Normal & abnormal radiology of brain part iv

Normal and Abnormal
Radiology of CNS (Part IV)
Mohammed Fathy Bayomy, MSc, MD
Lecturer
Clinical Oncology & Nuclear Medicine
Faculty of Medicine
Zagazig University

Approach To
Brain (Intra-Cranial)
Tumours

** benign vs. malignant distinction less clinically relevant for intracranial tumors
(mass effect, infiltration preventing removal, critical location)
Brain Neoplasm
Primary Metastatic
Extra-axial Intra-axial
Neural Glial
Meningioma
Astrocytoma
Ependymoma
Oligodendroglioma
Lung (50 %)
Breast (15%)
Melanoma (10%)
The most common primary brain tumors are
Gliomas (50%)
Meningiomas (20%)
Pituitary adenomas (15%)
Nerve sheath tumors (8%)
Classification

(I) Primary Brain Tumors (PBT)
(A) Brain Gliomas
• The most common brain tumors are gliomas, which
begin in the glial (supportive) tissue. There are several
types of gliomas:
• Astrocytomas arise from small, star-shaped cells
called astrocytes.
Glioblastoma multiforme (GBM) accounts for about
50% of all astrocytomas
• Ependymomas: lining of the ventricles.
• Oligodendrogliomas: the cells that produce myelin.
• Brain stem gliomas
Intra-cranial Tumors

• Medulloblastomas always located in the cerebellum,
These fast-growing high-grade tumors represent about
15 - 20% of pediatric brain tumors and 20% of adult
brain tumors.
• Meningiomas grow from the meninges
• Schwannomas are benign tumors that begin in
Schwann cells, which produce the myelin e.g. Acoustic
neuromas
• Craniopharyngiomas develop in the region of the
pituitary gland near the hypothalamus.
• Pituitary Adenomas. about 10% of PBT &are often
benign, slow-growing masses in pituitary gland.
(B) Brain Non-Gliomas

(II) Secondary Brain Tumors
(Brain Metastases)
Metastatic brain tumors are the most common brain
tumors.
Characteristics
• The primary cancer is usually in the lung, breast,
colon, kidney, or skin (melanoma), but can originate in
any part of the body
• Most are located in the cerebrum, but can also
develop in the cerebellum or brain stem
• More than half of people with metastatic tumors have
multiple lesions (tumors)

Differential diagnosis & patient age
Different incidence of suprasellar lesions between adults & children
Common
ADULTS
 Pituitary Macroadenoma
 Meningioma
 Schwannoma
 Saccular aneurysm
 Craniopharyngioma
(squamous papillary)
CHILDRE
N
 Pilocytic Astrocytoma
(adamantinous)
 Optic pathway glioma
 Arachnoid cyst
 Germinoma
 Metastasis
 Dermoid & Epidermoid cyst
 Leukemia & Lymphoma (met)
 Inflammatory/infective disease
 Hemangioblastoma
Less Common/Rare
 Hamartoma
 Inflammatory/infective disease
 Arachnoid cyst
 Germinoma
 Lipoma
 Pituitary stalk anomalies/Ectopic
neurohypophisis
 Teratoma
 Aneurysm
 Pituitary Macroadenoma
 Leukemia/Lymphoma (1ry)

10 20 30 40 50 60
Oligodendroglioma
Ependymom
a
Colloid cyst
Pituitary
Schwannoma
Ependymom
a
Medulloblastoma
Craniopharyngioma
Germinoma
Teratoma
Choroid
plex. pap
Astrocytoma
Hemangioblastoma
Meningioma
Metastases
Age distribution

Common Intra-cranial Tumors
Adult: Pediatric:
 Metastases ++
 Gliomas (25%)
- Fibrillary Astro
- Anaplastic Astro
- Glioblastoma Multi
- Oligodendroglioma
 Juvenile Pilocytic Astro
 PNET (Medulloblastoma)
 Ependymoma
 Brainstem Astrocytoma
 DNET
 Ganglioglioma
Age distribution

< 2 years
 Choroid plexus papillomas.
 Anaplastic astrocytomas.
 Teratomas.
 Medulloblastomas.
 Astrocytomas.
 Ependymomas.
 Craniopharyngiomas.
 Gliomas.
 Metastases: very rare
(neuroblastoma)
Adult
 Metastases (50%).
 Astrocytomas ‘‘GBM’’.
 Meningiomas.
 Oligodendrogliomas.
 Pituitary adenomas.
 Schwannomas.
Astrocytomas occur at any
age, but GBM is mostly seen
in older people.
2-10 years
Age distribution

