
  • 25.
  • 26.  Suggestive - enhancement of meninges
  • 27.  Invade to & through dura
  • 28. EXTRA AXIAL TUMOR  TheT2Wimagesshowaschwannoma locatedinthecerebellopontineangle (CPA).  Thiscasenicelydemonstratesthetypicalsignsofanextraaxialtumor.  ThereisaCSFcleft(yellowarrow).  Thesubarachnoidvesselsthatrunonthesurfaceofthebrainaredisplacedbythe lesion(bluearrow).  Thereisgraymatterbetweenthelesionandthewhitematter(curvedredarrow).  Thesubarachnoidspaceiswidenedbecausegrowthofanextraaxiallesiontends topushawaythebrain.  IntheregionoftheCPA90%oftheextraaxialtumorsareschwannomas.
  • 29. Intra-axial Intra-axial is a term that denotes lesions that are within the brain parenchyma Some authors include intraventricular lesions in the intra-axial group as most are lesions that arise from the brain parenchyma and grow exophytically into the ventricular system.
  • 30. 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
  • 31. 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
  • 32. Common intraaxial tumours in adults Supratentorial Metastases Gliomas Infratentorial Metastases Hemangioblastoma
  • 33.  Most intra-axial tumours are white matter based  Differential diagnosis for cortical based tumours:  DNET (Dysembryoplastic neuroepithelial tumour)  Ganglioglioma
  • 34.  Glioblastoma multiforme (GBM) frequently crosses the 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 midline via the subarachnoid space.  MScanalsopresentasamasslesioninthecorpuscallosum.
  • 35.
  • 36.  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
  • 37.
  • 38.  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
  • 39.  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  Tuberous sclerosis: subependymal tubers; ependymomas; intraventricular giant cell astrocytomas  Von Hipple Lindau: hemangioblastomas
  • 41.  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
  • 42.
  • 43. Intra-axial: • Astrocytoma • Ependymoma • Choroid plexus papilloma • Ganglioglioma Extra-axial: • Meningioma • Craniopharyngioma
  • 44.
  • 45. 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
  • 46.  Most tumors have a low or intermediate signal intensity on T1WI.  Exceptions to this rule can indicate a specific type of tumor.
  • 47.
  • 48.
  • 49. PITUTARY apoplexy. The high signal is due to hemorrhage in a pituitary macroadenoma. Glioblastoma multiforme, which caused a hemorrhage in the splenium of the corpus callosum. Metastasis of a melanoma. The high signal intensity is due to the melanin content.
  • 50.
  • 51.  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
  • 52. 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 • High grade glioma • Metastases • Abscess
  • 53.
  • 55. 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.
  • 57.  Most tumours do not show significant restriction of diffusion  High signal on DWI is seen with abscesses, epidermoid cysts and acute infarction
  • 58.  Dynamic susceptibility perfusion imaging is based on the premise that contrast material remains within the intravascular compartment.  Signal intensity depends on vascularity, not on breakdown of blood-brain barrier  Better correlation with grade of malignancy than degree of contrast enhancement
  • 59. Grade II astrocytoma. Left, Fluid-attenuated inversion recovery (FLAIR) image demonstrates an area of increased signal intensity in the parietooccipital region. Right, Perfusion MRI demonstrates decreased relative cerebral blood volume (rCBV), consistent with a low-grade neoplasm. The final pathologic diagnosis was a grade II astrocytoma. Axial MRI T1 showing hypointense mass in right frontal lobe which appears hyperintense on T2 and shows increased perfusion values with elevated choline peak values confirming a high grade glioma
  • 60. CT  CT is often the first modality employed to investigate neurological signs or symptoms, and often is the modality which detects an incidental lesion:  non-contrast CT  60% slightly hyperdense to normal brain, the rest are more isodense  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 also been suggested to be associated with anterior cranial fossa meningiomas
  • 61. 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 texture and 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
  • 62. T2 Contrasted T1 Perfusion-Weighted
  • 63. A number of helpful imaging signs have been 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
