Basic and advanced imaging in adult gliomas

BASIC AND ADVANCED
IMAGING IN ADULT GLIOMAS
DR. KANIKA BHARGAVA
P.G RESIDENT
MD RADIODIAGNOSIS

GLIOMAS
• Heterogeneous group of neoplasms.
• Earlier, tumours of putative glial cell orgin were called “glioms”
• Primary brain neoplasm arise from pluripotent stem cells (NSCs), which persist in
two areas:
Subventricular zone
Dentate gyrus of hippocampus
• Neuropil contains several subtypes of glial cells:
Astrocytes
Oligodendrocytes
Ependymal cells
Choroid plexus

ASTROCYTOMAS
• CLASSIFICATION ( histologic criteria + genetic parameters):
 LOCALIZED ASTOCYTOMAS
 IDH-MUTANT ASTROCYTOMAS
 IDH-WILD-TYPE ASTROCYTOMAS
 HISTONE H3 MUTANT GLIOMAS
• GRADING:
 Grade 1: low proliferative potential
 Grade 2(Diffuse astrocytomas): tumours with cytologic atypia alone
 Grade 3(anaplastic astrocytoma): anaplasia + mitotic activity
 Grade 4 (glioblastoma): additionally demonstrate microvascular proliferation (endothelium multilayering)

PILOCYTIC ASTROCYTOMAS
• Also called “juvenile pilocytic astrocytoma” or “cystic cerebellar astrocytoma”
• It is a well circumscribed, typically slow growing tumour of young patients.
• WHO Grade I tumours
• ETIOLOGY: Can be syndromic or sporadic:
NF-1 associated pilocytic astrocytomas : optic pathway gliomas
: NF-1 gene mutation
Sporadic : BRAF gene fusion
• AGE: middle age children (5 to 15 yrs)
• No sex predilection

LOCATION
• Cerebellum (60%, most common)
• Optic nerve/chiasm
• Hypothalamus/3rd ventricle 2nd most common
• Pons
• Medulla 3rd most common
• Tectum
• Cerebral hemispheres (uncommon)

IMAGING
• Image findings vary with location.
• Posterior fossa PA – most common appearance is “ well-delineated cerebellar cyst with a
mural nodule”
• PA around optic nerve/chiasm, 3rd ventricle and tectum –
solid, infiltrating and less well-marginated
expand the affected structures
PA in tecum can cause acqueductal obstruction
• Hemispheic PA : cortically based lesion, usually a cyst with a mural nodule

NCCT AND CECT
• Mixed solid/cystic or solid mass
• Focal mass effect
• Little adjacent edema
• Calcification (10-20%)
• Hemorrhage (uncommon, think about
PMA)
• Most PA s enhance on CT and MR
• “Non-enhancing cyst with a strongly
enhancing mural nodule” is the most
common appearance for posterior fossa
Pas
• 40% show solid enhancing mass with
central necrosis
• 10% solid homogenous enhancement

CECT
• CT of the brain demonstrates a large
partially cystic mass in the right
cerebellar hemisphere.
• 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 prepontine and
perimesencephalic cisterns
obliterated.

MRI
• T1
• solid component: iso to hypointense compared to adjacent brain
• cystic component: ~fluid signal unless hemorrhage
• T1 C+
• vivid contrast enhancement
• the cyst wall enhances in ~50% cases
• T2
• solid component: hyperintense compared to adjacent brain
• cystic component: high signal
• T2*:
• signal loss if calcification or hemorrhage present
• FLAIR:
• Cystic component: do not completely suppress on FLAIR
• Solid: hyperintense on FLAIR

• A large partially cystic mass
has its epicenter in the right
cerebellar hemisphere,
displacing and effacing the
fourth ventricle, resulting in
hydrocephalus (these ventricles
are far too large for an 8 year
old child).
• The mass has a solid
component, which is nodular,
and slightly hypointense on T1
compared to the cerebellum,
and hyperintense on T2.

It demonstrates bright contrast enhancement.

• Pilocytic astrocytoma.
• A, Axial postcontrast T1W MR image
demonstrates a cyst with an enhancing
mural nodule.
• B, Single-voxel MR spectroscopy (TE =
136) placed in the region of the
enhancing nodule demonstrates a more
ominous-appearing MR spectroscopy
pattern than would be expected for a
grade I lesion.
• Choline level is elevated, NAA level is
reduced, and lactate is
present (paradoxical)

PILOMYXOID ASTROCYTOMA
(PMA)
• Rare variant of pilocytic astrocytoma
• Negative for BRAF and overexpress developmental genes H19, IGH2BP3/IMP3 and DACT2.
• Large, bulky H shaped tumour, relatively well circumscribed masses
• Haemorrhage and necrosis more common
• More aggressive behaviour and frequent cns dissemination, therefore considered WHO Grade II
• AGE: <4 yrs, mean age = 2 yrs
• LOCATION:
 suprasellar region , most common – hypothalamic/optic chiasm extending into temporal lobes
 Cerebral hemispheres (40%)
 Cerebellum and 4th ventricle -RARE

IMAGING
• NCCT :
More often solid
Hypodense
Intratumoral haemorrhage common
(50%)
Calcification – RARE
Contrast-enhanced CT demonstrates a
minimally enhancing, solid, hypothalamic
lesion. Hydrocephalus is present.

Iso to hypointense on
T1W
Hyperintense on
T2/FLAIR
Peritumoral edema is
minimal
20% demonstrate
haemorrhage on
T2*(GRE,SWI)
No restriction on DWI
Strong homogenous
enhancement,
heterogeneous
enhancement if large
size
CSF dissemination
common, therefore
entire neuroaxis is
imaged

PLEOMORPHIC
XANTHOASTROCYTOMA
• WHO Grade II tumour
• BRAF point mutation in 50% cases
• LOCATION: supratentorial hemisphere (temporal>frontal>parietal)
• Superficial cortical based neoplasm
• Presentation: longstanding epilepsy
• Usually solitary lesions
• <3 cm size
• Mean age : 22 yr (tumour of children and young adults)
• Two common imaging patterns:
1. cyst + nodule
2. Solid mass + intratumoral cyst

• Well-delineated, peripheral
• Cortically based mass that contacts the
leptomeninges
• Overlying skull may be thinned or
remodelled
• Calcifications (40%)
• Haemorrhage – RARE
• Mural nodule shows moderate to intense
enhancement on CECT

• T1
• solid component iso to hypointense cf. grey matter
• cystic component low signal
• leptomeningeal involvement is seen in over 70% of cases
• T1 C+ (Gd)
• solid component usually enhances vividly
• T2
• solid component iso to hyperintense cf. grey matter
• cystic component high signal
• on T2 FLAIR sequence, cystic areas show hyperintensity relative to CSF
due to higher protein contents
little surrounding vasogenic edema

• Centered within the lateral
aspect of the right
temporal lobe (middle
temporal gyrus) with a
cortical/subcortical origin
is an intra-axial
multilobulated
predominantly solid mass
with cystic components.
• The solid mass is hypo to
isointense on T1 and
slightly hyperintense on T2
imaging.
• The cystic component is
hypointense on T1 and
hyperintense on T2.

• There is T2/FLAIR signal
abnormality in keeping with
vasogenic edema extending
from the right temporal
lobe into the anterior
parietal lobe, into the
posterior aspect of the sub
insular region and the
lateral aspect of the
posterior limb of the
internal capsule
• On post-contrast imaging,
the solid component of the
lesion enhances vividly with
non-enhancement of the
cystic component. No
evidence of blood products
within the lesion.