 Although cancer is rare in children, brain
tumors are the most common type of
childhood cancer after leukemia and
lymphoma.
 Most of the tumors in children are located
infratentorially.
Age distribution

 Metastases are by far the most common.
 It is important to realize that 50% of
metastases are solitary.
 Particularly in the posterior fossa, metastases
should be in the top 3 of the differential
diagnostic list.
 Supratentorially, metastases are also the most
common tumors, followed by gliomas.
Age distribution

NON-NEOPLASTIC
MASSES
CHILDHOOD
M-9 yrs, HAMARTOMA
 Congenital non-neoplastic heterotopias
 Isotense to grey matter on T1WI & T2WI
 They do not calcify, enhance, contain fat
or have cysts
 Clinical presentation (precocious puberty
and gelastic seizures)
F-10 yrs, OPTIC PATHWAY
GLIOMA
NEOPLASTIC
MASSES
 Frequently associated with NF1
 Iso-hypointense on T1WI & moderately
hyperintense on T2WI
 Moderate (variable) contrast
enhancement
 Necrosis, Hge, calcifications are rare
Age distribution

ADULTS
ANY AGE
F-50 yrs
CRANIOPHARYNGIOMA
(Papillary)
 Usually solid or predominantly solid
 Suprasellar location
 Rarely calcifies
CHILDREN
 Mostly cystic/predominantly cystic or rarely
mixed solid-cystic
 Suprasellar or intrasellar/suprasellar
 90% calcifies
M-15 yrs yrs
CRANIOPHARYNGIOMA
(Adamantinous)
Age distribution

It is often not possible to characterize suprasellar masses on the basis of radiological
findings alone > > > age and clinical presentation may drive to a diagnosis
NEUROFIBROMATOSIS type 1 (von Recklinghausen disease or
NF1)
Patients with two or more of following findings:
1) Six or more café-au-lait spots;
2) Two or more Lisch nodules (hamartoma) of
the iris
3) Two or more neurofibromatosis or one or
more plexiform neurofibromas;
4) Axillary/inguinal freckling;
5) One or more bone dysplasia or
pseudoarthrosis of a long bone;
6) A first degree relative with NF1
Correleation with clinical data
From 15% to 40% of patients with
NF1: OPTIC PATHWAY GLIOMAS
The involvement of optic chiasma & optic nerves
(white arrows)
CRANIAL NERVES
DYSFUNCTIONS
e.g. OCCULMOTOR NERVE PALSY
• Outward & downward deviation of the eye
• Ptosis of the eyelid
• Dilatation of ipsilateral pupil in complete
palsy
SCHWANNOMA OF III CRANIAL
NERVE
Intense & Homogenous CE of extra-axial mass
localized to site if III CN (white arrow)

PRECOCIOUS
PUBERTY
Appearance of physical and hormonal signs of
pubertal development at an earlier age than is
considered normal (before age 0f 6-8years for
girls and before age of 9 years for boys
HAMARTOMA
The absence of CE of mass localized in the
mammillary body (red arrow)
KNOWN/UNKNOWN PRIMARY
Breast cancer, melanoma, colorectal cancer.
Headache, cranial nerves dysfunction,
hormonal abnormalities.
INFUNDIBULARY METASTASIS
FROM BREAST CANCER
Intense CE of the mass thickening the stalk
(white arrow)
GELASTIC SEIZURES
Epileptic events characterized by laughter-like
vocalization usually combined with facial
contraction.

OTHER SYSTEMIC DISEASES
Children and young adults with involvement of
one or more body systems such as bone,
lymph nodes, liver, or various soft tissue.
LANGERHANS CELL
HISTOCYTOSIS
The thickened stalk with moderate CE after
gadolinium (green arrows)
In some case can occur in adults with
polycythemia and von Hippel-Lindau syndrome
(hemangioblastomas, visceral cysts, and renal
cell carcinoma)
HEMANGIOBLASTOMA
Intense CE (red arrow), the typical T2 signal
hyperintensity with characteristics flow voids in
the lesion (green arrow) and arterial
parenchymal blush in DSA (white arrow)

Abnormal Radiology
of Brain
Mohammed Fathy Bayomy
Assistant Lecturer of Clinical
Oncology Zagazig University

1- Location
 Intra- vs. Extra-axial
 Supra- vs. infra-tentorial.
 White matter vs. cortical based.
 Specific anatomic sites:
* Sella/suprasellar.
* Pineal region.
* Intraventricular.