  • 64. 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 AXIAL T1W T1C+
  • 65. 3.1a. Pre-contrast Axial T1 Wtd MRI 3.1b. Post-contrast Axial T1 Wtd MRI 3.1c. Post-contrast Coronal T1 Wtd MRI 3.1d. Post-contrast Sagittal T1 Wtd MRI 60 year-old lady with anosmia and short term memory loss. A well defined strikingly enhancing (arrows) classic meningioma is seen involving the floor of the anterior cranial fossa, particularly involving the PLANUM SPHENOIDALE and OLFACTORY GROOVE, finding responsible for anosmia. Olfactory groove Meningioma
  • 66. 3.3a. Pre-contrast Axial T1 Wtd MRI 3.3b. Axial T1 Wtd MRI (C+) 3.3c. Coronal T1 Wtd MRI (C+) A dural-based intensely enhancing (arrows) meningioma arising from the right side of the falx. Falcine Meningioma
  • 67. MRI images of a large sphenoidal wing meningioma. (A) Enplaque, (B) Globular MRI gadolinium. (A) Axial, (B) Coronal, (C) Sagittal images showing a pterional meningioma
  • 68. MENINGIOMA • Alanine – Doublet at 1.47 ppm Inverts at long TE • Decreased NAA, Cr • Increased Glx • Increased mI • Presence of Choline • Variable Lactate • Minimal lipids
  • 69. MRI gadolinium images of rarer meningiomas: (A) Falcotentorial meningioma, (B) Torcular meningioma, (C) Middle fossa meningioma extending through the foramen ovale, (D) Meningioma with pituitary microadenoma, (E) Cystic meningioma with a dural tail, (F) Multiple meningiomas A B C
  • 70.  Epi:  15% of Astrocytomas  Young Adults  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
  • 71. Low grade glioma CT: Well circumscribed, non enhancing, hypodense or isodense lesion
  • 72. Low grade glioma CT: Well circumscribed, non enhancing, hypodense or isodense lesion
  • 73. Low grade glioma CT: Well circumscribed, non enhancing, hypodense lesion WITH cyst S/O pilocytic astrocytoma
  • 74. TlWI o Homogeneous hypointense mass o May expand white matter and adjacent cortex o Appears circumscribed, but infiltrates adjacent brain o Ca++ and cysts uncommon o Hemorrhage or surrounding edema (rare) TI C+ o Usually no enhancement o Enhancement suggests progression to higher grade
  • 75. TlWI o Homogeneous hypointense mass o May expand white matter and adjacent cortex o Appears circumscribed, but infiltrates adjacent brain o Ca++ and cysts uncommon o Hemorrhage or surrounding edema (rare) TI C+ o Usually no enhancement o Enhancement suggests progression to higher grade
  • 76. Grade II astrocytoma in a 30-year- old man. Nonenhanced T2- weighted MRI shows a well- circumscribed area of increased signal intensity in the left temporal lobe. Grade II astrocytoma. Left, Fluid-attenuated inversion recovery (FLAIR) image demonstrates an area of increased signal intensity in the parietooccipital region. Right, Perfusion MRI demonstrates decreased relative cerebral blood volume (rCBV), consistent with a low-grade neoplasm. The final pathologic diagnosis was a grade II astrocytoma.
  • 77. 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
  • 78.  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.
  • 79.  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
  • 80. Non contrast axial CT CECT Axial
  • 81.  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
  • 82. •Axial T2WI MR shows a heterogeneous hyperintense mass with central necrosis and surrounding signalabnormality likely related to tumor extension and edema. Typical imaging of GBM. •Axial T1 C+ MR shows peripheral enhancement with central necrosis and extension across the splenium of the corpus callosum, characteristic of GBM.
  • 83. Axial (a) and coronal (b) fluid-attenuated inversion recovery MR images demonstrate the mass with a large amount of surrounding T2 prolongation, a finding that suggests edema.
  • 84. •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
  • 85. Axial CECT shows a peripherally enhancing, centrally necrotic mass with surrounding mass effect and midline shift. There is uncal herniation and early entrapment of the ventricular system. GBM. Single voxel MRS shows elevated Cho and decreased NAA. Note the lactate doublet at 1.33 (arrow), typical of high grade tumors. Patient with a history of AA that progressed to GBM.
  • 86. 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 CNS lymphoma -Periventricular enhancing mass.Often crosses corpus callosum. Typically isointense/hypointense on T2W.Necrosis common in AIDS related lymphoma.  Anaplastic astrocytoma (AA) -Often nonenhancing white matter mass. Enhancement may indicate degeneration to GBM.
