Radiological imaging of intracranial cystic lesions

Non-neoplastic
Non-infectious
Neoplastic
Intracranial cystic lesions
Infectious
Associated with
congenital
malformations
•Dermoid cyst
•Epidermoid cyst
•Arachnoid cyst
•Colloid cyst
•Neuroectodermal cyst
•Neuroglial cyst
•Ependymal cyst
•Porencephalic cyst
•Choroid plexus cyst
•Pineal cyst
•Hydatid
•NCC
•Abscesses
•Dandy-Walker
malformation
•Pilocytic astrocytoma
•Craniopharyngioma
•Ganglioglioma
•Hemangioblastoma

Cysts occurring as normal
anatomic variants
 Enlarged perivascular
(Virchow-Robin) spaces
Congenital inclusion cysts
 Dermoid cyst
 Epidermoid cyst
 Arachnoid cyst
Cysts derived from embryonic
endo- or ectoderm
•Colloid cyst
•Neuroectodermal
(neurenteric) cyst
Miscellaneous cysts
•Neuroglial cyst
•Ependymal cyst
(xanthogranuloma)
•Pineal cysts

 Intra-arachnoid CSF-filled sac that does not
communicate with ventricular system
Location
 50-60% middle cranial fossa
 10% cerebellopontine angle
 10% suprasellar arachnoid cyst

CT Findings
NECT
 Usually CSF density
 Hyperdense, if intracyst hemorrhage present (rare)
 May expand, thin/remodel bone
CECT: Doesn't enhance
CTA: Posterior displacement of MCA in MCF ACs
CT: Cisternography may demonstrate
communication with subarachnoid space

MR Findings
 TlWI: Sharply-marginated extra-axial fluid collection
isointense with CSF
 T2WI: Isointense with CSF
 FLAIR: Suppresses completely
 T2* GRE: No blooming unless hemorrhage present(rare)
 DWI: No restriction
 T1 C+: Doesn't enhance
 MRA: Cortical vessels displaced away from calvarium
 Phase-contrast cine MR - flow quantification can help
distinguish AC from enlarged subarachnoid space

Ultrasonographic Findings
 • Real Time: Useful for demonstrating sonolucent Acs
in infants < 1 Y
Angiographic Findings
MCA displaced posteriorly in MCF Acs
Nuclear Medicine Findings
 SPECT - May show hypoperfusion in brain adjacent to
cyst
Imaging Recommendations
 Best imaging tool: MR without, with contrast
 Protocol advice: Add FLAIR, DWI

DIFFERENTIAl. DIAGNOSIS
Epidermoid cyst
 Scalloped margins
 Insinuating growth pattern -
Creeps along, into CSF
cisterns
 Surrounds, engulfs vessels and
nerves
 Doesn't suppress on FLAIR
 Shows restricted diffusion
(bright) on DWI
Chronic subdural hematoma
 Signal not identical to CSF
 Often bilateral, lentiform-
shaped
 May show enhancing
membrane
Porencephalic cyst
•Surrounded by gliotic brain, not
compressed cortex
•History of trauma, stroke
common
Neurenteric cyst
•Rare; spine, posterior fossa =
most common locations
•Often proteinaceous fluid
Neuroglial (glioependyma) cyst
•Rare
•Usually intra-axial

Staging, Grading or Classification Criteria
Galassi classification:
 Type I: Small, spindle shaped, limited to anterior MCF
 Type II: Superior extent along sylvian fissure; temp lobe
displaced
 Type III: Huge, fills entire MCF; frontal/temp/parietal
displacement
Treatment
• Often none
• Resection (may be endoscopic)
• Fenestration
• Shunt (cystoperitoneal is common option)

Etiology
 From embryonic endoderm, not neuroectoderm!
 Similar to other foregut-derived cysts (neurenteric,
Rathke)
 Contents accumulate from mucinous secretions
desquamated epithelial cells
Epidemiology
 0.5-1.0% primary brain tumors
 15-20% intraventricular masses
 Associated abnormalities: Variable hydrocephalus

Presentation
 Headache (50-60%)
 Less common = nausea, vomiting, memory
loss,altered personality, gait disturbance, visual
changes
 Acute foramen of Monro obstruction may lead
torapid onset hydrocephalus, herniation, death
 40-50% asymptomatic, discovered incidentally

 Best diagnostic clue: Hyperdense foramen of Monro mass
on NECT
Location
 > 99% wedged into foramen of Monro
 Attached to anterosuperior 3rd ventricular roof
 Pillars of fornix straddle, drape around cyst
 Posterior part of frontal horns splayed laterally around cyst
 < 1% other sites - Lateral, 4th ventricles, Parenchyma
(cerebellum), Extra-axial (prepontine, meninges)
Size
 Variable (few mm up to 3 cm)
 Mean size == 15 mm

CT Findings
NECT
 Density correlates inversely with hydration state
 2/3 hyperdense
 1/3 iso/hypodense
 +/- Hydrocephalus
 Rare
 Hypodense
 Change in density/size
 Hemorrhage (cyst "apoplexy")
 Calcification
CECT
 Usually doesn't enhance
 Rare == rim enhancement

MR Findings
TlWI
 Signal correlates with cholesterol concentration
 2/3 hyperintense on Tl WI
 1/3 isointense (small CCs may be difficult to see!)
 May have associated ventriculomegaly
T2WI
 Signal more variable
 Generally reflects water content
 Majority isointense to brain on T2WI (small cysts
may be difficult to see!)

