Meningioma

ruhul006 1,717 views 64 slides Jul 11, 2017
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About This Presentation

meningioma


Slide Content

MeningiomaMeningioma
Dr Ruhul AminDr Ruhul Amin
Dept of medicineDept of medicine
jrrmchjrrmch

Meningioma
Etiology
Arise from specialized meningothelial cells called arachnoid cap cells
Incidence
* Most common non-glial primary brain tumor
* 15-20 % of primary brain tumor
88-95% typical meningioma
5-7% atypical meningioma
1-2% anaplastic(malignant) meningioma
Age& Gender

* Peak incidence 40-60 years
* F:M=2:1 to 4:1

Location
* Parasagital-25%
* Convexity-20%
* Sphenoid ridge-15-20%
* Para-sellar-5-10%
* Olfactory groove-5-10%
* Posterior fossa-10%
* Other(Intraventricular,pineal region,
optic nerve sheath)-2%
* Extra-cranial -1%
Imaging
Plain film
* Hyperostosis
* Erosion
* Enlarged vascular channels
* Tumor calcifications

ImagingImaging
NECT
70-75% Hyperdense
relative to adjacent brain
25% Isodense
1-5% hypodense
20-25% calcified
Bony hyperostosis
Cystic change or necrosis
8-23%
Perifocal oedema –60%
Haemorrhage-rare
CECT
Intensely enhanced in
90% cases
MR
Typically isointense with
gray matter
>95% enhance strongly
CSF cleft
60% have dural tail

Case No 01Case No 01
Pre Con Post Con

Case No-02Case No-02
Pre Con
Post Con

Case No-03Case No-03
Axial T1
Axial T2

Case No-03Case No-03
Axial T1 Contrast
Coronal T1 Contrast

Glioma(Low grade astrocytoma)Glioma(Low grade astrocytoma)
Pathology
Either focal well delineated or diffusely
infiltrating mass.WHO grade II
Incidence-10-15 % of astrocytoma
Age-Children & young adult between 20-40 yrs
Location-Cerebral haemispheres.
Natural history-7-10 yrs survival.
Death due to degeneration into higher grade
neoplasm

ImagingImaging
NECT-Focal/diffuse hypodense mass
Calcification-15-20%
Oedema-absent
CECT-Enhancement absent/Mild
MR-T1-hypo & T2 hyperintense.

T1 pre & post contrastT1 pre & post contrast

Glioblastoma multiforme(GBMGlioblastoma multiforme(GBM))
Pathology
Most malignant of all glial neoplasm.
Poorly delineated partially necrotic mass
WHO grade –IV
Incidence-50 % of all glial neoplasm
Age- Older patient >50 yrs; rare <30 yrs.
Location- Deep cerebral white matter
Natural history-Spread rapidly & diffusely
Postoperative survival of GBM is 08 month
05 yrs recurrence free survival rate is essentially zero.

ImagingImaging
NECT-Heterogeneous mixed density mass having necrosis or
cystic changes
Marked perifocal oedema
Haemorrhage common.Calcification rare
CECT- Strongly enhance but very inhomogeneous.Thick
irregular rim enhanement is common.
MR-T1-Mixed signal mass with necrosis or cyst
formation and a thick irregular wall.
Marked heterogeneous enhancement is noted.
T2-Heterogenously hyperintense with perifocal oedema.

P1 Pre conP1 Pre con

P1-Post conP1-Post con

Pre con Post con
P2P2

P3- T1 & T2P3- T1 & T2

P3 post conP3 post con

Pituitary AdenomaPituitary Adenoma
Pathology
Macroadenoma > 10 mm ,Microadenoma <10 mm
Necrosis,cyst formation & haemorrhagic foci common
Incidence
10% of all primary tumor
Microadenoma>>Macroadenoma
Imaged based-Macroadenoma twice as microadenoma
Age & Gender
Adult tumor(<10% in children)
F:M=4-5:1 for prolactinoma; M:F=2:1 for growth
hormone cell adenoma

ImagingImaging
Plain X-Ray
Sella is expanded,widened and eroded
CT
Microadenoma-Isodense/isointense on NECT/MR
Hypodense/hypointense on dynamic CECT-appears filling
defect within enhanced normal gland.
Macroadenoma-
NECT- Most are isodence with the cortex
Calcification rare-1-4%
Necrosis,cyst formation and haemorrhage causes
mixed density lesion
CECT - Moderate enhancement .
MR- Signal like cotrex on T1 & T2.
Variable if haemorrhage,necrosis or cyst formation is present.

Case No-01Case No-01
Skull

Case No- 01Case No- 01
Pre Contrast Post Contrast

Case No-01Case No-01
Pre Con Coro Post Con Coro

Case No-02Case No-02
Skull

Case No-02Case No-02
Pre Con
Post Con

CraniopharyngiomaCraniopharyngioma
Etiology
Arises from squamous rest along Rathke’s cleft
Pathology
Gross- Well delineated cyst with mural nodule most common
Micro-Squamous epthelium with necrosis,debris,cholesterol
clefts,keratin pearls.
Incidence
3-5% of all primary brain tumor
50% of paed.suprasellar tumors.
Age
Peak age-8-12 years
Second peak-40-60 years
Location
70% combined suprasellar/intrasellar,Intrasellar is rare.

ImagingImaging
NECTC- * Cystic appearing lobulated suprasellar mass with
* mural nodule
* Nodular or rim calcification-in 80% paed.case,50%-adult
* Density of cyst is slightly higher than CSF.
CECT- Nodular or rim enhancement in more than 90% cases.
MR - * Hypointense on TI & Hyperintense on T2
* Hyperintense on T1 if high protein concentration
* Nodular or rim enhancement after contrast.