DIFFUSE ASTROCYTOMAS
• Also referred to as low grade infiltrative astrocytomas
• WHO Grade II tumours
• Tend to grow slowly but tendency for malignant progression present
• Diffuse astrocytomas are divided into two molecular groups according to IDH status:
IDH mutant
IDH wild-type
If IDH status is unavailable, they are known as diffuse astrocytoma NOS (not otherwise
specified).
• if IDH is shown to be mutated, then 1p19q status must be determined and shown to be
not co-deleted (otherwise, 1p19q co-deleted tumor is now classified as
an oligodendroglioma).

• LOCATION : Cerebral hemisphere (mainly frontal lobes)
• AGE : mid 30s (20 – 50 yr)
• PATHOLOGY:
• Infiltrating lesions
• Illdefined borders
• Enlargement and distortion of invading structures
• Grey- white matter interface is blurred
• Occasional cysts and calcifications seen
• Hemorrhage - RARE

• Ill-defined homogenous mass lesion
hypodense to white matter
• No enhancement on CECT
• A relatively well circumscribed region
of low attenuation centered
immediately deep to the anterior part
of the right insular cortex, displacing
the lentiform nucleus
posteromedially.
• There is no evidence of hemorrhage
and no convincing contrast
enhancement.
• Despite its large size it exerts little
mass effect. The rest of the brain is
unremarkable.

• Frontal lobe predominance
• Infiltrating white matter
• Sparing of overlying cortex
• Moderate mass effect with adjacent gyral expansion
• T1W : hypointense
• T2W/FLAIR : hyperintense
• T2* : blooming if calcification present
• DWI and ADC : No diffusion restriction
• CEMR: No enhancement
• MRS :
choline peak, low NAA peak, elevated choline:creatine ratio
elevated myo-inositol and myo-inositol/creatine ratio
there is lack of the lactate peak seen at 1:33
the lactate peak represents the necrosis seen in aggressive mostly WHO grade IV tumors

• A well defined intra-
axial lesion in the
subcortical white
matter of left high
parietal lobe.
• The lesion is seen as
hypointense on T1W,
hyperintense on T2W
and FLAIR,

• No blooming is seen on
GRE
• No restriction on DWI.
• Poorly enhancing
• No perilesional edema is
noted.
• No evidence of necrosis,
hemorrhage or calcification
are seen in the lesion.
• Mild mass effect is seen in
the form of effacement the
underlying cortical sulci in
the parafalcine area.

• Mild elevation in choline with
decrease in the NAA and creatine
levels are seen within the lesion.
• Increased Choline / Creatine ratio
of 2.04 is seen. No lactate/lipid
peak is seen.
• Imaging and spectoscopic
findings are suggestive of low
grade glioma.

ANAPLASTIC ASTROCYTOMAS
• WHO grade III lesions
• Imaging appearances and prognosis between those of diffuse low-grade astrocytomas (WHO
grade II) and glioblastomas (WHO IV)
• They are classified on the basis of IDH mutation as IDH-mutant, IDH-wild-type and NOS (when
IDH status is unavailable).
• On imaging, these tumors share common features with diffuse low-grade astrocytomas,
however, they tend to present with focal , patchy contrast enhancement.
• AGE: adulthood with a peak incidence between 40 and 50 years of age.
• LOCATION: cerebral hemispheres (frontal and temporal lobes).
• Usually solitary, widely infiltrating lesions with variable sizes

• Ill-defined hypodense left frontal
lesion with no definite
enhancement is nonetheless
suspicious for a brain neoplasm,
most likely a primary tumor and
unlikely to be a metastasis given
the patient's age and pattern of
involvement.

• Intra-axial mass lesion
centered on the left
superior frontal gyrus
measuring 2.7 x 2.6 cm
with cortical expansion and
diffuse surrounding white
matter FLAIR/T2
hyperintense signal change
within the left frontal lobe
with the involvement of the
body of the corpus
callosum

• No susceptibility.
• No definite restricted
diffusion,
• but antero-medially there is
a moderate size region of
postcontrast enhancement
(some areas gyriform) and
with some increased CBV.
• There is resultant mass-
effect with asymmetry of
the left lateral ventricle and
left-to-right shift of midline
structures measuring 4 mm

• Spectroscopy shows
prominant choline peak with
reduction of NAA, increased
mI and mild lactate peak.

GLIOMATOSIS CEREBRI
• is a rare growth pattern of diffuse gliomas that involves at least three lobes by definition, have
frequent bilateral growth and may extend to infratentorial structures .
• There often is an important discordance between clinical and radiological findings, as it may be
clinically silent while it appears as a very extensive process radiologically.
• Importantly, whereas gliomatosis was previously considered a distinct entity since the 2016
update to the WHO classification of CNS tumours it is now merely thought of as a growth
pattern 8.
• Epidemiology
• peak incidence is 20-40 years of age
• Pathology
• . Gliomatosis cerebri growth pattern is seen in all diffuse gliomas and can contain areas of WHO
grade II or III tumours and rarely grade IV 6,7. It is most commonly encountered in anaplastic
astrocytomas 8.

• Classification
• Gliomatosis cerebri can be divided into two types 7:
• type 1: no discrete mass
• usually IDH wild-type 8
• type 2: discrete mass with further diffuse CNS
involvement
• IDH1 mutation more common in this subtype 7
• CT
• CT can be normal as lesions are often isodense to
normal brain parenchyma.
• There is a relative lack of mass effect and distortion
compared to the extensiveness of involvement.
• There may be an ill-defined asymmetry or subtle
hypoattenuation of the involved brain parenchyma.
A single image from a non-contrast CT
demonstrating widespread abnormality
involving both hemispheres. There is white
matter hypodensity, however, the cortex also
appears thickened.

• MRI
• Mass effect and enhancement are often minimal despite large portions of the
being involved. There is a loss of grey-white matter differentiation and diffuse gyral
thickening.
• Diffuse T1 and T2 prolongation throughout both white and grey matter:
• T1: iso to hypointense to grey matter 1
• T2: hyperintense to grey matter 1
• T1C+ (Gd): typically no or minimal enhancement
• DWI: usually no restriction
• MR spectroscopy
• elevated Cho:Cr and Cho:NAA ratios 2
• marked elevation of myoinositol (mI)
• perfusion MR
• low/normal rCBV: correlates with no vascular hyperplasia

• MRI confirms bilateral
abnormalities with high T2
signal within the white matter
and extensive thickening of
the cortex most easily seen
along the medial surface of
the right frontal lobe.
• Changes involve at least three
lobes and are consistent
with gliomatosis cerebri.
T1
T2
FLAIR

GLIOBLASTOMA
• Glioblastomas(GBM) are high grade astrocytomas; they are therefore generally aggressive, largely resistant
to therapy, and have a corresponding poor prognosis.
• WHO Grade IV
• They have a predilection for spreading along the condensed white matter tracts such as corticospinal
tracts and corpus callosum to involve the contralateral hemisphere.
• Primary vs secondary
• Glioblastomas have traditionally been divided into primary and secondary; the former arising de novo
(90%) whereas the latter developed from a pre-existing lower grade tumor (10%).
• These correlate closely to IDH mutation status:
• IDH mutant: generally secondary glioblastoma, almost always MGMT methylated 17
• IDH wild-type: generally primary glioblastoma
• If IDH status is unavailable or indeterminate then currently the diagnosis of glioblastoma NOS (not
otherwise specified) should be made