FLAIR: Does not suppress
DWI: Does not restrict
Tl C+
 Usually no enhancement
 Rare: May show peripheral (rim)
enhancement

Differential diagnosis -
Neurocysticercosis
 Multiple lesions within parenchyma and cisterns
 Associated ependymitis or basilar meningitis common
 Ca++ common
 Look for scolex
CSF flow artifact (MR "pseudocyst")
 Multiplanar technique confirms artifact
Subependymoma
 Frontal horn of lateral ventricle
 Attached to septum pellucidum
 Patchy/solid enhancement

Natural History & Prognosis
90% stable or stop enlarging
 Older age
 Small cyst
 No hydrocephalus
 Hyperdense on NECT, hypointense on T2 weightedMR
10% enlarge
 Younger patients
 Larger cyst, hydrocephalus
 Iso/hypodense on NECT, often hyperintense on T2WI
 May enlarge rapidly, cause coma/death!

Etiology
Embryology (two theories)
 Sequestration of surface ectoderm at lines of epithelial
fusion/along the course of normal embryonic invaginations
 Inclusion of cutaneous ectoderm at time of neural tube closure;
3rd-5th week of embryogenesis
Three classifications of dermoid inclusions, based on
pathogenesis -
1. Congenital cystic teratoma (true neoplasm derived from all
three embryonic germ layers)
2. Congenital dermoid inclusion cyst (nonneoplastic epithelial-
lined inclusion cyst)
3. Acquired implantation cyst (trauma, surgery, LP)

General Features
Best diagnostic clue: Fat appearance + droplets in cisterns, sulci,
ventricles if ruptured
Location
 Most often in sellar/parasellar/frontonasal region
 Posterior fossa - midline vermis & 4th ventricle
 Intraventricular within tela choroidea in lateral, 3rd, or 4th ventricles
 Extracranial sites = spine, orbit
 Ruptured: Subarachnoid/intraventricular spread of contents
Size: Variable
Morphology: Well-circumscribed lipid containing mass

CT Findings
NECT
 Round/lobulated, well-delineated, cystic mass
 Fat hypodensity
 20% capsular Ca++
 With rupture, droplets of fat disseminate in cisterns, may
cause fat-fluid level within ventricles
 Skull/scalp dermoid expands diploe
 Frontonasal: Bifid crista galli, large foramen cecum +
sinus tract
 Rare "dense" dermoid: Hyperattenuating on CT
CECT: Generally no enhancement

MR Findings
TlWI
 Unruptured: Hyperintense on Tl WI
 Ruptured: Droplets very hyperintense on Tl WI
o Fat suppression sequence confirms
o Fat-fluid level in cyst, ventricles common
 Rare "dense" dermoid: Very hyperintense on Tl WI
T2WI
 Unruptured: Heterogeneous, from hypo- to hyperintense on T2WI
 Chemical shift artifact in frequency encoding direction with long TR
 Ruptured: Typically hyperintense droplets on T2WI
 Rare "dense" dermoid: Very hypointense on T2
 With hair: Fine curvilinear hypointense elements
Tl C+: With rupture: Extensive MR enhancement
 possible from chemical meningitis
MRS: Very strong and broad resonances from mobile lipids at 0.9 and 1.3
ppm

 Normal or avascular mass effect
 If ruptured, can see vasospasm
 Dermoid-encased vessels may have increased
rupture risk
 Best imaging tool: MRI, especially in setting of
rupture
 Protocol advice
 Use fat-suppression sequence to confirm diagnosis
 Chemical shift-selective sequence useful to detect
tiny droplets

Epidermoid cyst
 Most epidermoid cysts resemble CSF, not fat
 No dermal appendages
 4-9x more common than dermoid
 Off-midline> midline: 40-50% in CPA, 10-15% para sellar/middle fossa, 10%
diploic
 MRI: Isointense to CSF except restricts on diffusion
Teratoma
 Location similar, but usually pineal region
 Mixture of two or more embryologic layers; ectoderm, mesoderm,
endoderm
 Often multicystic/multiloculated
 Heterogeneous appearance containing calcification,
 CSF, lipid, and soft tissue components
Lipoma
 • Homogeneous fat> heterogeneous lipid

Treatment
 Complete microsurgical excision
 Residual capsule may lead to recurrence
 Rare SCCa degeneration within surgical remnants
 Subarachnoid dissemination of contents may occur during
operative/postoperative course
 Cause aseptic meningitis or other complications
(hydrocephalus, seizures, CN deficits)
 Alternatively, disseminated fat particles can remain
 silent without radiological/neurological change
 Justifies wait-and-see approach
 Regular MRI and clinical exams are necessary to avoid
complication

Etiology
 Congenital: Arise from ectodermal inclusions during
neural tube closure
 Acquired: Develop as a result of trauma
 Uncommon etiology for intracranial tumors
 More common as spine etiology following LP
Epidemiology
 4-9x more common than dermoid
 Third most common CPA/lAC mass, after vestibular
schwannoma & meningioma
 Associated abnormalities: May have
occipital/nasofrontal dermal sinus tract

General Features
 •Best diagnostic clue: CSF-like mass insinuates cisterns, encases
nerves/vessels
Location
 90% intradural, primarily in basal cisterns
 Cerebellopontine angle (CPA) = 40-50%
 Fourth ventricle = 17%
 Para sellar/middle cranial fossa = 10-15%
 Rarely in cerebral hemispheres = 1.5%
 Brain stem location exceedingly rare
 Intraventricular within tela choroidea of temporal horn, 3rd, or 4th
ventricles
 10% extradural: Skull (intradiploic within frontal, parietal, occipital,
sphenoid skull) as well as spine
Size: Variable
Morphology: Lobulated, irregular, "cauliflower-like“ mass with "fronds"

CT Findings
NECT
 Round/lobulated mass
 > 95% hypodense, resembling CSF
 10-25% Ca++
 Intradiplioc epidermoid: Bony erosion with sharply
corticated margins
 Rare variant = "dense" epidermoid
 Secondary to hemorrhage, high protein, saponification
of cyst debris to calcium soaps or iron-containing
pigment
CECT: Usually none, although margin of cyst may
show minimal enhancement