  • 87.  On Imaging:  CT:  Well circumscribed, hypodense lesions with heavy calcification  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
  • 88.
  • 89.  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
  • 90. 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
  • 91. 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
  • 92.  Distinct type of (usually) benign supratentorial astrocytoma found almost exclusively in young adults. Presentation  Majority with long-standing epilepsy, often partial complex seizures (temporal lobe)  Other signs/symptoms: Headache, focal neurologic deficits Age  Tumor of children/young adults  2/3 < 18 years. Location  Peripherally located hemispheric mass, often involves cortex and meninges.  98% supratentorial-Temporal lobe most common.
  • 93. General Features  Best diagnostic clue- Supratentorial cortical mass with adjacent enhancing dural "tail“.  Cyst and enhancing mural nodule typical. CT Findings  Cystic/solid mass: Hypodense with mixed density nodule  Solid mass: Variable; hypodense, hyperdense or mixed. Minimal or no edema is typical. Ca++, hemorrhage, frank skull erosion rare.  Strong, sometimes heterogeneous enhancement of tumor nodule. MR Findings  TlWI-Mass is hypointense or isointense to gray matter.  T2WI-Hyperintense or mixed signal intensity mass  Cystic portion isointense to CSF. Surrounding edema rare
  • 94.  T1 C+- Enhancement usually moderate/strong, well-delineated  Enhancement of adjacent meninges, dural"tail"common (approximately 70%)  Enhancing nodule often abuts pial surface.
  • 95. Axial and coronal FLAIR, T2W and T1C+ scans showing solid cystic mass with ehhancing mural nodule.
  • 96. 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 remodel calvarium 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
  • 97.  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).
  • 98. General Features  Best diagnostic clue: Partially cystic, enhancing,cortically-based mass in child/young adult with TLE. CT Findings  40% hypodense,30% mixed hypodense (cyst), isodense (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. MR Findings  TIWI-Mass is hypo to isointense to gray matter.  T2WI-Hyperintense, heterogeneous.  Tl C+:Variable enhancement, usually moderate
  • 99. Axial FLAIR MR shows a cortically- based hyperintense mass in the right frontal lobe. Note the lack of edema and mass effect. Coronal T1 C+ MR shows a temporal lobe circumscribed cystic and solid mass with intense enhancement of the mural nodule (arrow). Long history of temporal lobe epilepsy. Ganglioglioma.
  • 100. (Left) Axial T2WI MR shows a hyperintense temporal lobe 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+ MR shows a cystic and solid temporal lobe mass with marked enhancement of the solid portion, a typical enhancement pattern of ganglioglioma.
  • 101. Best diagnostic clue: Well-demarcated, wedge-shaped "bubbly" intracortical mass in young patient with longstanding partial seizures Location  Temporal lobe (often amygdala/hippocampus) most 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)
  • 102.  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
  • 103. Non-enhanced CT scan reveals a parietal lesion with calcific hyperdensity. Calvarial remodeling is evident on bone window CT scan.
  • 104. MRI axial images showing multicystic lesion in the right temporal lobe which appears (A)hypointense on T1, (B and C) Hyperintense on T2 and FLAIR, (D) No significant enhancement on contrast imaging A B C D
  • 105. DNET Axial T2WI MR in a 5 year old with seizures shows multicentric, "bubbly", DNET with involvement of the body of the caudate nucleus (arrow). Axial T2WI MR shows bubbly temporal lobe DNET expanding involved gyri and remodeling the inner calvarial table (arrow).
  • 106. 23 May 2016 106 ■ General characteristics – Solid, cystic, or combination – Classically described as globular/ exophytic suprasellar mass ■ 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
  • 107. Radiology Vol. 243, No. 2: 539-550 ©RSNA, 2007
  • 108.  Age and clinical feature should always considered.  Neuroradiology provides details of the structural pathology, the functional and physiological data.  MRI is the choice of neuroimaging; CT still has a role.  MRI (FLAIR) increases the conspicuity of lesions at brain- CSF interfaces.  MRI (STIR) suppresses fat, which is useful for skull base and orbital imaging.  fMRI and DTI decide the surgical approach.  Advanced imaging helps in narrowing the D/Ds  Good preoperative work up & team approach is key to success.