Meningiomas are tumors that arise from meningothelial cells of the arachnoid mater. They constitute 20% of all primary intracranial tumors with an incidence of 2.3 per 100,000 people. On pathology, meningiomas are graded based on their malignant potential from Grade I to Grade III. Grade I meningiomas include meningothelial, fibrous, transitional and psammomatous subtypes. Grade II are atypical meningiomas and Grade III include anaplastic, papillary and rhabdoid subtypes. Diagnosis is typically made based on imaging features seen on CT and MRI scans. Treatment involves surgical resection although radiation and medical management may

1. Meningiomas
Dr Kvv Raja Shekhar

2. • There is today nothing in the whole realm of
surgery more gratifying than the successful
removal of a meningioma with subsequent perfect
functional recovery. The difficulties are admittedly
great, sometimes insurmountable, & though the
disappointments are still many, another
generation of neurosurgeons will unquestionably
see them largely overcome
Harvey Cushing, 1922

3. • Meningioma was the term coined by Harvey
Cushing in 1922
• In 1864, John Cleland speculated that they arise
from arachnoid cell clusters
• In 1915, Cushing & Weed reconfirmed this

4. The meninges: embryology &
histology
• Consist of 3 layers – dura( i.e., pachymeninx)
• Arachnoid & pia (leptomeninges)
• At 22 to 24 days of gestation a monocellular layer
of cells of neural crest origin surround the neural
tube – the pia
• At 33 to 41 days the CNS is surrounded by a
multiple layer of mesenchymal cells – gives rise to
dura & arachnoid mater

5. • The arachnoid has 2 cell populations
• One subgroup follows the dura closely & is formed
by the arachnoid barrier cells
• The other consists of arachnoid trabecular cells &
bridges the subarachnoid space to attach to the
pia mater
• CSF is reabsorbed by the arachnoid villi
• Arachnoid villi protrude into venous sinuses

6. • Venous endothelium in contact with arachnoid cap
cells, the rest of the granulation is covered by a
fibrous capsule
• Arachnoid villi are numerous in – SSS, cavernous
sinus, tuberculam sella, lamina cribrosa, foramen
magnum & torcular herophili
• Arachnoid granulations & pacchionian bodies are
larger & more pronounced versions of arachnoid
villi

8. Incidence
• Constitute 20% of all intracranial neoplasms
• Overall incidence 2.3/100,000
• Male:Female – 1:2
• 1—4% of childhood(< 18) tumors
• Mean age of pt – 58 ± 15 yrs

9. Etiology
• Head trauma – Cushing
• Recent information suggests that head trauma is
not significant in the etiology of meningiomas

10. Viruses
• Inoue-Melnick (IMV) virus
• DNA virus causing subacute myelo-
opticoneuropathy
• In a study from Japan 84.6% of meningioma pt
were positive for the IMV antibody
• Though there is a strong biochemical evidence their
role in the development of tumor remains
undefined

11. Irradiation
• Radiation injury is a proven factor in the
development of meningiomas
• 4 times more common in pt irradiated as per
Kienbock-Adamson technique
• Does the use of mobile phones increase the risk for
meningiomas?

12. Neurofibromatosis
• Are more common with type 2 NF
• Frequently multiple
• Can be spinal or cranial

13. Oncogenes related to meningiomas
Oncogene Aberration Reference
sis Amplification Fujimoto
myc Amplification Sauceda
Ha-ras Ampilfication Diedrich
c-mos Rare allele Diedrich
merlin Ampilfication Kimura

14. Meningiomas & receptors
• Donnell described estrogen receptor in
meningiomas
• Progesterone receptors have been more
consistently identified in the cytoplasm of
meningiomas
• somatostatin, glucocorticoid,androgen & dopamine
receptors have also been found
• Increased levels of CEA & PRL
• Interfere with glucose metabolism by increasing
insulin levels

15. Grade 1 – meningothelial
fibrous (fibroblastic)
transitional (mixed)
psammomatous
angiomatous
microcystic
secretory
lymphoplasmacyte-rich
metaplastic
Grade II – atypical
clear cell
chordoid
Grade III – rhabdoid
papillary
anaplastic