MR Findings
TlWI
 Uncommonly hyperintense to brain ("white epidermoid") due to high
triglycerides & unsaturated fatty acids
 Uncommonly hypointense to CSF ("black epidermoid")
 Presence of solid crystal cholesterol & keratin
 Lack of triglycerides & unsaturated fatty acid
T2WI
 Often isointense (65%) to slightly hyperintense (35%) to CSF on T2WI
FLAIR: Usually doesn't completely null
DWI: Restricted diffusion
Tl C+
 margin of cyst may show minimal enhancement (35%)
 With malignant degeneration changes into enhancing tumour
MRS: Resonances from lactate

 Best imaging tool: MRI
 Protocol advice
 FLAIR will often distinguish where as conventional
sequences may not
 Diffusion definitively distinguishes from
arachnoid cyst

Differential Diagnosis –
Arachnoid cyst
 Completely nulls on FLAIR
 No restricted diffusion
 Rather than insinuate and engulf local structures, ACs
displace them
 Smooth surface, unlike lobulations of epidermoids
Cystic neoplasm
 Attenuation/signal intensity not that of CSF
 Often enhances
Dermoid cyst
 Usually at or near midline
 Resembles fat, not CSF
 contains dermal appendages

Etiology
 Intraparenchymal
 Lining of embryonic neural tube becomes sequestered
within developing WM
 Evagination of neuroectoderm along choroidal fissure
 May contain ependymal or choroid cells as cyst lining
 Subarachnoid space
 Leptomeningeal neuroglial heterotopia postulated
Epidemiology: Uncommon « 1% of intracranial cysts

General Features
Best diagnostic clue: Nonenhancing CSF-like parenchymal
cyst with minimal/no surrounding signal abnormality
Location
 May occur anywhere throughout neuraxis
 Frontal lobe most common site
 Intraparenchymal > extraparenchymal
Size: Varies from a few mm up to several cm
Morphology: Smooth, rounded, unilocular benign-appearing
cyst

CT Findings
NECT
 Well-delineated low density cyst
 Unilocular
 No Ca++
CECT: Wall does not enhance

MR Findings
 Tl WI: Usually hypo intense, resembles CSF
 T2WI: Hyperintense
 FLAIR: Usually suppresses
 DWI: Typically no diffusion restriction
 Tl C+: No enhancement
• Best imaging tool: MR without, with contrast
• Protocol advice: Include FLAIR, DWI

Differential diagnosis –
Porencephalic cyst
 Communicates with ventricles
 Usually adjacent brain shows gliosis, spongiosis
Enlarged perivascular spaces (PVSs)
 Clusters of variable-sized cysts> single, unilocular cyst
 Usually midbrain, around anterior commissure
Arachnoid cyst
 • Extra-axial
 • Does not have epithelial lining
Infectious cyst
 Cysts usually in subarachnoid space, ventricles
 Ca++, enhancement common
 Cysts usually < 1 cm

Definition:
 Pial-lined interstitial fluid (ISF)-filled structures that accompany
penetrating arteries but do not communicate directly with
subarachnoid space
Presentation
Usually normal, discovered incidentally at imaging/autopsy
Demographics
 PVSs occur in all locations, at all ages and are easily seen in most
patients on 3T imaging
 Present in 25-30% of children (benign normal variant)
 Enlarged PVSs - Mean age = mid 40s
 Gender: Giant PVSs: M:F = 1.8: 1

General Features
Best diagnostic clue: Fluid-filled spaces that look like CSF,
surround/accompany penetrating arteries
Location
 Most common site for normal PVSs = basal ganglia(cluster around
anterior commissure)
 Other common locations
 Midbrain
 Deep white matter
 Subinsular cortex, extreme capsule
 Most common location for expanded ("giant" or "tumefactive") PVSs
= midbrain
 Can be found almost anywhere
 BUT almost never involve cortex (PVSs expand within subcortical
white matter)

CT Findings
NECT
 Clusters of round/ovoid/linear/punctate cyst-
like lesions
 Low density (attenuation = CSF)
 No Ca++
CECT: Don't enhance

MR Findings
TlWI
 Multiple well-delineated cysts isointense with CSF
 Midbrain enlarged PVSs may compress aqueduct/3rd ventricle, cause
hydrocephalus
T2WI
 Appear isointense with CSF
 No edema in adjacent brain
FLAIR
 Suppress completely
 25% have minimal increased signal in brain surrounding enlarged PVSs
T2* GRE: No blooming
DWI: No restricted diffusion
Tl C+
 No enhancement
 +/- Visualization of penetrating arteries with contrast

Lacunar infarcts
• Older patients
• Common in basal ganglia,
white matter
• Adjacent parenchymal
hyperintensity
Infectious/inflammatory cysts
 Neurocysticercosis
scolex
most are < 1 cm
don't typically occur in cluster
cyst walls often enhances
surrounding edema often
present
Other parasites
Hydatid cysts often
unilocular, almost all in
children
Multilocular parasitic cysts
typically enhance, mimic
neoplasm more than PVS

 Usually remain stable in size
 Occasionally continue to expand
Treatment
 "Leave me alone" lesion that should not be
mistaken for serious disease
 Shunt ventricles if midbrain lesions cause
obstructive hydrocephalus

Etiology-pathogenesis: 3 major theories
 Enlargement of embryonic pineal cavity
 Ischemic glial degeneration +/- hemorrhagic
expansion
 Small pre-existing cysts enlarge with hormonal
influences
Epidemiology
 1-4% prevalence at imaging
 20-40% microscopic cysts within pineal gland
found at autopsy

General Features
Best diagnostic clue: Homogeneous fluid-filled mass above,
clearly distinct from tectum
Location: Above tectum, below internal cerebral
veins(ICVs)
Size: Most are small « 1 cm, but may be up to 2 cm or more
Morphology
 Round/ovoid, relatively thin-walled cyst
 May flatten tectum, occasionally compressaqueduct
 variable hydrocephalus (enlarged 3rd, lateral ventricles;
normal 4th V) with large cysts