PRIMARY GBM, IDH-WILD TYPE
• Primary glioblastomas are those that arise de novo, without a pre-existing lower grade diffuse
astrocytoma.
• LOCATION:
• Distributed throughout the cerebral hemispheres
• Preferentially involves subcortical and deep periventricular white matter
• Easily spreads along compact tracts such as corpus callosum and corticospinal tracts
• Vary widely in size
• Spreads quickly and extensively (20% appear multifocal at initial diagnosis)
• AGE: any age, peak age = 60 to 75 yr
• Mean survival <1 yr

IMAGING
General features:
• Demonstrates a thick, irregular, enhancing “rind” of tumour surrounding a necrotic core in majority of cases
• Rare- tumour extends diffusely throughout white matter, no dominant mass present
• Rarer- primary diffuse leptomeningeal gliomatosis- between pia and glia limitans of cortex
CT:
• irregular thick margins: iso to slightly hyperattenuating (high cellularity)
• irregular hypodense centre representing necrosis
• marked mass effect
• surrounding vasogenic edema
• haemorrhage is occasionally seen
• calcification is uncommon
• intense irregular, heterogeneous enhancement of the margins is almost always present

• The mass in the right temporal lobe has a liquid (necrotic) center ( blue * ) surrounded by
a slightly hyperdense irregular rim (yellow arrows) which enhances following contrast
administration. The whole mass is surrounded by low density change in the white matter
(red * ) consistent with edema.
• There is significant mass effect with shift of the brain's midline to the left (dotted green
line).

MRI
• T1
• hypo to isointense mass within
white matter
• central heterogeneous signal
(necrosis, intratumoral
hemorrhage)
• T2/FLAIR
• hyperintense
• surrounded by vasogenic
edema
• flow voids are occasionally seen
T1 FLAIR
T2

• T1 C+ (Gd)
• enhancement is
variable but is
almost always
present
• typically peripheral
and irregular with
nodular
components
• usually surrounds
necrosis

• GE/SWI
• susceptibility artefact on T2* from blood products (or occasionally
calcification)
• DWI/ADC
• solid component
• elevated signal on DWI is common in solid/enhancing component
• diffusion restriction is typically intermediate similar to normal white matter,
but significantly elevated compared to surrounding vasogenic edema (which
has facilitated diffusion)
• ADC values correlate with grade 13
• WHO IV (GBM) = 745 ± 135 x 10-6 mm2/s
• WHO III (anaplastic) = 1067 ± 276 x 10-6 mm2/s
• WHO II (low grade) = 1273 ± 293 x 10-6 mm2/s
• ADC threshold value of 1185 x 10-6 mm2/s sensitivity (97.6%) and specificity
(53.1%) in the discrimination of high-grade (WHO grade III & IV) and low-grade
(WHO grade II) gliomas 13
• non-enhancing necrotic/cystic component
• the vast majority (>90%) have facilitated diffusion (ADC values >1000 x 10-
6 mm2/s)
• care must be taken in interpreting cavities with blood product

• MR perfusion: rCBV elevated
compared to lower grade
and normal brain
• MR spectroscopy
• typical spectroscopic
characteristics include
• choline: increased
• lactate: increased
• lipids: increased
• NAA: decreased
• myoinositol: decreased

• GBM typical imaging features.
Large infiltrative and necrotic
lesion in the right cerebral
hemisphere with heterogeneous
gadolinium enhancement (a),
• low ADC foci mostly in periphery
of the lesion (b and e),
• increased rCBV areas on DSC
perfusion (c and f),
• haemorrhagic deposits and flow-
voids/neoangiogenic zones on
SWI sequence (d)
• and lipids peak on MR
spectroscopy, compatible with
necrosis

PATTERNS OF GBM SPREAD
White matter spread:
• Most common
• Dissemination along compact white matter fibres such as corpus callosum,
fornices, anterior commissure and corticospinal tract
• Supratentorial tumors usually spread in an anterior-posterior direction, and
infratentorial neoplasms more often extend in a craneo-caudal direction.
CSF dissemination
Ependymal and subependymal spread
Skull-dura matastasis
Extra-CNS manifestations

• Butterfly pattern GBM.
Brain MRI (a and b)
demonstrating
heterogeneous lesion
in the corpus callosum,
with irregular
gadolinium
enhancement and
central necrosis,
infiltrating the frontal
lobes.

• Multicentric GBM.
Brain CT (a) and
MRI (b to f)
demonstrating
heterogeneous
lesions in the left
frontal and
temporal lobes,
with non-
homogenous
enhancement and
central necrosis.

• T1 weighted axial MRI(A) and after
IV contrast administration CT (B).
Ependymal spread of GBM.
Leptomeningeal dissemination
of GBM.

SECONDARY GBM, IDH-MUTANT
• Secondary glioblastomas, in contrast, are those which arise from a pre-
existing lower grade diffuse astrocytoma.
• They are relatively uncommon, only accounting for approximately 10% of all
glioblastomas.
• These tumors tend to be less aggressive than primary glioblastomas and they tend
to occur in younger patients .
• Peak age = 45 yrs
• they have a predilection for the frontal lobes .
• Less prominent necrosis
• Significant non-enhancing areas

• Glioblastoma with IDH-mutation status. FLAIR (a), T2WI (b), DWI (c) and T1WI Gd+ (d) sequences
displaying infiltrative lesion with ill-defined borders in the right frontal lobe with mass effect, vasogenic
edema/tumor infiltrative area, and subtle gadolinium enhancement foci.

• GBM IDH-wildtype versus GBM IDH-mutation. Superior line (a to e) showing GBM IDH-
wildtype; Inferior line (f to j) demonstrating GBM IDH-mutated, both with
histopathological and molecular confirmation. ADC values (D and I) were lower in the
GBM IDH-wildtype, corresponding to higher cellularity density.

GLIOSARCOMA
• GBM with glial (gliomatous)and mesenchymal (sarcomatous) differentiation
• PATHOLOGY:
Biphasic tissue pattern: neoplastic glial + metaplastic mesenchymal
2 gross phenotypes:
1. Meningioma-like with superficial location
2. GBM-like with deep location, necrotic centre + hypervascular tumour rind
• Mean age = 60 yr
• Overall survival = 13 months

RADIOGRAPHIC FEATURES
• Gliosarcomas can be very similar to glioblastomas in appearance.
• They are usually broad-based peripherally located lesions with possible direct
dural invasion or only reactive dural thickening (dural tail).
• CT
• Gliosarcomas may be seen on CT as a sharply defined (often due to sarcomatous
component 5), round or lobulated, hyperdense solid mass.
• They can have relatively homogeneous contrast enhancement and peritumoral
edema.
• MRI
• T1: heterogeneous and hypointense mass
• T2: heterogeneous signal due hemorrhagic and necrotic components
• T1C+ (Gd): thick irregular and rim-like or ring enhancement 8

• Cerebral CT-Scan in axial sections before (A) and after (B) contrast showing left
hypodense frontal parasagittal process (arrow), with ring enhacement and
surrounded by a significant perilesional edema (Asterix).

• Cerebral MRI in AXIAL T1-WI
(A) and axial post contrast T1-
WI (B), T2-WI (C), sagittal T1
(D) and coronal post contrast
T1-WI (E)
• showing a left frontal
parasagittal process (arrow), in
which is iso-intense on T1,
hyyperintense on T2-WI, with
peripheral enhancement and
central necrosis, surrounded
by an important cerebral
edema (ring) with a mass
effect on the median-line
structures.