1- Location
 Determine whether mass arises from within
brain parenchyma (intraaxial) or from outside
the brain parenchyma (extra-axial).
 Extra-axial tumor: mass lies outside the brain,
so the tumor not originate from brain but
derived from the lining of the brain or
surrounding structures, 80% of these extra-
axial lesions will be either a meningioma or a
schwannoma.
Extra-axial vs Intra-axial

1- Location
 Intra-axial tumor: mass lies inside the brain,
so the tumor originate from brain itself, in
adult will be a metastasis or astrocytoma in
75% of cases.

1- Location
Narrows CSF space
Displaces cortex toward periphery
Widens CSF space
Displaces brain deeper
Broad base toward dura

1- Location
INTRA-AXIALEXTRA-AXIAL
–Glioma
–Medulloblastoma
–Hemangioblastoma
–Metastases
–Meningioma
–Pituitary adenoma
–Craniopharyngioma
–Schwannoma
–Chordoma
–Dermoid/epidermoid cyst
–Lipoma
–Metastases

1- Location
Common Intra-Axial Tumors in Pediatric
Supratentorial: Infratentorial:
 Astrocytoma
 Pleomorphic xanoastro (PXA)
 PNET
 DNET
 Ganglioglioma
 PNET (medulloblastoma)
 Ependymoma

1- Location
Common Intra-Axial Tumors in Adult
 Metastases ++
 Gliomas (25%)
- Fibrillary Astro
- Anaplastic Astro
- Glioblastoma Multiformi
- Oligodendroglioma
 Metastases ++++

1- Location
Extra-Axial
lesions
ADULTS
 Germinoma
(squamous-papillary)
 Leukemia/lymphoma
(metastatic)
 Meningioma
 Schwannoma
 Metastasis
 Epidermoid/dermoid cyst
 Aneurysm
 Infectious/inflammatory
- Pituitary stalk
- Infundibulum
- Meninges
- Vessels
CHILDREN
 Germinoma
(adamantinous)
 Leukemia/lymphoma
(primary)
 Epidermoid/dermoid cyst
 Aneurysm
 Infectious/inflammatory
 Stalk anomalies &
ectopic neurohypophisis
Intra-Axial
lesions
- Optic chiasma
- Hypothalamus
- 3rd ventricle
ADULTS
 Metastasis
 Glioma
CHILDREN
 Pilocytic astrocytoma
 Optic pathway glioma
 Hamartoma
 Lipoma

1- Location
• Variable signal, often isotense to brain
parenchyma on T1WI & T2WI.
• Homogenous, intense enhancement.
• Linear, enhancing dural tail (highly suggestive,
not pathognomonic)
F-45 years
Tuberculum Sellae Meningioma
EXTRA-
AXIALADULT
s
CHILDRE
NM-19 years
Arachnoid cyst
• CSF-like signal in all sequences, without CE
after gadolinium

1- Location
EXTRA-
AXIAL
Signs of extra-axial location
 CSF cleft: widens CSF space
 Displaced and expand subarachnoid space: because
growth of an extra-axial lesion tends to push away the brain.
 Displaced subarachnoid vessels: The subarachnoid vessels
that run on the surface of the brain are displaced by the
lesion.
 Cortical gray matter between mass and white matter:
displaces brain deeper.

1- Location
EXTRA-
AXIAL
Signs of extra-axial location
 Broad dural base: broad base toward dura, typically seen in
meningiomas.
 Homogenous enhancement: not derived from brain tissue
and do not have a blood-brain-barrier.
 Bony reaction: are seen in bone tumors like chordomas,
chondrosarcomas and metastases, can also be secondary,
as is seen in meningiomas and other tumors.

1- Location
EXTRA-
AXIAL
CSF cleft (Definitive sign)

1- Location
EXTRA-
AXIAL
Vessels b/n lesion & brain (Definitive sign)

1- Location
EXTRA-
AXIAL
Cortex b/n lesion & brain (Definitive sign)

1- Location
EXTRA-
AXIAL
Broad based towards calvarium (Suggestive
sign)

1- Location
EXTRA-
AXIAL
Adjacent bone changes (Suggestive sign)

1- Location
EXTRA-
AXIAL
Enhancement of meninges (Suggestive sign)
Meningeal tail

1- Location
EXTRA-
AXIAL
Invade to & through dura

1- Location
EXTRA-
AXIAL
CSF cleft (yellow arrow).
Subarachnoid vessels that run on surface of brain are displaced by the
lesion (blue arrow).
There is gray matter between lesion & white matter (curved red arrow).

1- Location
EXTRA-
AXIAL
• Broad dural base
• Hyperostosis of
adjacent bone
• Homogenous
enhancement

1- Location
EXTRA-
AXIALDifferentiation between intra-axial versus
extra-axial is usually straight forward, but
sometimes it can be very difficult and
imaging in multiple planes may be necessary
Thought to be a falcine meningioma, i.e. extra-axial:
hypointense on T2.
However, there is gray matter on the anteromedial and
posteromedial side of the lesion (red arrow), this
indicates that the lesion is intra-axial.
If the lesion was extra-axial the gray matter should
have been pushed away.