CT Findings
NECT
 Sharply-demarcated, smooth cyst behind 3rd
Ventricle
 Fluid iso-/slightly hyperdense to CSF
 25% Ca++ in cyst wall
 Rare: Very hyperdense cyst with acute hemorrhage
("pineal apoplexy")
CECT: Rim or nodular enhancement

MR Findings
TlWI
 55-60% slightly hyperintense to CSF on Tl WI
 1-2%: Hemorrhage (heterogenous signal intensity)
T2WI: Iso / hyperintense to CSF
FLAIR: Doesn't suppress (moderately hyperintense)
T2* GRE
 Uncommon: Blooming caused by old or recent hemorrhage
Tl C+
 60% enhance
 Partial/complete rim, nodular
 Cystic areas may fill in on delayed scans, resemble solid tumor
MRV: Internal cerebral veins (ICVs) may be elevated
 by large lesions

 Best imaging tool: MR without, with contrast
 Protocol advice: Use thin sections (3 mm or less) for
detecting, defining lesions in this anatomically
complex region

DIFFERENTIAL DIAGNOSIS
Normal pineal gland (can be cystic)
 Three anatomic appearances on contrast-enhanced imaging
 Nodule (52%)
 Crescent (26%)
 Ring-like (22%)
Pineocytoma
 Usually solid components present; purely cystic tumors occur
but are less common
 Cystic pineocytomas occur, may be indistinguishable on
imaging studies, require histology for definitive diagnosis
 Both pineal cyst, indolent pineocytoma may not change on
serial imaging

 Size generally remains unchanged in males
 Cystic expansion of pineal in some females
begins in adolescence, decreases with aging
 Rare: Sudden expansion, hemorrhage ("pineal
apoplexy")
Treatment
 Usually none
 Atypical/symptomatic lesions may require
stereotactic aspiration or biopsy/resection
 Preferred approach == infra tentorial supra
cerebellar

CPC commonly found at autopsy or imaging in middle-aged, older
adults
Etiology
 Lipid from desquamating, degenerating choroid epithelium
accumulates in choroid plexus
 Lipid provokes xanthomatous response
Epidemiology
 Most common type of neuroepithelial cyst
 1% of all pregnancies on routine US
 50% of fetuses with Trisomy 18
 Small asymptomatic CPCs found incidentally in >1/3 of all
autopsied adults

Age
 Adult CPC: Prevalence increases with age
 Fetal CPC: Prevalence decreases with age
Associated abnormalities
 Fetal CPC
 Trisomy 18 (mildly increased risk < 2x baseline
risk)
 Trisomy 21 (only if other markers present)
 Adult CPC: May cause obstructive
hydrocephalus (rare)

General Features
Best diagnostic clue
 Older patient with "bright" choroid plexi on MRI
 Fetus or newborn with large (> 2 mm) choroid plexus cyst(s) on US
Location
 Atria of lateral ventricles most common site
 Attached to or within choroid plexus
 Usually bilateral
Size
 Usually small (2-8 mm)
 Often multiple
 Rare: Large cysts (> 2 cm)
Morphology: Cystic or nodular/partially cystic mass(es) in choroid
plexus glomi

CT Findings
NECT
 Iso- or slightly hyperdense compared to CSF
 Irregular, peripheral Ca++ in majority of adult cases
CECT: Varies from none to rim or solid enhancement
MR Findings
 T1 WI: Iso/slightly hyperintense compared to CSF
 T2WI: Hyperintense compared to CSF
 FLAIR: 2/3rd iso-, 1/3rd hypointense on FLAIR
 T2* GRE: Blooms with intracystic hemorrhage (rare)
 DWI: 65% show restricted diffusion (high signal)
 Tl C+
 Enhancement varies from none to strong
 variable pattern (solid, ring, nodular)
 Delayed scans may show filling in of contrast within cysts

Ultrasonographic Findings
Prenatal US
 Cyst> 2 mm surrounded by echogenic choroid
 In absence of other abnormalities, low risk for
chromosomal abnormalities

Best imaging tool
 Adults: MR without, with contrast
 Fetus, newborn
 Antenatal: Maternal US or MR
 Postnatal: US of infant with anterior, posterior,
mastoid fontanelles as acoustic windows
Protocol advice
 MR without/with contrast, FLAIR
 U/S transverse view of lateral ventricle at atrial level

Ultrasound "pseudolesion"
 Tiny anechoic areas in fetal choroid are normal, not CPC
 Normal fluid-filled atria can be confused with CPC on transverse
view
 "Split" or "truncated" choroid can mimic CPC
Ependymal cyst
 Doesn't enhance
 Usually unilateral
 Attenuation, signal more like CSF
Neoplasm
 Choroid plexus papilloma (children < 10 y; strong relatively uniform
enhancement; cystic variant reported but rare)
 Metastasis (rarely cystic)
 Cystic astrocytoma (rare in older patients)

Sturge-Weber syndrome
 Enlarged "angiomatous" choroid plexus ipsilateral
tomalformation
Infectious/inflammatory cysts
 Neurocysticercosis
 Multiple cysts common (parenchyma,
subarachnoid space, ventricles)
 Not associated with choroid plexus
 May be migratory
 Look for scolex, other signs of NCC (e.g.,
parenchymal Ca++)

Villous hyperplasia of choroid plexus
 Very rare
 Often overproduces CSF
 Causes hydrocephalus
Choroid plexus infarct
 Usually seen in choroid artery infarct
 May cause increased intraventricular signal on DW