DIFFUSE MIDLINE GLIOMA,
H3 K-27M MUTANT
• Infiltrative high grade glioma with predominantly astroctytic differentiation and K27 mutation.
• Location
• Diffuse midline glioma H3 K27M–mutant can be found throughout the midline structures of the central
nervous system:
• thalamus
• brainstem
• mesencephalic
• pontine: most common
• medullary
• spinal cord
• Any age, Median age of diagnosis of pontine tumors = 7 yrs
• IMAGING
• Enlarged thalamus with T2/FLAIR hyperintensity
• Minimal or patchy enhancement
• Leptomeningeal dissemination or “brain to brain” metastasis common

• DIFFUSE INTRINSIC PONTINE GLIOMAS:
• Diffusely infiltrate the pons “fat pons”
• Indistinct margins
• Hypointense on T1W
• Hyperintense on T2/FLAIR
• Expand anteriorly, enfolding and sometimes
completely engulfing the basilar artery
• Foci of necrosis and intratumoral
may be present
• No or little patchy enhancement

• Multiplanar multisequence MRI
shows the pons is swollen with a
T1 hypointense / T2 hyperintense
mass suggestive of intrinsic
pontine glioma.
• Post-contrast T1 images show
minimal focal enhancement is
present.
• Note absence of hydrocephalus
despite size of mass.
• DWI and spectroscopy confirms
the malignant nature of the
disease.
• MR spectroscopy demonstrates
increased Cho and decreased
NAA.

ADVANCED MRI IMAGING IN
GLIOMAS

FUNCTIONAL MRI
Improved magnetic resonance (MR) imaging techniques have shown much
potentials in evaluating the key pathological features of the gliomas
including;
• cellularity,
• invasiveness,
• mitotic activity,
• angiogenesis, and
• necrosis.

MR IMAGING OF CELLULARITY AND
INVASIVENESS
1. Tumor Cellularity by Diffusion-Weighted Imaging
• measures free water molecular diffusion and has been widely used in the diagnosis
of acute cerebral infarction and in differentiating tumor necrosis from abscess cavity
• high cellularity may impede free water diffusion, resulting in a reduction of apparent
diffusion coefficient (ADC) values.
• Generally, lower ADC values correspond to increased cellularity and high-grade
gliomas
• This correlation is, however, not linear.
• In a study by Higano et al. the minimum ADC varies significantly between WHO
grade III ((1.06 ± 0.21) × 10−3 mm2/sec) and WHO grade IV gliomas ((0.83 ± 0.14) ×
10−3 mm2/sec) at b value of 1000 sec/mm2

• Contrast-enhanced T1-weighted
image shows a glioblastoma with
strong enhancement after
intravenous gadolinium injection.
• (b) The tumor shows decreased
ADC values on ADC map (arrow
in (b)).

2. Tumor Invasiveness by Diffusion Tensor Imaging
• Peritumoral invasion is another index of tumor aggressiveness.
• However, conventional MR imaging cannot accurately evaluate this invasive behavior due
overlapping of the edema and tumor cells.
• The DTI measures direction and magnitude of water diffusion based on the data obtained
from 6 or more gradient directions as opposed to 3 directions in DWI.
• The water movement within the white matter tracts is mainly restricted across the myelin
sheaths, a principal contributor to directionally dependent water diffusion, that is,
anisotropy.
• Mathematic indices such as fractional anisotropy (FA) derived from DTI data can imply
microstructural integrity of brain tissue.
• Further application using fiber-tracking techniques can reveal the relationship between
gliomas and adjacent white matter tracts
• Low-grade gliomas tend to deviate, rather than destruct or infiltrate, the adjacent white
matter. Therefore, FA value is less reduced in low-grade gliomas.

Low-grade gliomas
tend to deviate,
rather than destruct
or infiltrate, the
adjacent white
matter.
Therefore, FA value
is less reduced in
low-grade gliomas.

(a) Contrast-enhanced T1-weighted image
demonstrates a butterfly glioblastoma
involving the genu of corpus callosum with
small areas of low ADC value on ADC map
(arrows in (b)).
(b) On color-coded diffusion tensor imaging, the
normal left-right-oriented red color (arrow in
(c)) is lost due to destruction of the transverse
tracts.

(a) Contrast-enhanced T1-weighted
image shows a necrotic
glioblastoma with rim-like
enhancement.
(b) (b) On FA map, attenuated FA
(arrows) of the adjacent tracts is
shown, indicating tumor infiltration.

(a) Contrast-enhanced T1-weighted image shows
an oligodendroglioma, WHO grade II, in the
left frontal lobe.
(b) (b) Functional MR imaging and DTI
tractography
(c) (c) demonstrate the activation of Broca's area
(arrow in (b)) anterior to the tumor and the
elevated arcuate fasciculus (arrow in (c)),
respectively.
(d) The grey sphere indicates the location of
tumor.

• 3. Non-Gaussian Diffusion Kurtosis Imaging (DKI)
• The computational algorithms of DTI are based on the ideal Gaussian
distribution of water movement.
• However, this is not realistic in vivo as the brain represents a complex
environment where the movement of water is restricted.
• Diffusion kurtosis imaging (DKI) is an extension of the DTI model capable of
measuring the degree of non-Gaussian water diffusion.
• The value of DKI has been shown in a study of Van Cauter et al. with
parameters contributing to better discrimination between high-grade and
low-grade gliomas than with conventional diffusion parameters.

MR IMAGING OF MITOTIC ACTIVITY
• Tumor Activity and Image-Guided Biopsy by Proton MR Spectroscopy
• Proton MR spectroscopy (MRS) can noninvasively measure the brain metabolites in
vivo.
• Some metabolites commonly used in clinical MRS study include but are not limited
to N-acetyl aspartate (NAA, at 2.02 ppm), choline (Cho, at 3.2 ppm),
creatine/phosphocreatine (Cr, 3.0 ppm), lactate (Lac, at 1.33 ppm), lipids (Lip, at 0.9–
1.5 ppm range), and myo-inositol (mI, at 3.56 ppm).
• Although no tumor-specific metabolite has been labeled, the ratios of metabolites
such as Cho/Cr ratio have been used to assess cellular proliferation.

image depicts a glioblastoma
involving the genu of corpus
callosum.
(b) The arrows point two hot spots
(targets) for stereotactic biopsy
based on the regions of increased
Cho/Cr ratios ((b) Cho/Cr map).

image shows a nonenhanced low-
grade astrocytoma in the right superior
frontal lobe with a high mI level on
spectrum of proton MRS (arrow in
(b)).