16. Pathology
• 2000 WHO classification
• Listed under the heading “tumors of the meninges”
• Subheading “tumors of meningothelial cells”
• Recognizes three grades based on pathologic
criteria & reflects on their risk of recurrence &
aggressive growth

17. Gross
• Globular, encapsulated tumors
• Attached to dura & compress the underlying brain
without invasion
• Are usually easily separated from pia
• May occur as a flattened sheath of tumor, taking
the shape of the under lying bone, meningioma en
plaque more common in the area of the sphenoid
bone

19. • Cut surface pale & translucent or homogenous &
reddish-brown, depending on the degree of
vascularity
• Gritty in consistency
• Cut surface has a whorled pattern after fixation
• Intratumoral hemorrhage is rare, & necrosis is
generally absent (occurs with malignant
degeneration)

21. Distribution of intracranial
meningiomas
• Convexity-35%
• Parasagittal-20%
• Sphenoid ridge-20%
• Infratentorial-13%
• Intraventricular-5%
• Tuberculam sella-3%
• Others-4%

22. Microscopy
• Meningotheliomatous- characterized by a lobular microarchitecture
and are populated by cells having delicate round or oval nuclei,
inconspicuous nucleoli, lightly eosinophilic cytoplasm, and indistinct
cytoplasmic borders (thus their alternative designation as syncytial
meningiomas).
• Common to these (and other subtypes) are tumor cells concentrically
wrapped in tight whorls, pale nuclear "pseudoinclusions" consisting of
invaginated cytoplasm (orphan Annie’s eye), and the lamellated
calcospherules known as psammoma bodies
• While none of these features are pathognomonic of meningioma, their
demonstration in the setting of an extra-axial, dural-based mass carries
considerable diagnostic weight.

25. Fibroblastic
• Fibroblastic or fibrous meningiomas adopt a
mesenchymal profile, being variably collagenized
and consisting of spindly tumor cells in fascicular or
storiform array.
• Syncitial nature is lacking
• Palisading of nuclei may lead to confusion with
schwannoma

27. Transitional
• As their name implies, are hybrids, maintaining a lobular arrangement
but evidencing a tendency to cellular elongation and streaming.
• These are often particularly rich in compact cellular whorls and
endowed with psammoma bodies in conspicuous numbers.
• When the latter are present in profusion, the term psammomatous
meningioma may be applied.
• Such tumors exhibit a particular predilection for the intraspinal
compartment.
• It should be noted that none of the foregoing growth patterns is of any
special biologic significance, most neuropathologists dispensing with
these qualifying adjectives in their reporting of surgical material.

29. Secretory
• A variant of the meningotheliomatous subtype, is
distinguished by its content of "pseudopsammoma
bodies"—globular hyaline inclusions that are
eosinophilic, intensely PAS positive
• Although entirely benign, the secretory
meningioma may masquerade as a malignant
neoplasm by virtue of its occasional association
with elevated serum CEA levels

31. Angiomatous
• Hypervascular, characterized by the presence of
exuberant large & small, well differentiated
vascular channels
• Intervening btw these are small nests of
meningotheliomatous, fibroblastic or transitional
meningiomas

33. Microcystic
• Mason – for soft, glistening & succulent tumors on
macroscopy
• Is named for its content of variably sized
intercellular vacuoles, these often appearing empty
but in someinstances containing a lightly PAS-
positive fluid derived in all likelihood via the
transudation of plasma across the neoplasm's
characteristically rich,and frequently hyalinized,
stromal vasculature

34. Lymphoplastic
• Have infiltrates of mononuclear cells
• Behave in a benign fashion

35. Atypical
• Associated with higher recurrence rate &
aggressive behaviour
• Criteria are increased mitotic activity (4 or more
mitosis/10 high power fields) or 3 or more of the
following features: increased cellularity, high
nucleus to cytoplasm ratio, prominent nucleoli,
sheet like growth, & foci of spontaneous or
geographic necrosis

40. Papillary
• Characterized by the ependymoma-like perivascular
structuring of its constituent cells.
• The latter can be seen to extend variably elongated
cytoplasmic processes toward vessel walls, fashioning
pseudorosettes that frequently appear to float unanchored
in tissue sections
• Usually depart from the typical in evidencing worrisome
hypercellularity, brisk mitotic activity, and in some cases,
foci of coagulative necrosis.
• Papillary meningiomas are potentially aggressive
neoplasms noted for their tendency for stubborn local
recurrence, their capacity for extraneural metastasis, and
their often fatal outcome.
• An excess of reported cases have presented in childhood or
adolescence.