Fetal CPCs
 Transient finding; typically resolve in 3rd trimester regardless of
whether isolated or with associated anomalies
 CPC + minor markers = 20% risk for chromosome abnormality
 CPC + major markers = 50% risk for chromosome abnormality
Adult CPCs
 Usually remain asymptomatic, nonprogressive
Treatment
Adult CPC: Usually none
 Rare: Shunt for obstructive hydrocephalus
Fetal CPC
 In absence of other markers, none
 With other markers, amniocentesis warranted

 Etiology: Thought to arise from sequestration of
developing neuroectoderm
Demographics -
 Age: Typically young adults, less than 40 years
 Gender: Male predominance

General Features
 Best diagnostic clue: Non-enhancing thin-walled cyst with
CSF density/intensity
Location
 Intraventricular common, typically lateral ventricle
 Intraparenchymal, central white matter of temporo-
parietal and frontal lobes
 Subarachnoid space, less common
Size: Variable, typically small, 2-3 mm up to 8-9 cm
Morphology: Smooth, thin-walled cyst

CT Findings
 NECT: Cyst is isodense to CSF; Ca++ extremely
rare
 CECT: No enhancement
MR Findings
 Tl WI: Isointense to CSF, cyst wall may be seen
 T2WI: Isointense to hyperintense to CSF (protein
content)
 FLAIR: Isointense to CSF
 DWI: No diffusion restriction

Choroid plexus cyst
• May be indistinguishable
• Typically bilateral and arise in choroid plexus glomus
• Commonly DWI positive, enhance
Arachnoid cyst
• May be indistinguishable; CSF intensity
Porencephalic cyst
• Focal encephalomalacia, +/- surrounding gliosis
• Typically communicates with the ventricle

 Uncommon so natural history is unknown
 Interval follow-up typically shows no clinical or
imaging changes in asymptomatic lesions
 Recurrence after surgical intervention uncommon
Treatment
 If symptomatic, surgical excision or decompression
 Rapid resolution of symptoms after surgery
 Conservative management if asymptomatic

Definition - CSF-filled cavity with smooth walls, lined by white
matter of cerebral hemisphere
Etiology
 Congenital: In utero destructive process caused by cerebral
vascular events or infectious injury (CMV)
 Acquired: Injury later in life, following head trauma, vascular
occlusion, or infection
 Amygdala-hippocampal atrophy often coexists with congenital
porencephaly (95% in some reports)
 This atrophy may be bilateral despite unilateral porencephalic
cysts
 Familial porencephaly may be associated with inherited
thrombophilia

General Features
 Best diagnostic clue: Cystic space in brain parenchyma,
enlarged adjacent ventricle on CT, MRI
Location
 Usually corresponds to territories supplied by cerebral
arteries (ischemic injury in mid-gestation)
 Cortical/subcortical cavity, unilateral/bilateral
 Usually connected with one of the lateral ventricles
 Size: Variable
 Morphology: Rounded or oval

CT Findings
NECT
 Intraparenchymal smooth-walled cavity, CSF-
isointense
 Communication with ventricle or separating
membrane
CECT: No contrast enhancement of fluid-filled
cavity
CTA: Absence of vessels at site of porencephaly

MR Findings
Tl WI: Smooth-walled cavity within brain parenchyma,
isointense to CSF
T2WI: Common adjacent brain atrophy, gliosis
FLAIR
 Accurately depicts CSF content of cyst
 More accurate in differentiating neoplastic/inflammatory
from porencephalic cysts
Tl C+: Nonenhancing cyst
MRA: Absence of vessels at site of porencephaly
MRS: Absence of normal brain metabolites

USG
 Prenatal ultrasound for congenital porencephaly
 Best imaging tool: MR
 Protocol advice: FLAIR
 Assess hippocampal structures in patients with
 porencephaly-related seizures

Treatment
 Usually no treatment is required
 Indications for surgery: Mass effect
(hemimacrocephaly, midline displacement),
ocalized/generalized symptoms
 Procedures
 Cystoperitoneal shunt (preferred)
 If no communication with ventricular system:
Fenestration or partial resection of cyst wall
 Children with intractable seizures and
porencephalybenefit from uncapping and cyst
fenestration to lateral ventricle

AKA – enterogenous cys
Etiology: Persistent neurenteric canal (connection
between embryonic foregut, developing neural tube)
Epidemiology
 Only 35 intracranial cases reported
 < 1% of all spinal masses
 Vertebral anomalies in 50% of spinal NECs
 Anterior segmentation defects

General Features
Best diagnostic clue: Round/lobulated nonenhancing,
slightly hyperintense (to CSF) mass in front of medulla
Location
 Spine> > brain
 Most of intracranial NECs found in posterior fossa
Midline, anterior to brain stem
Other: CPA, clivus
Rare: Suprasellar, quadrigeminal cisterns; anterior fossa
Size: Variable; usually < 2 cm
Morphology: Smooth, lobulated, well-demarcated

CT Findings
NECT: Hypo-/isodense mass anterior to brainstem
CECT: No enhancement
MR Findings
 T1WI: Iso-/slightly hyperintense to CSF
 T2WI: Hyperintense to CSF
 FLAIR: Hyperintense to CSF
 T2* GRE: No blooming

Epidermoid or dermoid cyst
 CPA most common site for epidermoid
 "White" epidermoid (rare) is hyperintense on Tl
WI, can be difficult to distinguish if midline
Arachnoid cyst
 Like CSF on all sequences
Consider
• A midline mass in front of the brain stem that is
slightly hyperdense/intense to CSF may be an NEC

Non-neoplastic
Non-infectious
Neoplastic
Intracranial cystic lesions
Infectious
Associated with
congenital
malformations
•Dermoid cyst
•Epidermoid cyst
•Arachnoid cyst
•Colloid cyst
•Neuroectodermal cyst
•Neuroglial cyst
•Ependymal cyst
•Pineal cyst
•Hydatid
•NCC
•Abscesses
•Dandy-Walker
malformation
•Pilocytic astrocytoma
•Ganglioglioma
•Hemangioblastoma
•Cystic metastases