IMAGING OF ANGIOGENESIS
Perfusion-Weighted MR Imaging
• Malignant gliomas are characterized by high degree of angiogenesis, a marker of histological grading system.
• The principal proangiogenic factor is vascular endothelial growth factor (VEGF), which can result in increased
neovasculature, microvascular permeability, and vasodilatation.
• The neovasculatures in gliomas function abnormally with irregularity of the endothelial lining and disruption of the blood-
brain barrier (BBB).
• The abnormal caliber and number of tumor vessels resulting from abnormal angiogenesis can be histologically measured
by microvascular density or area (MVA), which may represent an independent prognostic biomarker .
• However, the MVA calculation is time consuming and clinically arduous.
• A fast and noninvasive alternative in assessing MVA is dynamic susceptibility-weighted contrast-enhanced (DSC) MR
imaging, which measures changes in tissue T2* following injection of contrast agent.
• DSC MR imaging can generate a series of perfusion parameters, including relative cerebral blood volume (rCBV), referring
to volume of blood in a given region of brain tissue, relative cerebral blood flow, referring to volume of blood per unit
time passing through a given region of brain tissue, and mean transit time, referring to the average time for blood to pass
through a given region of brain tissue.
• Among the parameters, rCBV is generally considered associated with tumor energy metabolism and provides a reliable
estimate of tumor MVA

• Dynamic contrast-enhanced (DCE) MR imaging is another perfusion method, which relies on the relaxivity effects,
rather than the susceptibility effects assessed in DSC method, and measures T1 signal changes following injection
of contrast agent.
• Because gadolinium exerts stronger relaxivity effects than the susceptibility ones, DCE method requires a smaller
amount of contrast agent than DSC method does, allowing multiple repeated studies and better quantitation of
the perfusion parameters
• Tumor neovasculatures tend to have leaky BBB, so the small molecular-weight gadolinium-based contrast agent
readily extravasates, causing underestimation of the tumor rCBV.
• Consequently, the correlation between the rCBV and histologic tumor grading may not be always consistent
unless rCBV is corrected for contrast extravasation.
• Low-grade gliomas usually show no increase in tumor rCBV while high-grade gliomas may demonstrate high rCBV
that in some cases extends outside the contrast-enhancing portion of the tumor.
• Contrast enhancement in tumor may suggest impaired blood brain barrier with leakage of contrast agents into the
extravascular spaces.
• Tumor with relatively intact BBB may show no enhancement.
• Therefore, conventional contrast-enhanced T1-weighted images and rCBV map can complement each other in
outlining tumor extent and differentiating tumor from perifocal edema

(a) FLAIR image shows a hyperintense
low-grade glioma, WHO grade II, without
significant contrast enhancement on T1-
weighted image (b) or increase of the
rCBV (c).

demonstrates a ring-enhancing glioblastoma in
the left parietal lobe with avid increase of rCBV
(b) extending beyond the extent of the contrast
enhancement.

shows a butterfly glioblastoma, involving the
genu of corpus callosum. (b) The right aspect of
the lesion appears to be heterogeneously
contrast enhanced. (c) On rCBV map, the
nonenhanced left aspect of the tumor (arrow)
shows high rCBV (arrow in (c)). This helps
differentiate tumor infiltration from perifocal
edema.

• Capillary Permeability Imaging
• In addition to MVA, capillary permeability is another feature of angiogenesis in high-grade
gliomas.
• MR imaging is capable of estimating the capillary permeability based on measuring the
contrast leakage rate between the intravascular and extravascular spaces, known as the
contrast transfer coefficient (K trans).
• K trans generally correlates with histological grading and length of survival in gliomas.

(a) Contrast-enhanced T1-weighted image depicts
a nonenhanced astrocytoma, WHO grade II. (b)
The K transmap shows consistently no leakage of
contrast medium in the tumor region, suggesting
a low grade.

An anaplastic
oligodendroglioma, WHO grade
III, in the left frontal lobe shows
contrast enhancement and
leakage on T1-weighted image
(a) and K trans map (b),
respectively.

MR IMAGING OF TUMOR
NECROSIS
• Contrast-Enhanced T1-Weighted Imaging and Proton MRS
• Necrosis is the hallmark of glioblastoma and is caused by tumor hypoxia as a result
of increased cell proliferation and mitotic activity, as well as insufficient tissue
perfusion.
• On conventional contrast-enhanced T1-weighted images, tumor necrosis can be
easily diagnosed with the fact that necrotic zones are typically less enhanced,
giving the tumor an appearance of irregular rim enhancing mass.
• However, imaging diagnosis of necrosis can be problematic in early stages or in
micronecrosis in which the necrotic region may show to be enhanced or not
enhanced at all.
• MRS is an imaging tool of choice to show characteristic metabolites accumulated
in the necrotic regions, even when necrosis is not overtly seen on contrast-
enhanced T1-weighted images.
• The anaerobic glycolysis and cell death with membrane breakdown in the hypoxic
tumor can be revealed by the increased Lac and Lip peaks on MRS.

demonstrates a necrotic glioblastoma in
the right parietal lobe with increased
rCBV
(b) (b) in the periphery of the tumor and
peritumoral regions.
(c) (c) A single-voxel MRS, echo time
135 ms, obtained from region 1 of
increased rCBV (b) shows a high Lip
peak, suggesting micronecrosis.
(d) (d) MRS obtained from the region 2 of
low rCBV (b) depicts an inverted Lac
peak, representing hypoxia in the necrotic
region.

OLIGODENDROGLIOMAS
• 3rd most common glial neoplasm
• WHO classification of CNS tumors, therefore, recognizes four diagnoses related to
oligodendrogliomas:
• Oligodendroglioma (WHO grade II): IDH-mt, 1p19q co-deleted
• anaplastic oligodendroglioma (WHO grade III): IDH-mt, 1p19q co-deleted
• oligodendroglioma NOS (WHO grade II): IDH and 1p19q indeterminate
• anaplastic oligodendroglioma NOS (WHO grade III): IDH and 1p19q indeterminate
• In addition, oligoastrocytomas are also recognized

OLIGODENDROGLIOMA,
IDH-MUTANT AND 1P/9Q CODELETION
• Ogs are primary tumour of adults, mean age = 35-55 yrs (peak
=40-45 yr) with moderate male predominance.
• Diffusely infiltrating, slow growing gliomas, but locally aggressive
• WHO Grade II
• Arise in the grey-white matter junction
• 85-90% supratentorial (most common site- frontal lobe(50-65%))
• Ogs in children occur unusual sites- posterior fossa and spinal
cord
• Microscopically, “fried-egg” appearance with network of delicated
angulated capillaries “chicken-wire” pattern is present.
• 5 yr survival 80%
• Local recurrence after resection is very common

IMAGING
• Seen as round or oval, relatively sharply
delineated masses that involve the cortex
and sub-cortical white matter
• On CT:
 Peripheral and cortically based
 Focal gyral expansion
 Thinning and remodelling of overlying
calvaria is common
 2/3rd are hypodense and 1/3rd are mixed
density patterns
 Coarsed nodular or clumped calcification
(70-90%)
 Gyriform calcification highly suggestive
 Cystic degeneration (20%)
 Gross haemorrhage and peritumoral edema
is less common
 Enhancement varies from none to
moderate
 Patchy multifocal enhancement (50%)

MRI
• Hypointense to grey matter on T1W
• Heterogeneously hyperintense on T2/FLAIR
• Vasogenic edema is uncommon
• T2* blooming present (calcification)
• Moderate heterogenous enhancement seen in 50% cases
• Do not restrict on DWI
• MRS: elevated choline and decreased NAA
• Perfusion MR: high relative cerebral blood volume (rCBV) that reflects prominent “chicken-wire”
vascularity, therefore elevated rCBV doed not necessarily indicate high grade histopathology!!