42. Anaplastic meningioma
• Exhibits frank features of malignancy
• Have an appearance similar to sarcoma or
carcinoma
• High mitotic index(20 or more/10 HP fields)

44. Features suggesting aggressiveness
• Hypercellularity
• Loss of architecture
• Nuclear pleomorphism
• Increased mitotic index
• Focal necrosis
• Hypervascularity
• Hemosiderin deposition
• Small cell formation

45. Extra-neuraxial meningiomas
• Orbit
• Paranasal
• Sinuses
• Nasopharynx
• Skin & subcutis
• Lungs
• Mediastinum
• Adrenals

46. • Can metastasise to lungs, liver, pleura & lymph
nodes
• Abscesses can occur within meningiomas

47. Meningiomas & brain edema
• 4 major theories
1- disruption of BBB
2- mechanical compression
3- vascular compression
4- secretion of edemogenic
factors

48. Management
• Investigations –xray skull, ct / mri plain &
contrast , Angiography, Somatostatin receptor
scintigraphy(Indium 111) , FDG PET , MRS ,
DD on Radiology – NEUROSARCOIDOSIS , Superficial
mets ,solitary fibroid tumours
• Treatment—Observation, surgery , embolization ,
radiation, medical management

49. Plain radiographs
• Hyperostosis (38-61%)
• Calcifications (3-18%)
Increased
vascular marking

50. Diagnosis of meningioma made on
basis of
• A) morphology- the configuration of the mass, it’s
location, & it’s effect on adjacent brain
• B) the density (CT), intensity (MRI), & enhancement
features of the mass
• C) the presence of ancillary findings

51. CT of intracranial meningiomas
• Plain CT- isodense to slightly hyperdense relative to
brain parenchyma
• Density homogenous & sharply marginated
• Calcification- a) tiny punctate (psammomatous)
is common
b) dense calcification of entire
lesion
c) nodular calcification, less
common

52. Contrast CT
• Homogenous, intense enhancement
• Result of passage of iodinated contrast material
into the interstitial space of neoplasm, rather than
hypervascularity
• Being extra-axial has no blood brain barrier
• Margins sharp & broadly based against a bony
structure or a free dural edge

54. Coronal scanning
• Relationship to bony
structures, as well as
dural structures
demonstrated
• Displacement of vessels

55. • Contiguous bony structures altered, either due to
direct infiltration or because of reactive changes to
hypervascularity of the neoplasm
• Commonest finding is hyperostoses
• New bone less homogenous & has irregular
margins
• Bony erosion by pressure from an adjacent tumor

56. CT signs S/O aggressive course
• Heterogeneous contrast enhancement
• Indistinct or irregular margins
• Minimal or no calcification
• Marked surrounding edema
• Mushroom-like projections

57. MRI
• Extra-axial dural based lesion- a mass is said to be
dural based when the greatest diameter occurs at
the margin of the tumor that abuts against the
dural surface
• Extra-axial- interface present, dilated subarachnoid
space, buckling of white matter
• Displacement, encasement, narrowing & occlusion
of surrounding vessels better visualized

58. • T1 – 60% are isointense,
30% mildly hypointense
to gray matter

59. MRI-T2
• On proton density & T2
isointense(50%), mild to
moderate
hyperintensity(40%)
• Hyperintensity S/O
higher water content-
probably
meningothelial,vascular,
aggressive,microcystic

60. Contrast MRI
• Homogenous contrast
enhancement-intense
and uniform
• Dural tails-histologically
has connective tissue .
Vascular tissue
,meningioma cell nests