1- Location
INTRA-AXIAL
 Intra-axial is a term that denotes
lesions that are within the brain
parenchyma
 Some authors include intra-
ventricular lesions in the intra-axial
group as most are lesions that
arise from the brain parenchyma
and grow exophytically into
ventricular system.

1- Location
• A linear ependymal enhancement is evident in
III ventricle anterior recesses.
• Pineal recess nodular localization &
leptomeningeal spread
F-45 years, Metastatic Ependymal
intraventricular spread (melanoma)
INTRA-AXIAL
ADULT
s
CHILDRE
NM- 2 years, pilocytic
astrocytoma
• Solid & cystic mass.
• Solid portion T1-hypointense, T2-
hyperintense with strong enhancement.
• Cystic portion present variable T1 & T2 signal
according to protein content.

1- Location
Supratentorial vs Infratentorial
Common Intra-Axial Tumors in Pediatric
 Astrocytoma
 Pleomorphic xanoastro (PXA)
 PNET
 DNET
 Ganglioglioma
 PNET (medulloblastoma)
 Ependymoma

1- Location
Common Intra-Axial Tumors in Adult
 Metastases ++
 Gliomas (25%)
- Fibrillary Astro
- Anaplastic Astro
- Glioblastoma Multiformi
- Oligodendroglioma
 Metastases ++++
Supratentorial vs Infratentorial

1- Location
Suprasellar
SUPRASELLAR
LESIONS
Neoplastic & Non-
neoplastic masses
-Macroadenoma
-Meningioma
-Schwannoma
-Craniopharyngioma
-Pilocytic astrocytoma
-Optic pathways glioma
-Metastasis
-Lymphoma &
Leukemia
-Arachnoid cyst
-Dermoid cyst
-Epidermoid cyst
-Ectopic
neurohypophysis
-Hemangioblastoma
Infectious & inflammatory
lesions
-Granulomatous diseases
-Abscesses/ Hypophyisitis
Vascular anomalies
-Aneurysm Most Common
diagnosis
(big five: >75% of all
suprasellar masses)
-Macroadenoma
-Meningioma
-Aneurysm
-Craniopharyngioma
-Pilocytic astrocytoma

1- Location
Pineal Region
Common Pineal Region
Tumors
 Pineocytoma
 Germ cell tumours
 PNET
 Tectal Glioma
 Meningioma
 Dermoid
 Arachnoid cyst

1- Location
Pineal Region
Differential diagnosis
-Pineocytoma
-Pineoblastoma
-Papillary tumor of pineal gland
-Astrocytoma of pineal gland
-Meningioma near pineal gland

1- Location
Pineal Region
-Pineocytoma
-Papillary tumor of pineal gland
-Germinoma
-Astrocytoma of pineal gland
-Pineal cyst

1- Location
Intraventricular
Common Intraventricular Tumors
 Ependymoma
 Subependymoma
 Central Neurocytoma
 Meningioma
 Giant cell Astrocytoma
 Choroid plexus papilloma
 Colloid cyst

1- Location
-Ependymoma
-Intraventricular meningioma
-Subependymal giant cells astrocytoma
-Choroid plexus papilloma
-Choroid plexus carcinoma
-Oligodendroglioma
Intraventricular

1- Location
-Central Neurocytoma
-Choroid plexus papilloma
-Choroid plexus carcinoma
Intraventricular

1- Location
Posterior Fossa
Posterior Fossa Tumours in Pediatric
Brainstem:
 Glioma
 Ganglioglioma
 Astrocytoma
Tectum/Cerebellum:
 Pilocytic Astrocytoma
 Medulloblastoma
Fourth Ventricle:
 Medulloblastoma
 Ependymoma
 Choroid Plexus Papilloma
CP Angle:
 Acoustic neuroma
 Meningioma
 Epidermoid Cyst

1- Location
CP Angle
Common CP Angle Tumors
 Schwannoma
 Meningioma
 Epidermoid
 Arachnoid Cyst
 Paraganglioma
 Metastasis

1- Location
Fourth Ventricle
Common Fourth Ventricle Tumors
 Astrocytoma
 Medulloblastoma
 Ependymoma
 Brainstem gliomas
(Exophytic)
 Metastases
 Dermoid & Epidermoid

1- Location
Skull Base
Common Skull Base Tumors
 Chordoma
 Chondrosarcoma
 Esthesioneuroblastoma
 Lymphoma
 Metastases
 Myeloma
 Paraganglioma
 Sinonasal Carcinoma

2- Peritumoral edema
 Vasogenic cerebral oedema: a type of cerebral
edema in which blood brain barrier (BBB) is
disrupted (N.B. cytotoxic edema where BBB is
intact).
 Extracellular oedema which mainly affects the white
matter, through leakage of fluid out of capillaries.
 May be minor or major
 Rounded or irregular
 Most frequently seen around brain tumors (both
primary & secondary) but is may be seen around
non tumorous conditions.