• Left frontal lobe intra-axial lesion that
involves cortex as well as subcortical
white matter, expanding both, with
moderate regional mass effect,
compressing the frontal horns of the
lateral ventricles and effacing regional
sulci.
• Bowing of the anterior aspect of the
falx cerebri approximately 7.5 mm to
the right.
• No hydrocephalus.
• Scattered within the tumor are small
nodular areas of contrast
enhancement, particularly at the
medial aspect and at the rim, with no
discrete mass enhancing mass
demonstrated.
• There are also multiple prominent
vessels seen traversing the tumor, felt
to be sulcal. Surrounding T2 FLAIR
hyperintensity in the left frontal lobe.

• The rim of the tumor also demonstrates
restricted diffusion (ADC 600-800 x 10^-6
mm^2/s).
• There are areas of susceptibility artefact
within and surrounding the tumor, some
representing products of blood
degradation.
• A small amount of calcification is probably
also present within the lesion.
• The contrast enhancing components show
increased rCBV, again more noticeably at
the medial aspect.
• MRS through the enhancing components
also shows increased choline, increased
lipid/lactate and slightly reduced NAA.

ANAPLASTIC
OLIGODENDROGLIOMA (AO)
• IDH-mutant and 1p/19q codeletion OG with focal or diffuse histologic features of anaplasia.
• Can develop de-novo or arise from progression of pre-existing WHO grade II gliomas.
(mean progression time = 6-7 yrs)
• WHO Grade III tumours
• Mean age= 50 yrs
• Preference for frontal lobe, temporal lobe is 2nd most common site
• Imaging of AO similar to OG but,
• Peritumoral edema , haemorrhage and foci of cystic degeneration are more common
• Variable enhancement from none to striking
• rCBV is misleading as OGs are quite vascular
• MRS: Cho/Cr ratio >2.33 is s/o AO

• Anaplastic oligodendroglioma. (a) Axial CT image shows a heterogeneous mass with
both cyst-like and calcified components (arrows). Extension through the corpus
callosum with involvement of both frontal lobes is seen. (b) Axial contrast-enhanced
CT image shows ringlike enhancement of the cystlike portion (arrowheads).

• Anaplastic oligodendroglioma. (a) Axial T1-weighted MR image shows a mass in the
right temporal lobe (arrows) with both soft-tissue and cystlike components. (b) Axial
T2-weighted MR image shows heterogeneity of the mass and minimal surrounding
vasogenic edema. (c) Axial contrast-enhanced MR image shows irregular ring-like
enhancement of the mass (arrowheads). This appearance mimics that of a
glioblastoma multiforme.

CLASSIFICATION
• Ependymomas are WHO grade II tumors, with more histologically aggressive tumors denoted WHO
III (anaplastic ependymoma),
• In the current (2016 update) WHO classification of CNS tumors the following entities are accepted as
belonging to the ependymoma family of tumors 11:
• WHO grade I
• subependymoma
• myxopapillary ependymoma
• WHO grade II
• ependymoma -
• papillary ependymoma
• clear cell ependymoma
• tanycytic ependymoma
• RELA fusion-positive (a new entity in 2016 update)
• WHO grade III
• anaplastic ependymoma
• Note: the 2016 update to WHO classification of CNS tumors has deleted the variant cellular
ependymoma as it was felt that it overlapped that of a standard ependymoma too closely

• Ependymomas represent a relatively broad group of glial tumors most often
arising from the lining the ventricles of the brain or the central canal of the spinal
cord
• Ependymomas can occur anywhere within the neuraxis, but distribution is not
1. posterior fossa: 60%
1. molecular subgroups: Posterior Fossa A and Posterior Fossa B
2. supratentorial ependymoma: 30%
1. molecular subgroups: RELA fusion and YAP1 fusion
3. spinal cord/canal: 10%
1. spinal cord ependymoma
2. myxopapillary ependymoma

• Each molecular subgroup has different epidemiological profile:
• infratentorial
• Posterior Fossa A
• M:F = 2:1
• age: young children
• Posterior Fossa B
• M:F = 1:1
• age: older children and teenagers
• supratentorial
• RELA fusion
• M:F = 2:1
• age: older children
• YAP1 fusion
• M:F = 1:3
• age: <3 years of age
• Microscopically, these tumors are characterized by well-
differentiated cells. Characteristic features include ependymal
rosettes, i.e tumour cells arranged radially around blood vessels
It shows true ependymal rosette
consisting of tumor cells
arranged around well-defined
lumens forming gland-like
structures.

IMAGING
General features:
• INFRATENTORIAL
Well delineated “plastic” tumours
Typically rise from floor of 4th ventricle
Extend laterally through Foramen of
Luschka to CPA cistern
Extend posterior-inferiorly through
Foramen of Magendie to cisterna
magna
Obstructive hydrocephalous
CSF dissemination
Cysts, calcification haemorrhage more
common
• SUPRATENTORIAL
Large, bulky, aggressive looking
hemispheric tumours

CT
• Generally mixed density
on NCCT
• Hypodense intratumoral
cysts intermixed with iso
and hyperdense soft
tissue portions
• Coarse calcifications
(50%)
• Macroscopic
haemorrhage (10%)
• Mild to moderate
heterogenous
enhancement
A large rounded mass is present in the posterior fossa, centered on the
fourth ventricle. Centrally it is of high attenuation, consistent with
hemorrhage. Following administration of contrast, moderate
enhancement of the solid component is seen.
There is marked obstructive hydrocephalus and a little blood is also seen
pooling in the occipital horns.

MRI
• T1
• solid portions of ependymoma typically are isointense to hypointense relative to white matter
• T2
• hyperintense to white matter
• more reliable in differentiating tumor margins than non-contrast T1-weighted images (but less reliable than contrast
enhanced T1)
• T2* (e.g. SWI)
• foci of blooming from hemorrhage or calcification
• T1 C+ (Gd)
• enhancement present but heterogeneous
• enhancement with gadolinium is useful in differentiating tumor from adjacent vasogenic edema and normal brain
parenchyma
• DWI/ADC
• restricted diffusion may be seen in solid components, especially in anaplastic tumor
• diffusion should be interpreted with caution in masses with significant hemorrhage or calcification
• MRS
• Choline peak elevation according to the cellularity of tumor
• NAA peak reduction
• elevated Cho/Cr ratio
• lipid and lactate rise when degeneration occurs

• Classic MRI appearance of posterior
fossa ependymoma in a 2-year-old
child. Fourth ventricular mass
demonstrates
• a low T1 signal intensity,
• b predominantly solid enhancement
on postgadolinium T1-weighted
images, and
• c heterogeneous T2 hyperintensity.
• d Sagittal postgadolinium T1-weighted
image demonstrates extension inferior
through the foramen of Magendie
onto the posterior aspect of the upper
cervical cord, a feature that is highly
suggestive of ependymoma

• Axial and sagittal T2-weighted images
through a typical fourth ventricle
ependymoma demonstrate signal
intensity similar to gray matter
throughout most of the lesion.
• Extension through the foramina of
Luschka is demonstrated by black
arrowheads in a and white
arrows in b and d, and
• extension through foramen of
Magendie by black arrows in e.
• Dashed lines in a indicate planes at
which sagittal images (b, d) are
located.
• The lesion insinuates around and
encases vessels, as shown in c and f.
• Cystic/necrotic areas (black
arrows in aand d) are closer to
cerebrospinal fluid signal intensity