• Pilocytic astrocytoma
• Pleomorphic xanthoastrocytoma
• Craniopharyngioma
• Ganglioglioma
• Hemangioblastoma

Etiology: Astrocytic precursor cell
Epidemiology
 5-10% of all gliomas
 Most common primary brain tumor in children
 Major source of morbidity in NF l
 15% of NF l patients develop PAs, most commonly in optic
pathway
 Up to 1/3 of patients with optic pathway PAs have NF l
 Frequently causes obstructive hydrocephalus
 May be a greater clinical management problem than tumor
itself

Demographics
Age
 > 80% under 20 y
 Peak incidence: 5-15 years of age
 Older than children with medulloblastoma
Gender: M = F
WHO grade I

General Features
 Cystic cerebellar mass with enhancing mural
nodule
 Enlarged optic nerve/chiasm/tract with variable
enhancement
Location: Cerebellum (60%) > optic nerve/chiasm
(25-30%) > adjacent to 3rd ventricle> brainstem
Size
 Large lesions in cerebellum
 Optic nerve lesions typically smaller

CT Findings
NECT
 Discrete cystic/solid mass
 May have little or no surrounding edema
 Solid component hypo- to isodense
 Ca++ 20%, hemorrhage rare
 Often cause obstructive hydrocephalus
CECT
 50% non enhancing cyst, strongly enhancing mural
nodule
 Cyst may accumulate contrast on delayed images

MR Findings
TlWI
 Solid portions iso/hypointense to GM
 Cyst contents iso- to slightly hyperintense to CSF
T2WI
 Solid portions hyperintense to GM
 Cyst contents hyperintense to CSF
FLAIR
 Solid portions hyperintense to GM
 Cyst contents do not suppress: Hyperintense to CSF
T1 C+
Intense but heterogeneous enhancement of solid portion
Cyst wall occasionally enhances
MRS
Aggressive-appearing metabolite pattern - High choline, low NAA, high lactate
Paradoxical finding: MRS does not accurately reflect historical behavior of tumor

 Best imaging tool: Contrast-enhanced MR
 Protocol advice
 Multiplanar or 3D volume post contrast imaging key
to showing point of origin and degree of extension
 MRS pattern is contradictory to clinical behavior
 Small residual tumor on post-operative studies may
not negatively impact prognosis

Ganglioglioma
 Discrete, solid/cystic, cortically-based enhancing
mass
 Ca++ common
Hemangioblastoma
 Large cyst with small enhancing mural nodule
 Adult tumor!
 Associated with von Hippel Lindau disease

 Tumor may spread through subarachnoid space in rare
cases (but is still WHO grade I)
Median survival rates at 20 y > 70%
Treatment
 Cerebellar or hemispheric: Resection
 Adjuvant chemotherapy or radiation only if residual
progressive unresectable tumor
 Opticochiasmatic/hypothalamic: Often none
 Stable or slowly progressive tumors watched
 Debulking or palliative surgery considered after vision loss
 Radiation or chemotherapy for rapidly progressive disease

Epidemiology
 < 1% of all astrocytomas
 Rare but important cause of temporal lobe epilepsy
WHO grade II
Age
 Tumor of children/young adults
 Typically first three decades
 2/3 < 18 years
Gender: No gender predominance

General Features
 Supratentorial cortical mass with adjacent enhancing dural "tail"
 Cyst and enhancing mural nodule typical
Location
 Peripherally located hemispheric mass, often involves cortex and
meninges
 98% supratentorial
 Temporal lobe most common
 Parietal> occipital> frontal lobes
 Rarely found in cerebellum, sella, spinal cord, retina
Morphology
 50-60% cyst + mural nodule that abuts meninges
 (may be solid)

CT Findings
NECT
 Cystic/solid mass: Hypodense with mixed
density nodule
 Minimal or no edema is typical
 Ca++, hemorrhage, frank skull erosion rare
CECT: Strong, sometimes heterogeneous
enhancement of tumor nodule

MR Findings
TlWI
 Cystic portion isointense to CSF
 Associated cortical dysplasia may be seen (rare)
T2WI
 Hyperintense or mixed signal intensity mass
 Surrounding edema rare
FLAIR
 Hyperintense or mixed signal intensity mass
T1 C+
 Enhancement usually moderate/strong, well-delineated
 Enhancement of adjacent meninges, dural"tail“ common
(approximately 70%)
 Enhancing nodule often abuts pial surface
Rare: Deep tumor extension, distant metastases

Best imaging tool
 Multiplanar MR is most sensitive
 CT may be helpful for calvarial changes
Protocol advice: Contrast-enhanced MR
including
 coronal images to better evaluate temporal
lobes

Ganglioglioma
 Cortically based hemispheric mass, solid/cystic or solid
 Mural nodule typical, often not adjacent to meninges
 no enhancing dural "tail"
 Ca++ is common
Pilocytic astrocytoma
 Supratentorial location other than hypothalamus/chiasm rare
 Enhancement but no dural "tail"
Dysembryoplastic neuroepithelial tumor (DNET)
 Superficial cortical tumor, well demarcated
 Multicystic "bubbly" ,appearance
 T2 hyperintense mass with rare, mild enhancement
 May remodel calvarium

Treatment
 Surgical resection is treatment of choice
 Repeat resection for recurrent tumors
 Radiation therapy and chemotherapy show no
significant improvement in outcome
REMEMBER !!!
 Cortical mass & meningeal thickening in a young
adult with long seizure history? Think PXA!
 Meningioma-like lesion in young patient should raise
suspicion of PXA
 Ganglioglioma may mimic PXA clinically and by
imaging

 Well differentiated, slowly growing neuroepithelial tumor
composed of neoplastic ganglion cells and neoplastic
glial cells
 WHO grade I or II
 Most common neoplasm causing chronic temporal lobe
epilepsy
Age
 Tumor of children, young adults
 80% of patients < 30 years
 Gender: Slight male predominance