3- Effect on surroundings
 Primary brain tumors are derived from brain cells
and often have less mass effect for their size than
you would expect, due to their infiltrative growth.
 This is not case with metastases and extra-axial
tumors like meningiomas or schwannomas, which
have more mass effect due to their expansive
growth.

EXPANSIVE GROWTH
PATTERN
INFILRATIVE GROWTH
PATTERNVSINTRA-
AXIAL
EXTRA-
AXIAL
Intra-axial or extra-axial bulky lesion,
with usually well-defined margins,
compressing adjacent structure:
(a) Craniopharyngioma (papillary
variant) wedging in to foramina of
Monro & displace nerves & Chiasma.
(b) Tuberculum Sellae Meningioma
displacing the fronto-basal
parenchyma & splaying the optic
nerves.
INTRA/EXTRA-
AXIAL
Lesions with ill-defined margins that
predominantly infiltrate rather than
compress structure:
(c) Hypothalamus, pituitary stalk,
suprasellar and interpeduncular
cistern invasion from infiltrative high
grade diencephalic glioma.

(A) Tumor Spread
 Along the white matter tracts spread: astrocytomas
have infiltrative growth that do not respect boundaries
of lobes >>>> the tumor is actually larger than can be
depicted with MRI.
 Trans-foramens extension: ependymomas of fourth
ventricle in children tend to extend through the
foramen of Magendie to cisterna magna & through
the lateral foramina of Luschka to cerebellopontine
angle.
 Cortical extension: oligodendrogliomas typically show
extension to the cortex.

(A) Tumor Spread
Extension into foramen magnum
(red arrow).
Extension to prepontine area
(blue arrows).

(A) Tumor Spread
 Subarachnoid seeding: some tumors show
subarachnoid seeding and form tumoral nodules
along brain & spinal cord. This is seen in PNET,
ependymomas, GBMs, lymphomas,
oligodendrogliomas , choroid plexus papillomas.
 Primitive neuroectodermal tumours (PNET) form a
rare group of tumors, which develop from primitive
or undifferentiated nerve cells. These include
medulloblastomas and pineoblastomas.

(A) Tumor Spread
 Extracranial extension: one of the most important roles
of imaging is to assess extracranial extent of a tumor.
 Patient who presented with left multiple
cranial nerve abnormalities.
 On the images we see an extra-axial
tumor in region of left cavernous sinus.
 There is homogeneous enhancement
with a broad dural tail.
 This is typical for meningioma.
 Only by studying all the images we do
appreciate that actual extent of the tumor
is greater than expected.
 The tumor is situated in pterygopalatine
fossa & extends into orbit.
 It also spreads anteriorly into middle
cranial fossa

(B) Mass Effect
The effect of a growing mass (or of the edema surrounding
the mass) compressing (and infiltrating) brain structures.
Mechanical
displacement of
adjacent brain
Compression
foramina of Monro &
Ventricles
Obstructive
Hydrocephalus
Midline Shift/Brain
Herniation
MASS
(large or
small with
or without
EDEMA)
Compression of pituitary
gland & adjacent
cerebral parenchyma
(Diencephalon, temporal
& frontal lobes

(B) Mass Effect
PILOCYTIC ASTROCYTOMA
CRANIOPHARINGIOMA (Sq.
papillary)
PILOMYXOID ASTROCYTOMA

(B) Mass Effect
 Minimal mass effect: occur in diffusely infiltrating
intra-axial tumors, with variable enhancement pattern
e.g. astrocytomas
Low grade astrocytoma shows typical infiltrative growth occupying most of the
right hemisphere with only a minimal mass effect.

(B) Mass Effect
 Midline crossing: ability of tumors to cross midline:-
• Glioblastoma multiforme (GBM) frequently crosses
midline by infiltrating white matter tracts of corpus
callosum.
• Radiation necrosis can look like recurrent GBM &
can sometimes cross midline.
• Meningioma is an extra-axial tumor and can
spread along the meninges to the contralateral
side.
• Lymphoma is usually located near midline.
• Epidermoid cysts can cross midline via
subarachnoid space.
• MS can also present as mass lesion in corpus
callosum.