63. Observation
• 3mo-9mo-yearly for 5 years-biannually thereafter
• Symptomatic / rapid growth
• 2 exceptions-younger patients <45 yrs
tuberculum sella meningioma(d/t
rapid visual deterioration)

64. Surgery
• Simpson
• Kobayashi and associates-microscopic
• Location decides extent of resection and thus
recurrence
• Yamasaki&colleagues-3 yr followup(VEGF&MIB-1)
• Extent of removal*

67. Radiation
• Malignant meningioma
• Following incomplete resection
• Multiple recurrent tumours
• Inoperable patients

68. THANK YOU

71. Convexity Meningiomas
• A meningioma whose
attachment does not lie
on the dura mater of the
skull base & does not
invade any of the dural
venous sinuses
• Most common subtype

72. Types of convexity meningiomas
• Anterior- attachment lies at or in front of the coronal
suture & include meningiomas of the pterion growing
solely or mainly towards the frontal bone
• Median- those astride the Rolandic fissure
• Posterior- those attached to the posterior parietal &
occipital regions
• Temporal- both tumors developing in the temporal
lobe & those of the pterion that grow postmed &
project on to the temporal side of the sylvian fissure

73. Clinical presentations
• Anterior- altered mentation
• Seizures
• Symptoms of raised ICT
• Motor deficit affects face & upper limb
• Vague signs of pyramidal involvement

74. Median
• Sensory & motor signs
• Jacksonian seizures, preceded by motor or less
often sensory aura
• Speech disturbance when the lesion affects the
dominant lobe

75. Posterior
• Least common variant
• Signs of raised ICT
• Sensor motor symptoms
• Field defect- homonymous hemianopsia

76. Temporal
• Epileptic fits
• Contralateral motor deficit
• Visual field deficits
• Speech disturbances- dominant lobe
• Ipsilateral motor disturbance- if it compresses the
peduncle against the edge of the tent

77. Parasagittal Meningiomas
• As one that fills the
parasagittal angle with
no brain tissue btw the
tumor & SSS
• Anterior, middle ( MC) &
posterior third

79. Symptomatology
• Anterior- long H/O headache associated with
secondary optic atrophy
• Mental deterioration as evidence by memory
impairment, change of personality, self neglect
• Hyperostosis of skull presenting as a swelling

80. Middle
• Jacksonian seizures beginning in the foot
• Followed by spastic paralysis which begins in the
corresponding leg

81. Posterior
• Symptoms of raised ICP
• Seizures
• Visual field defects

82. Falcine Meningiomas
• The falx meningioma
arises from the falx
cerebri & does not
involve the SSS
• Should lie in complete
concealment by the
overlying cerebral cortex

83. Types
• Anterior ,middle(MC) & posterior third falcine
meningimas
• Anterior- from crista galli to coronal suture
• Middle- from the coronal to lambdoid suture
• Posterior- from the lambdoid to the torcula

84. Clinical features
• Anterior falx- symptoms raised ICP, progressive
dementia, gradual personality changes, seizures
infrequent & nonfocal
• Middle- focal motor or Jacksonian sensory march
seizure. Progressive loss of neuro function &
spaticity of lower extremities may also accompany
• Posterior- headache, symptoms of raised ICT, visual
field defects

85. Tentorial
• May present with psychiatric symptoms or seizures
• Can extend infratentorially & produce cerebellar
symptoms

86. Classification
• Medial tentorial meningiomas
• Lateral tentorial meningiomas
Medial & lateral are sub-divided into anterior,
middle & posterior
 Falcotentorial (para straight sinus) meningiomas

87. Olfactory groove meningiomas
• Arise in the midline of the AF over the cribriform
plate of the ethmoid & the area of the suture
joining this structure & the planum sphenoidale.
May extend from crista to post planum sphenoidale
• Blood supply from br of ethmoidal, meningeal, &
ophthalmic arteries
• Olfactory nerves displaced laterally

88. Clinical features
• Grow to large size before causing symptoms
• Features of raised ICP, personality changes
• Anosmia not an important symptom but picked up
on clinical evaluation