General Features
Best diagnostic clue: Partially cystic, enhancing, cortically-based mass in
child/young adult with TLE
Location
 Can occur anywhere but most commonly superficial hemispheres, temporal
lobe
 Parietal and frontal lobes next most common
Size
 Variable, typically 2-3 cm in adults
 Larger in children, typically> 4 cm
Morphology - Three patterns
 Most common: Circumscribed cyst + mural nodule
 Solid tumor (often thickens, expands gyri)
 Calcification is common
 In younger patients « 10 years), gangliogliomas are larger and more cystic

CT Findings
NECT
 Variable density
 40% hypodense
 30% mixed hypodense (cyst), isodense (nodule)
 Ca++ common, 35-50%
 Superficial lesions may expand cortex, remodel bone
CECT
 Approximately 50% enhance
 Varies from moderate, uniform to heterogeneous
 Can be solid, rim or nodular

MR Findings
TIWI
 Mass is hypointense to isointense to gray matter
 Ca++ may be variable intensity
 May see associated cortical dysplasia
T2WI
 Hyperintense mass typical
 May be heterogeneous
T2* GRE: May show Ca++ as areas of "blooming"
Tl C+
 Variable enhancement, usually moderate but heterogeneous
 May be minimal, ring-like, homogeneous
 Meningeal enhancement rarely seen
MRS: Elevated Cho has been described

PET
 Typically decreased activity with FDG-PET
indicating tumour hypometabolism
 Best imaging tool: Multiplanar MR
 Protocol advice: Contrast-enhanced MR to
include coronal T2 images to better evaluate
temporal lobes

Pleomorphic xanthoastrocytoma (PXA)
• Supratentorial cortical mass, dural "tail" common
• Often cyst and mural nodule, may be solid
• Enhancing nodule abuts pial surface
• Temporal lobe most common location
Dysembryoplastic neuroepithelial tumor(DNET)
• Superficial cortical tumor, well demarcated
• Multicystic "bubbly" appearance
• T2 hyperintense mass with rare, mild enhancement
• May remodel calvarium

 Excellent prognosis if surgical resection complete
 Well-differentiated tumor with slow growth pattern
 Malignant degeneration is rare, approximately 5-10% (glial
component)
Treatment
 Surgical resection is treatment of choice
 Radiation therapy and/or chemotherapy for aggressiveor
unresectable tumors
REMEMBER !!!
 In children under 10 years old, gangliogliomas are larger and
more cystic
 In young patient with history of temporal lobe epilepsy,
think ganglioglioma

 Vascular tumor of unknown origin
 WHO grade I
Age
 Sporadic HGBL
 Peak 40-60 y
 Rare in children
 Familial
 VHL-associated HGBLs occur at younger age but are rare <
15Y
 Retinal HGBL: Mean onset 25 y
Gender: Slight male predominance

General features –
Best diagnostic clue – adult with intra-axial posterior fossa
cystic mass with enhancing mural nodule abuttin pia
Location –
90-95% posterior fossa (80% cerebellar hemispheres)
Morphology –
60% with cyst + mural nodule

CT
NECT –
 mural nodule is isodense to brain
 fluid density surrounding cyst.
CECT –
 Bright enhancement of the nodule
 The cyst walls do not usually enhance.
 Calcification is not a feature.

MRI
T1
 hypo intense to iso intense mural nodule, vividly
enhancing
 fluid filled cyst
T2
 hyper intense mural nodule
 flow-voids due to enlarged vessels may be evident
especially at the periphery of the cyst, seen in 60-
70% of cases
 fluid filled cyst, similar to CSF

 Highly vascular nodule
 Prolonged blush
 +/- AV shunting (early draining vein)
 Best imaging tool: Contrast-enhanced MR (sensitivity
> > CT for small HGBLs)
Protocol advice
 Begin MRI screening of patients from VHL families
after age 10 Y
 Screen complete spine

Metastasis
 most common parenchymal posterior fossa mass
in middle-aged, older adults is metastasis!
 Solid> cystic
 Multiple> single
Pilocytic astrocytoma
 usually in children

 Usually benign tumor with slow growth pattern
 Symptoms usually associated with cyst expansion
(may occur rapidly)
Treatment
 En bloc surgical resection (piecemeal may result
in catastrophic hemorrhage)
 Pre-operative embolization
 Sometimes used if large tumor nodule present (3.5
cm)

 Squamous cell ca lung
 Adenocarcinoma lung
 Carcinoma thyroid
 Multiple
 Typically at gray-white matter junction
 Disproportionate edema
 May show peripheral enhancement

• Hydatid
• NCC
• Abscesses

Vesicular stage:
 Larva is a small, marginal nodule projecting into small cyst with
clear fluid
 little or no inflammation
 May remain in this stage for years or degenerate
Colloidal vesicular stage: Larva begins to degenerate
 Scolex shows hyaline degeneration, slowly shrinks
 Cyst fluid becomes turbid and capsule thickens
 Surrounding edema and inflammation
Granular nodular stage: Cyst wall thickens and
 scolex is mineralized granule
 Surrounding edema regresses
Nodular calcified stage: Lesion is completely
 mineralized and small; no edema

Best diagnostic clue: Cyst with "dot" inside
Location
 May involve cisterns> parenchyma> ventricles
 Parenchymal cysts often hemispheric, at gray-white
junction
 Intraventricular cysts are often isolated
 Fourth ventricle is most common
 Rare CNS locations: Sella, orbit, spinal cord
Size
 Cysts variable, typically 1 cm, range from 5-20 mm
 scolex 1-4 mm