(B) Mass Effect

4- Single vs Multiple
 Single tumors: typically in primary brain tumors
 Multiple tumors: meningiomas & schwannomas
can be multiple tumors especially in NFII
 Multiple lesions: usually indicate metastatic
disease.
 Multifocal tumors: may occur in brain lymphomas,
multicentric glioblastomas gliomatosis cerebri.
 Seeding metastases: medulloblastomas (PNET-
MB), ependymomas, GBMs, oligodendrogliomas.

Metastases
Multiple meningiomas and a
schwannoma in a patient with
Neurofibromatosis II

Multiple brain tumors can be seen in phacomatoses:
• Neurofibromatosis I: optic gliomas & astrocytomas
• Neurofibromatosis II: meningiomas, ependymomas,
choroid plexus papillomas
• Tuberous Sclerosis: subependymal tubers,
intraventricular giant cell astrocytomas, ependymomas
• Von Hippel Lindau: hemangioblastomas

5- Cortical based tumors
 Most intra-axial tumors are located in WM.
 Some tumors spread to or are located in GM.
 Differential diagnosis: pilocytic astrocytoma,
oligodendroglioma, ganglioglioma,
Dysembryoplastic Neuroepithial Tumor (DNET).
 Patients with a cortically based tumor usually
present with complex seizures.

Non-enhancing, cortically based tumor (ganglioglioma).

CT shows a mass with
calcifications, which extends all
the way to cortex.
Although this is a large tumor
there is only limited mass effect
on surrounding structures, which
indicates that this is an infiltrating
tumor.

6- CT Density
For example: fat containing tumors
lipomas, dermoid cysts, teratomas
CT: low density on CT (- 100HU).
MRI: high signal intensity on both
T1- & T2WI while low on fat
suppression
Coronal T1WI
CT without contrast
For example: lymphoma, colloid
cyst , PNET-MB
(medulloblastoma).
*High density:-
*Low density:-

7- MR signal intensity
 Most tumors have a low/intermediate signal intensity
on T1WI.
 Exceptions to this rule can indicate a specific type of
tumor.
 Calcifications are mostly dark on T1WI, but
depending on matrix, they can sometimes be bright
on T1.
 If you only do an enhanced scan, remember that
high signal is not always enhancement.
(A) High on T1WI

(A) High on T1WI
High Intensity on T1WI
 Met-hemoglobin: e.g. hemorrhagic tumors or metastasis
 High protein: e.g. dermoid cyst
 Fat: e.g. Lipoma, dermoid cyst
 Cholesterol: e.g. Colloid cyst
 Melanin: e.g. Melanoma metastases
 Flow effects: e.g. Slow flow
 Paramagnetic cations: e.g. Cu, Mn, ………etc

(A) High on T1WI
Pituitary Macroadenoma
with hemorrhage
GBM with hemorrhage Metastasis of melanoma

 Most tumors will be bright on T2WI due to high water
content.
 When tumors have low water content they are very
dense & hypercellular & cells have a high nuclear-
cytoplasmasmic ratio >>>> dark on T2WI, e.g. CNS
lymphoma & PNET (hyperdense on CT).
 Calcifications are mostly dark on T2WI.
(B) Low on T2WI

 Paramagnetic effects cause signal drop and are seen
in tumors that contain hemosiderin.
 Proteinaceous material can be dark on T2 depending
on content of protein itself, e.g. colloid cyst.
 Flow voids are also dark on T2 & indicate presence
of vessels or flow within lesion, seen in tumors that
contain a lot of vessels like hemangioblastomas, but
also in non-tumorous lesions like vascular
malformations.
(B) Low on T2WI

(B) Low on T2WI
Low Intensity on T2WI
 Hyper-cellularity: e.g. lymphoma, Meningioma, PNET,
Germinoma, GBM, Oligodendroglioma, Mucinous adeno-
metastases (GI, Lung, Breast, GU)
 Calcification: see calcification
 Blood: e.g. old hemorrhage or vascular mal.
 Protein: e.g. colloid cyst
 Melanin: e.g. Melanoma metastases
 Flow-void: e.g. Hemangioblastoma, vascular mal.