• Supratentorial ependymoma in a
10-year-old girl on a noncontrast
CT, b T2-weighted, c FLAIR,
and d–fpostgadolinium T1-
weighted MRI.
• Unlike posterior fossa
ependymomas, most
supratentorial ependymomas
(70%) are extraventricular in
origin.
• Supratentorial ependymomas
usually demonstrate more
heterogeneous T1 and T2 signal
than their infratentorial
counterparts, due to a greater
tendency toward cyst formation,
calcifications, and hemorrhage.
• Avidly enhancing areas are
generally present, but are often
intermixed with poorly or
nonenhancing areas

• Perfusion MRI can be performed using several techniques, including T2*-
weighted dynamic susceptibility and fast spoiled gradient-echo techniques, which
require bolus administration of gadolinium contrast, and
• arterial spin labeling, which does not require gadolinium.
• When performed, perfusion MRI of ependymoma generally demonstrates
markedly elevated cerebral blood volume and, unlike many other glial neoplasms,
poor return to baseline that may be attributable to fenestrated blood vessels and
an incomplete blood–brain
• Proton MR spectroscopy usually demonstrates elevated choline and reduced N-
acetylaspartate (NAA) in ependymomas, as in many other brain tumors.
• MR spectroscopy is currently used primarily to differentiate tumor recurrence from
postradiation or posttreatment change rather than to confirm a histologic
diagnosis [

• Supratentorial ependymoma
on a postgadolinium T1; b FLAIR (inset:
noncontrast CT); c diffusion-weighted
images (DWI); d apparent diffusion
coefficient; and e perfusion MRI
with f cerebral blood volume
measurements.
• DWI demonstrates reduced diffusion
within the soft tissue components of some
ependymomas due to high cellularity.
• Perfusion-weighted imaging generally
demonstrates elevated blood volume
within the tumor, with poor return to
baseline likely attributable to lack of a
blood–brain barrier.

• Supratentorial grade 2
ependymoma in a 12-year-
old girl.
• a Axial FLAIR, b axial
perfusion MRI, cpostcontrast
axial T1, d axial cerebral blood
volume map derived from
perfusion MRI, e axial ADC
coefficient, and f perfusion
MRI T2*-weighted dynamic
susceptibility curves

ANAPLASTIC
EPENDYMOMA
• Anaplastic ependymoma in a 2-
month-old infant who presented with
increasing head circumference.
• T2-weighted sequences in a and c and
postgadolinium T1-weighted
sequences in b, d, e, and f.
• This tumor is characterized by multiple
cysts, heterogeneous postcontrast
enhancement, and large size resulting
in severe obstructive hydrocephalus.
• c, d Upward extension of the tumor
through the tentorial incisura

• Leptomeningeal and multiple intraventricular
metastases discovered 13 months after
treatment of a posterior fossa ependymoma
in a 2-year-old girl.
• Although initial MRI of the lumbar spine was
suggestive of possible leptomeningeal
disease, CSF cytology was negative.
• a) Original coronal FLAIR images at time of
diagnosis.
• b) Sagittal and c), d) axial postgadolinium T1-
weighted images of the lumbar spine at time
of diagnosis.
• e) Thirteen months later, the resection site of
the original fourth ventricular tumor
demonstrates no evidence of locally
recurrent disease.
• f) However, multiple intraventricular
leptomeningeal metastases are seen and
may have been attributable to CSF spread at
the time of initial diagnosis

SUBEPENDYMOMA
• Rare, benign, slowly-growing, non-invasive tumour
• Incidental finding
• WHO Grade I
• Middle age and older adults, children –very rare
• Solitary
• <2 cm in size, some upto several cm
• LOCATION:
Most common- frontal horn of lateral ventricle (50%), near foramen of monro
where they are attached to septum pellucidi
Fourth ventricle
Occipital horn of lateral ventricle

IMAGING
• General Features:
• Well-demarcated nodular masses
• May expand the ventricle
• Little mass effect
• Larger lesions may cause obstructive
hydrocephalous
• On CT:
• Iso to slightly hypodense
• Calcification and intratumoral cysts may
be present
• Haemorrhage – RARE
• Little or No enhancement on CECT
No intracranial hemorrhage identified. Grey white matter
differentiation is preserved. An irregular, heterogenous,
27 mm, intraventricular mass is seen within the right
lateral ventricle, possibly arising from the
septum pellucidum. It does not show calcification. Mild
prominence of the right lateral ventricle is probably due
to normal asymmetry.

• Hypo to isointense on T1W
• Intratumoral cysts are common in
larger lesions
• Heterogeneously hyperintense on
T2W/FLAIR
• Peritumoral edema is usually absent
• T2*(GRE,SWI) may show “blooming”
foci (secondary to calcification)
• Haemorrhage (10-12%)
• Enhancement- none or mild to
moderate
• No restriction on DWI
• MRS: Normal choline with mildly
decreased NAA

MYXOPAPILLARY EPENDYMOMA
• Very slow growing tumor
• Mostly in young adults
• Almost exclusively a tumor of conus medullaris,
cauda equina and filum terminale
• On MRI scan (T1 weighted, post-contrast), two
tumors can be seen.
• The larger of the two (yellow arrow) is located at L2
level just below the conus medullaris.
• The smaller tumor (blue arrow) is located in the
thecal cul-de-sac.
• The patient underwent laminectomy and resection
of the larger tumor, both for symptom relief and
diagnosis.
• Histology revealed typical myxopapillary
ependymoma (WHO Grade 1).

CLASSIFICATION
• 3 HISTOLOGICAL SUBTYES:
1. Choroid plexus papilloma (CPP)
2. Atypical choroid plexus papilloma (aCPP)
3. Choroid plexus carcinoma (CPC)
• MOLECULAR SUBGROUPS(methylation profiling):
Pediatric low-risk choroid plexus tumours (CLUSTER 1)-
Young age
Supratentorial location
Adult low-risk choroid plexus tumours (CLUSTER2)-
Adult age
Infratentorial location
Pediatric high risk choroid plexus tumours (CLUSTER3)-
Young age
Supratentorial location

CHOROID PLEXUS PAPILLOMA
• Most benign choroid plexus neoplasm
• CPPs are well circumscribed papillary or cauliflower-like masses that may adhere to but
usually do not invade the ventricular wall.
• Cysts and haemorrhage are common.
• Location: There is strong effect of age on CPP location
In infants- atrium of lateral ventricle (80%)
In adults- 4th ventricle and CPA cisterns
In older patients- lateral ventricles (rare)
• Usually solitary lesion
• Size varies from small to huge masses

• Median age of presentation:
• 1.5 years for lateral and 3rd ventricle
• 22.5 years for 4th ventricle
• 35.5 years for CPA CPPs
• Presentation:
• Infants- hydrocephalous
• Children and adults- headache, nausea
vomiting
• CT imaging:
• Iso-hyperdense on NECT scans
• Hydrocephalous
• CECT- shows intense homogenous
enhancement
The mass is relatively well circumscribed, slightly hyperdense
compared to grey matter on CT, and following administration of
contrast demonstrates vivid enhancement.

MRI
• Sharply marginated
lobular mass
• Iso to slightly
hypointense on T1W
• Iso to hyperintense on
T2/FLAIR
• Linear branching
internal “flow-voids”
• T2* may show
hypointense foci
• Intense homogeneous
enhancement
• Do not restrict on DWI
• MRS may show elevated
myo-inositol

CHOROID PLEXUS CARCINOMA
• Rare malignant tumours
• Seen exclusively in young children (<3 years, median age = 18 months)
• WHO Grade III, Methylation cluster 3
• Almost always arise in lateral ventricle
• Heterogeneous, bulky intraventricular tumour with invasion into adjacent brain
parenchyma
• Often displays gross haemorrhage and necrotic foci
• Strong heterogeneous enhancement
• CSF dissemination is common

Transcranial ultrasound demonstrates
hydrocephalus and a large intraventricular mass
located in the trigone of the lateral ventricle on the
left.
CT obtained following insertion of a right sided VP
shunt demonstrates a large vividly enhancing
intraventricular mass, located at the trigone of the
lateral ventricle on the left.