Morphology
 Rounded or ovoid cyst, solitary in 20-50%
 Disseminated form ("miliary" NCC) rare
 Imaging varies with development stage, host
response
 Lesions may be at different stages in same patient
 Inflammatory response around cyst may seal sulcus,
make lesions appear intra-axial

CT Findings
NECT
 Vesicular stage (viable larva): Smooth, thin-walled cyst, isodense to
CSF, no edema
 Hyperdense "dot" within cyst = proto scolex
 Colloidal vesicular stage (degenerating larva): Hyperdense cyst fluid
with surrounding edema
 Granular nodular (healing) stage: Mild edema
 Nodular calcified (healed) stage: Small, Ca++ nodule
CECT
 Vesicular stage: No (or mild) wall enhancement
 Colloidal vesicular stage: Thick ring-enhancing fibrous capsule
 Granular nodular stage: Involuting enhancing nodule
 Nodular calcified stage: Shrunken, calcified nodule
 Subarachnoid lesions: Multiple isodense cysts without scolex, may
cause meningitis
 Intraventricular cysts not well seen on CT, may see hydrocephalus

MR Findings
TlWI
 Vesicular stage: Cystic lesion isointense to CSF
 May see discrete, eccentric scolex (hyperintense)
 Colloidal vesicular stage: Cyst is mildly hyperintense to CSF
 Granular nodular stage: Thickened, retracted cyst wall
 Nodular calcified stage: Shrunken, Ca++ lesion
 Useful to detect intraventricular cysts
T2WI
 May see discrete, eccentric scolex
 No surrounding edema
 Colloidal vesicular stage: Cyst is hyperintense to CSF
 Surrounding edema, mild to marked
 Granular nodular stage: Thickened, retracted cyst wall; edema
decreases
 Nodular calcified stage: Shrunken, Ca++ lesion

FLAIR
 • May see discrete, eccentric scolex (hyperintense to
CSF); no edema
 Colloidal vesicular stage: Cyst is hyperintense to CSF
 Surrounding edema, mild to marked
 Useful to detect intraventricular cysts (hyperintense)
T2* GRE: Useful to demonstrate calcified scolex
DWI: Cystic lesion typically isointense to CSF
ADC values usually higher than tuberculomas

TI C+
 Vesicular stage: No enhancement typical
 May see discrete, eccentric scolex enhancement
 Colloidal vesicular stage: Thick cyst wall enhances
 Enhancing marginal nodule (scolex)
 Granular nodular stage: Thickened, retracted cyst wall; may have
nodular or ring-enhancement
 Nodular calcified stage: rare minimal enhancement
 In children, may see "encephalitic cysticercosis" with multiple small
enhancing lesions and diffuse edema
 Intraventricular cysts may cause ventriculitis and/or hydrocephalus
 Cisternal NCC may appear racemose (multilobulated, grape-like),
typically lacks scolex)
 Complications: Meningitis, hydrocephalus, vasculitis

Arachnoid cyst
 Solitary lesion with CSF density/intensity
 No enhancement
Enlarged perivascular spaces
 Follow CSF on all MR sequences
 No enhancement
Tuberculosis
 Tuberculomas often occur with meningitis
 Typically not cystic
 Usually lower ADC values

 Most common cause of epilepsy in endemic areas
 Intraventricular NCC has increased morbidity and
mortality
 Increased morbidity related to acute obstructive
hydrocephalus
Treatment
 Oral albendazole (reduces parasitic burden, seizures)
 Steroids often required to decrease edema during medical
therapy
 CSF diversion often required - hydrocephalus
 Endoscopic resection of intraventricular lesions in selected
cases
 Antiparasitic agents contraindicated in patients with
encephalitic cysticercosis

 Parietal lobe common; MCA territory
 Large uni- or multilocular cyst +/-detached germinal
membrane, daughter cysts, no edema
CT Findings
NECT
 Unilocular or multilocular cyst
 isodense to CSF
 no edema
 Ca++ rare (< 1%)
CECT – No enhancement typical

MR Findings
TlWI
 Cyst isointense to CSF
T2WI
 Cyst isointense to CSF with hypointense rim
 No perilesional edema
Tl C+
 No enhancement typical
 May see fine peripheral enhancement

 Large PF +
 big cerebrospinal fluid (CSF) cyst +
 normal 4th ventricle (V) absent
Location: Posterior fossa
Classic" DWM:
 Small hypoplastic vermis - superiorly rotated by cyst
 torcular arrested in fetal position (cyst mechanically hinders caudal
migration)
Dandy Walker Variant (DWV) - mild form of DW complex
 Variable vermian hypoplasia
 no or small cyst
 normal
 sized PF/brainstem

Radiography –
 Enlarged calvarium, particularly posterior fossa
 Lambdoid-torcular inversion (transverse sinus grooves
elevated above lambda)
 Sinuses are originally above lambda in fetus, cyst mechanically
hinders descent
CT Findings
NECT
 Large posterior fossa
 Variable-sized cyst communicates with 4th V
 Torcular-lambdoid inversion (torcular above lambdoid suture
 Occipital bone may appear scalloped

MR Findings
TIWI
 Floor 4th V present
 4th v opens dorsally to variable-sized CSF cyst
 Cyst wall difficult to discern
 Vermian remnant - rotated up
 +/- Remnant fused to tentorium
 Elevated torcular with high/steeply sloping tentorium (classic)
T2WI
 Associated anomalies
 Cortical dysplasia, heterotopias, myelination delays (syndromic
DWS)
FLAIR: Very slight differentiation between cyst, compressed basal
cisterns may be present
DWI: Very slight diffusion restriction in cyst may be seen
MRV: Elevated torcular Herophili (DWM)

 Cystic intracranial lesions – varied etiology
 MRI – preferred modality
 FLAIR and DWI – important sequences
 Prenatal diagnosis – congenital lesions
 Diagnosis important – treatment varies

 Diagnostic Imaging, Brain – first edition, Osborn.
 www.radiopedia.org

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