(B) Low on T2WI
Melanoma Met. PNETGBM Oligodendroglioma Ependymoma
Mucinous Carcinoma Lymphoma Lymphoma-FLAIR Meningioma

8- Solid vs Cystic
Is the lesion Solid, Mixed solid-cystic, Cystic or Vascular?
• Optic pathway glioma
(pilocytic/pilomyxoid
astrocytoma
• Craniopharyngioma
• Hamartoma
• Schwannoma
• Meningioma
• Ectopic posterior pituitary
• Metastasis
• Granulomatous diseases
• Adenoma
• Optic pathway glioma
(pilocytic/pilomyxoid
astrocytoma
• Arachnoid cyst
• Epidermoid cyst
• Dermoid cyst
SOLID
MIXEDCYSTIC-
SOLID
CYSTI
C
• Aneurysm
VASCULA
R

8- Solid vs Cystic
(A) Cystic Mass
 There are many cystic lesions that can simulate a CNS
tumor.
 These include epidermoid, dermoid, arachnoid,
neuroenteric and neuroglial cysts.
 Enlarged perivascular spaces of Virchow Robin can
simulate a tumor.
 To determine whether a lesion is a cyst or cystic mass look
for the following characteristics:
• Morphology
• Fluid/fluid level
• Content usually isointense to CSF on T1, T2 & FLAIR
• DWI: restricted diffusion

8- Solid vs Cystic
(A) Cystic Mass
T2W FLAIR
DW
I
T1C+
EPIDERMOID CYST
 Isointense to CSF in T1WI
and T2WI without CE after
gadolinium
 T2-FLAIR high signal & DWI
restricted diffusivity due to
desquamating
epithelium/cholesterol
accumulation
FLAIRT2W
T1C+DW
I
ARACHNOID CYST
 Signal and diffusivity equal
to CSF. No CE.
 CSF containing cyst with
thin walls
T2W
DW
I
T1C+
T1W
 Hyperintense to CSF in
T1WI and hypointense in
T2WI >>>> (crankcase) like
oily material (cholesterol,
protein, blood product)
 Cyst walls enhance.
 DWI MR typically presents
a low signal
CRANIOPHARYNGIO
MA
Variable Signal Intensity according to content of cyst

8- Solid vs Cystic
(A) Cystic Mass
Medulloblastoma WHO grade IV
Ependymoma WHO grade II
 Neoplastic cysts (arises
within tumour & has
enhancing walls).
 Non-neoplastic cysts
(reactive, arising in
neighbouring
parenchyma & mural
enhancement is absent).

8- Solid vs Cystic
(A) Cystic Mass
Craniopharyngioma Neurentric Cyst GBM
Enhancing rim
surrounding cystic
component
Contents of which have
the same signal
intensity as CSF
Central cystic
component & irregular
enhancement

8- Solid vs Cystic
(A) Cystic Mass
Glioblastoma Multiforme
WHO grade IV

8- Solid vs Cystic
(B) Solid lesions

9- Necrosis
 Caused by sudden vascular occlusion.
 Endothelial proliferation and thrombosis are
predisposing factors.
 Poor prognosis in adult glioma.

10- Calcification
 It is usually a sign of slowly growing lesion.
 It is best assessed in CT.
 When we think of a calcified intra-axial tumor, we
think oligodendroglioma since these tumors nearly
always have calcifications.
 Intraaxial calcified tumor in brain is more likely to be
an astrocytoma than a oligodendrogliomas, since
astrocytomas, although less frequently calcified, are
far more common.
 Pineocytoma itself does not calcify, but instead it
'explodes' calcifications of pineal gland.

10- Calcification
Tumors Associated with Calcification
Intra-axial tumours:
 Astrocytomas (20%)
 Oligodendrogliomas (90%)
 Metastases
 Ependymoma (50%)
(25%)
 Ganglioglioma
Extra-axial tumours:
 Meningioma (25%)
 Craniopharyngioma (90%)
 Chordomas
 Chondrosarcomas

10- Calcification
Oligodendroglioma
PDWI CT
Ependymoma Medulloblastoma
(A) Calcification in Intra-axial Tumours
Pilocytic Astrocytoma

10- Calcification
(B) Calcification in Extra-axial Tumours
Craniopharyngioma
Meningioma
T1W
Coronal
T1W Sagittal CT

11- Hemorrhage
 Due to pathological changes in the tumor vessels.
 It is rare (0.8-10.2%).
 Usually typical of malignant tumors
Hemorrhagic metastatic
melanoma
Stage
Hyperacut
e
Acute
Early Subacute
Late Subacute
Chronic
Time
<24hrs
1-3 d
3-7 d
>7d
>14d
T1
Iso
Iso
Hyper
Hyper
Iso, Hypo
T2
Hyper
Hypo
Hypo
Hyper
Hypo

12- Enhancement
 The brain has a unique triple layered blood-brain
barrier (BBB) with tight endothelial junctions in order to
maintain consistent internal milieu.
 Contrast will not leak into brain unless this barrier is
damaged.
 Enhancement is seen when CNS tumor destroys BBB.
 Extra-axial tumors not drive from brain cells >>> not
have a blood-brain barrier >>> enhance.
 No blood-brain barrier in pituitary, pineal choroid
plexus regions.