MRI obtained only 2 month later demonstrates the mass to have markedly increased in size with
intraventricular and leptomeningeal spread. The 4th ventricle is now trapped and ballooned.

GANGLIOGLIOMA
• Well-differentiated, slow growing tumours (WHO GradeI)
• Biphasic tumour with variable neuronal and glial elements
• Associated with Turcot syndrome, NF-1 and NF-2
• Location:
Throughout the CNS
Most are located superficially
75% arise in temporal lobe
10% in frontal lobe
15% in posterior fossa (brainstem or cerebellum)
Rare- ventricles, CPA cistern, intramedullary cord
• Solitary lesions
• Size = 1 to 6 cm
• Never metastasize

• AGE: <30 years age(80%), peak age = 15 to 20 years
• No sex predilection
• PRESENTATION: pharmacologically resistant temporal lobe epilepsy (complex
partial type)
• Malignant degeneration is uncommon
IMAGING:
• Cortically based superficial parenchymal lesions
• Two general imaging patterns-
1. A well-defined solid or partially cystic mass with mural nodule
2. Diffusely infiltrating less delineated mass with ill-defined borders and patchy
enhancement (uncommon)

• CT SCAN: varying attenuation
• Cystic component (60%)
• Well-circumscribed hypodense cyst with
isodense mural nodule (30%)
• Primarily hypodense (40%)
• Calcification (30-50%)
• Haemorrhage is rare
• Only 50% enhance following contrast
administration
• Patterns- solid, rim, or nodular to cystic with
an enhancing nodule
• MRI:
• Iso – hypointense on T1W as compared to
cortex
• Hyperintense on T2/FLAIR
• Surrounding edema is absent
• Focal cortical dysplasia adjacent to tumour in
some cases
• Enhancement from none to minimal to
moderate but heterogeneous
• Classic pattern : cystic mass with enhancing
mural nodule

Ganglioglioma is the most common tumor associated with temporal lobe epilepsy.
Calcification is common in ganglioglioma and is an important distinguishing factor from DNET
and pleomorphic xanthoastrocytoma.

ANAPLASTIC GANGLIOGLIOMA
• Rare, aggressive glioneuronal tumour (WHO Grade III)
• Most are malignant transformation of previously diagnosed benign GG
• Composed of = dysplastic ganglion cell + anaplastic (usually glial) component
• Affect children and young adults
• Most are supratentorial
• Most common site is temporal lobe
• Radiological findings are non-specific and overlap those of GG and diffuse
astrocytomas
• Atypical location common (i.e deep rather than cortical)
• Often larger, more infiltrative/poorly demarcated

• Large lesion in the right temporal lobe
with a heterogeneous slightly
hyperdense lobulated mass associated
with a rounded well-circumscribed low
attenuation component in the posterior
superior aspect.
• Moderate enhancement after
administering IV contrast.
• Associated white matter edema,
although the amount of associated
edema is less that what would be
expected for a tumor this size.
• Positive mass effect: near complete
effacement of the right lateral ventricle,
contralateral midline shift of 3mm with
subfalcine herniation
• No overlying bony permeative change.

• Selected MR sequences
through the brain.
Findings:
• Confirms the large lesion
in the right temporal
region with solid and
cystic components.
• Heterogeneous
enhancement of the solid
component, rim
enhancement of the
cystic component.

DESMOPLASTIC INFANTILE
ASTROCYTOMA/GANGLIOGLIOMA
• Rare , usually benign, mostly cystic lesion of young children
• WHO Grade I
• Have aggressive appearance radiologically
• Two histologic forms:
1. Desmoplastic infantile astrocytoma (DIA)
2. Desmoplastic infantile ganglioma (DIG)
• Because elements of both types are often present in a single lesion, WHO considers DIA/DIG
a single tumour entity
• Large, bulky, supratentorial hemispheric masses with mean diameter aproaching 8 cm.
• They are sharply demarcated, mixed cystic-solid tumours that involve superficial cortex and
adjacent leptomeninges (appears attached to the dura)

• Common sites: Frontal and parietal lobe
• AGE: <5 years, large majority within 1st year of life
• Presentation : intense head circumference with tense bulging fontanelles in a
lethargic infant with “sunset eyes”
• Benign prognosis, very rarely metastasizes
• IMAGING:
• Massive, heterogeneous peripherally located mixed cystic-solid suratentorial mass.
• Cystic portion is relatively deep inside the hemispheric white matter
• Solid portion is typically peripheral, often directly abutting the dura

• Large, multiseptate cystic mass located predominantly in the right frontal and
temporal lobes, causing right lateral ventricular compression and subfalcine
herniation

• Large tumor that consists of both
enhancing solid component and multiple
cystic components with marked
surrounding edema, centered within the
right frontal lobe.
• It causes subfalcine herniation to the
left and obstructs the third ventricle at
the level of foramen of Monro resulting in
marked hydrocephalus Mass effect on
mid-brain causing shift of mid-brain to
the left and uncal herniation is noted.
• MR spectroscopy obtained from solid
enhancing component of the lesion
demonstrates markedly increased choline
peak, consistent with high cellularity of
this mass. NAA peak is not seen. The solid
components of the tumor have restricted
diffusion.

DNET
• Dysembryoplastic neuroepithelial tumour is a benign, usually
cortically based lesion with multinodular architecture.
• Often associated with cortical dysplasia
• WHO Grade I
• LOCATION: any part of supratentorial cortex
Temporal lobes (45-50%)
Frontal lobe (1/3rd)
Rare- lateral ventricle
• Solitary lesion
• Variable sizes from few millimetres to several centimetres
• Intracortical tumours that thicken and expand the gyri
• Malignant transformation is rare
• Tumour of children and young adults (<20years)

• Presentation: pharmacologically resistant partial complex
seizures
• Little or no growth over time.
• IMAGING
• A well demarcated, triangular, “pseudocystic” or “bubbly”
cortical/subcortical mass in young patients with long
standing partial epilepsy
• “points” towards ventricle
• CT scan:
• Hypodense cortical/subcortical mass
• Gross intratumoural haemorrhage – rare
• Focal bony scalloping or calvarial remodelling is common (
if tumour is adjacent to inner table of the skull)

MRI
• Multilobulated, hypointense, “bubbly” cortical mass that may involve subcortical
white matter on T1W
• Strikingly hyperintense on T2W images with multicystic or septated appearance
• on FLAIR a characteristic, hyperintense rim along tumour periphery is present in
75% cases
• Peritumoural edema is absent
• Blooming on T2 * occurs in few cases ( calcification>haemorrhage)
• Little on no enhancement on T1+C, when present mild or nodular punctate
pattern
• MRS : decreased NA without elevated choline or Cho:Cr ratio

• Multiple MR images demonstrate a multilobulated multiseptated nonenhancing mass in
the left occipital lobe. The mass is not associated with surrounding edema. No
hemorrhagic change or restricted diffusion is confirmed.

Basic and advanced imaging in adult gliomas

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