Case No -01Case No -01
Axial T1
Axial T2

Case No-01Case No-01
Axial T1 Post Con
Coronal T1 Post Con

Acoustic SchwannomaAcoustic Schwannoma
Pathology
Arises from schwann cells
Encapsulated,Focal & Round
Cyst,necrosis & haemorrhage common
Don’t undergo malignant transformation.
Multiple –NF 2
Incidence - 6-8% of primary brain tumor
Age - 40-60 yrs common
Location-CN VIII - CP angle

ImagingImaging
Plain X-Ray-Widening of the internal auditory canal
NECT
Isodense or slightly hyperdense to adjacent brain
Mixed density if cystic change or necrosis is present.
CECT
Virtually all schwannoma enhancee strongly following
contrast.
Heterogeneous enhancement occurs if cystic change or
necrosis is present.
MR-
T1-2/3
rd
hypointense,1/3
rd
isointense
 T2-Hyperintense
Strongly enhance after contrast.

P1 PreconP1 Precon

P1-Post conP1-Post con

P2 axial T2P2 axial T2

MedulloblastomaMedulloblastoma
Pathology
75% in the vermis,25% in the lateral cerebellum
Uncapsulated but relatively well circumscribed spherical midline
posterior cranial fossa mass
Anteriorly bulges into 4
th
ventricle & posteriorly into cisterna magna
Densely cellular
Gross calcification,cyst formation and haemorrhage are rare
Incidence-15-25% 0f primary CNS tumor in children.
one third of posterior fossa tumor in children common.
75% in the vermis
Age & Sex-75% <15 yrs of age
50% in the first decade
Second smaller peak age in adult 24-30 yrs
M:F=1.5 to 3:I

ImagingImaging
CT
Hyperdense on NECT; Enhance strongly following
contrast
Obstructive hydrocephalus is common
Calcification –15%
MR
Hypointense on T1W1,Variable on T2W2
Moderately intense enhancement is typical
Heterogenous –if cystic changes is present.

Case no 1Case no 1

Case no 1Case no 1

Axial T1 Axial T2
Case No -01Case No -01

Case No-01Case No-01
Axia T1 post Con

Case No-01Case No-01
SAG T1
SAG T1 Post Con

Arachnoid cystArachnoid cyst
Etiology-Meningeal maldevelopment
Pathology
Thin walled CSF like fluid filled cavity that
lie entirely within the arachnoid membrane
lined by flattened arachnoid cells.
Incidence-1% of all intracranial mass.
Age and sex-Any age but 75% in
children.M:F=3:1
Clinical presentation-headache,seizures and
focal neurological sign.

Arachnoid cyst Cont.Arachnoid cyst Cont.
Location
Middle cranial fossa- 50-60%
Supracellar cistern- 5-10 %
Quadrigeminal cistern- 5-10 %
Cerebral convexity- 5 %
Posterior fossa
-CP angle
-Cisterna magna

ImagingImaging
CT
Smoothly marginated nonenhancing extra-
axial mass similar to CSF attenuation
Pressure erosion of adjacent calvaria can
occur.
MR
They parallel CSF signal intensity on all
pulse sequence.The cyst has no internal
character unless haemorrhage or high
protein content.

Pre & post contrast CTPre & post contrast CT

Axial T1 & T2Axial T1 & T2

Parenchymal metastasesParenchymal metastases
Etiology
Lung,Breast.Melanoma,GIT & Genitourinary
tumor
Pathology-Rounded solid/partially cystic mass
with oedema.
Incidence-1/3
rd
of all brain tumor
Age-Most common in older adults->40 yrs
rare in children.
Location-Any where; gray-white matter junction is
common.

ImagingImaging
NECT-
Iso/hyperdence with perifocal oedema
Cystic
CECT
Strong solid/ring enhancement.
MR-T1-hypo & T2 hyperintence.

P1 Pre conP1 Pre con

P1-Post conP1-Post con

P2P2
Pre con Post con

AVMAVM
Pathology
AVMs are complex network of abnormal
vascular channels that consists of arterial
feeders,arterial collaterals,the AVM nidus
and enlarged venous out flow channels.
Congenital
Dilated arteries and veins without capillary
bed.
May contains non funtional gliotic brain.

AVMs Cont.AVMs Cont.
Location
85% supratentorial,15% posterior fossa
Age- Peak age-20-40 yrs,25% in
chlidren/adolescence
Symptoms
Haemorrhage-50% ,Seizures-25%
Neurological deficit-20 to 25 %.

ImagingImaging
NECT-Isointense or slightly hyperintense lesion.
Calcification is noted in 25-40%
Haemorrhage may be found.
CECT-Intense serpiginous enhancement is noted in
the vessels.
MR-Tightly packed of honeycomb of flow void.
Areas of increased signal if vessels are
thrombosed or slow and turbulence flow.
Haemorrhage in different stage of evolution.

Axial Pre Con
Axial Post Con

SchizencephalySchizencephaly
Gray matter lined CSF filled clrft that
extended from the ependymal surface of the
brain through white matter to the pia.
Type-I Closed lip-in which the cleft walls are
in apposition
Type-II Open lip-in which the cleft walls are
separated.

Axial CT

HydranencephalyHydranencephaly

Spinal Nerve sheath tomourSpinal Nerve sheath tomour

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