12- Enhancement
 High grade gliomas: infiltration of surroundings >>>
Break BBB >>> Enhancement
 Low grade tumors: no infiltration of surroundings >>>
No Break BBB >>> No Enhancement
 Ganglioglioma & pilocytic astrocytomas are exceptions
to this rule: they are low-grade tumors, but they
enhance vividly.

12- Enhancement
Contrast Enhancement
 Extra-axial tumors: Meningioma, Schwannoma
 High grade gliomas
 Low grade gliomas: ganglioglioma, pilocytic astrocytoma
 Lymphoma
 Metastases
 Non-tumoral: infection, abscess, MS, infarction

12- Enhancement
Meningioma WHO grade I Schwannoma

12- Enhancement
GBM WHO grade IV

12- Enhancement
Ganglioglioma Pilocytic astrocytoma

12- Enhancement
Primary CNS lymphoma

12- Enhancement
Choroid plexus papilloma
WHO grade I

12- Enhancement
Dysembryoplastic Neuroepithelial Tumor (DNET)
WHO grade I

12- Enhancement
Low-grade astrocytoma of temporal lobe
no enhancement & DWI was normal

12- Enhancement
 Contrast enhancement cannot visualize full extent
of tumor in cases of infiltrating tumors, like gliomas
>> reason for this is that tumor cells blend with
normal brain parenchyma where the blood brain
barrier is still intact.
 Tumor cells can be found beyond enhancing
margins of tumor & beyond any MR signal alteration
-even beyond area of edema.

12- Enhancement
 In gliomas - like astrocytomas, oligodendrogliomas
glioblastoma multiforme - enhancement usually
indicates a higher degree of malignancy.
 Therefore when during follow up of low-grade glioma
tumor starts to enhance, it is a sign of malignant
transformation.
 Tumor angiogenesis as shown by perfusion MR
correlates better with tumor grade than enhancement
after administration of intravenous contrast.

12- Enhancement
Contrast enhancement patterns
No Enhancement
Homogeneous Enhancement
Patchy Enhancement
Ring Enhancement
 Low grade astrocytoma
 Cystic non-tumoral lesions
 Germinoma
 Pineal tumours
 Pituitary adenoma
 Pilocytic astrocytoma (solid
component)
 Haemangioblastoma
 Ganglioglioma
 Meningioma
 Schwannoma
 Radiation necrosis
 High grade glioma
 Metastases
 Abscess

12- Enhancement
(A) No enhancement
 Low grade astrocytomas
 Cystic non-tumoral lesions:
• Dermoid cyst
• Epidermoid cyst
• Arachnoid cyst
T1WI T1WI+
C
T2WI
Diffuse Infiltrative
Astrocytoma
(WHO grade II)

12- Enhancement
(A) No enhancement
 Low grade astrocytomas
 Cystic non-tumoral
lesions:
• Dermoid cyst
• Epidermoid cyst
• Arachnoid cyst
T1WI T1WI+
C
T2WI
Diffuse Infiltrative Astrocytoma (WHO grade II)
T2WI T2WI T1WI+
C
T1WI+
C
Low-grade astrocytoma

12- Enhancement
(B) Homogeneous enhancement
 Metastases
 Meningioma
 Pituitary macroadenoma
 Pilocytic astrocytoma (solid part)
 Pineal gland tumors
 Lymphoma
 Germinoma
 Ganglioglioma
 Hemangioblastoma (solid part)
 Schwannoma

12- Enhancement
(B) Homogeneous enhancement
Meningioma Schwannoma Lymphoma
Hemangioblastoma Pilocytic Astrocytoma Ganglioglioma
Choroid
plexus
papilloma

12- Enhancement
(C) Patchy enhancement
 Metastases
 Oligodendroglioma
 Glioblastoma multiforme
 Radiation necrosis
T1WI+
C
FLAIR
Glioblastoma multiforme (GBM)
Partial enhancement
Cystic component with ring
enhancement

12- Enhancement
(C) Patchy enhancement
FLAIR
T1WI+
C
T1WI+
C
T1WI
T2WI
Glioblastoma multiforme (GBM)
Large tumor with limited mass-effect
Heterogeneity on both T2WI &
FLAIR.
There is patchy enhancement.

12- Enhancement
(D) Ring enhancement
 Metastases
 Glioblastoma multiforme
 Abscess, Infectious disease
 Multiple sclerosis
 Chronic hematoma
GBMMetastases
Abscess

Normal & abnormal radiology of brain part iv

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