89. Tuberculam sella meningiomas
• Arise from the tuberculam sellae, chiasmatic sulcus,
limbus sphenoidale & diapragma sellae
• Optic nerve elevated & laterally displaced
• Blood supply from the posterior ethmoidal arteries
& small br from the ACA
• Large tumors compress the hypothalamus & third
ventricle
• 5-10% of intracranial meningiomas

90. Cushing’s classification
• Based on size
• I: initial stage
• II: presymptomatic
• III: favorable for
surgery
• IV: late or inoperable

91. Clinical findings
• Chiasmal syndrome- bitemporal field defect
• Optic atrophy
• Headache
• Anosmia & personality changes
• Rarely hypothalamic dysfunction

92. Lateral & Middle Sphenoid Wing
Meningiomas

93. Group A
• Extend from the dura of
the cavernous sinus, the
anterior clinoid process
& from the internal part
of the sphenoid wing. In
close contact with optic
nerve & with the carotid
& it’s branches

94. Group B
• Meningiomatous cells
invade the hyperostosing
bone, the plaque
spreads into the dura of
the sphenoid wing &
cavernous sinus.
• Compress the optic
nerve
• Extend down through
base of skull

95. Group C
• Are very invasive
• Spread over the midline
& the clivus

96. Group D
• Non-invading
meningioma that can be
easily manipulated
because it’s stalk is small
• No close connection to
internal carotid or optic
tract

97. Group E
• Fastened to the external
part of the sphenoid
wing, at the border of
the skull base & the
vault
• Distort the frontal &
temporal bone

98. Clinoidal meningiomas
• Divide into three subgroups based on the presence of
an interfacing arachnoidal membrane btw the tumor
& cerebral vessels
• Group I: origin proximal to the end of the carotid
cistern, as in the case of a meningioma originating at
the inferior aspect of clinoid process
• Tumor enwraps the carotid lacking an interfacing
arach membrane
• Accounts for inability to dissect tumor from vessel

99. Group I tumor

100. Group II
• Originates from the superior &/or lateral aspect of
ant clinoid process above the segment of the
carotid artery invested in the cistern
• There is an arachnoidal membrane of the carotid
cistern & distally of the sylvian cistern separating
the tumor from vessel
• Microsurgical dissection feasible

102. Group III
• Originates at the optic foramen, extending into the
canal & the tip of the ant clinoid process
• Usually small tumors
• Arachnoidal investment btw the vessels & tumor is
present but may be absent btw tumor & optic
nerve

104. Clinical features
• Unilateral visual loss, Foster-Kennedy syndrome
• Invasion of SOF & cavernous sinus leads to cranial
nerve palsies & exophthalmos
• Seizures, mental changes, hemiparesis, & anosmia,
depending on tumor size

105. Meningiomas of the cavernous sinus
• Meningiomas involving the CS may start in areas
outside the CS & invade it secondarily, or start
within it & spread outside

108. Cerebellar convexity meningiomas
• 1- 2% of all meningiomas
• 10-18% of posterior fossa meningiomas
• Present with headache, progressive cerebellar signs
• Raised ICP & symptoms of hydrocephalus
• Tend to be large before causing symptoms
• Very often detected incidentally

109. CP angle meningiomas (post pyramid
menigios)
• Tumors located anterior to IAM- present with
decreased hearing. En plaque type more common
• Tumors located posterior to IAM- presenting with
cerebellar signs

110. Clival & Petroclival meningiomas
• Clival meningiomas are defined as those attached
at any of the lateral sites along the petroclival
borderline where the sphenoid, petrous & occipital
bones meet

111. • Clinical findings can be grouped into 4 major
etiologies based on
A) Cranial nerve involvement
B) Cerebellar compression
C) Brain stem compression
D) Increased ICP

112. Meningiomas of the temporal bone
• Slow growing tumors
• Earliest presentation is feeling of fullness in
ipsilateral ear
• Vestibular dysfunction may occur
• Anterior extension involves Vth or CS
• Posterior extension into PF, causes CP angle
syndrome