Meningioma are the common extraxial tumor of brain meningothelial tumor arising from the arachnoid cap cells of arachnoid granulation.

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BASIC PRINCIPLES IN
MENINGIOMAS
DR. SURESH BISHOKARMA
MCH NEUROSURGERY ®
UPENDRA DEVKOTA MEMORIAL NATIONAL INSTITUTE OF
NEUROLOGICAL AND ALLIED SCIENCES
BANSBARI, NEPAL

2.  1922: Harvey Cushing coined the term meningioma to describe a benign
globoid tumor arising from the leptomeninges.
 Eisenhardt believed meningioma arises from arachnoid cap cells that are
particularly abundant in the arachnoid granulation.
 Virchow was the first to describe the classic pathologic feature of the
meningioma with the term psammoma body (sand like, rightly describing
the granules noted within the tumor).
 1957: Donald Simpson's 1957 paper described the correlation between
surgical resection of meningiomas and the rates of symptomatic
recurrence:
HISTORY

3.  Slow growing, extra-axial tumor, usually benign neoplasms thought to
arise from meningothelial cells found within arachnoid granulations (not
dura).
 Concentrated in the walls of the major venous sinuses, these structures,
which contain “arachnoid cap cells,” account for the dural localization of
most meningiomas within the cranium and spinal cord.
 Although most are benign (70-75%), a few are classified as atypical (20-
24%) or anaplastic (4%).
 Metastases are uncommon and may be seen with benign or malignant
meningiomas.
INTRODUCTION

4.  Meningiomas: 13 to 26% of all intracranial tumors.
 Skull base meningiomas comprise approximately 44% of all skull base
tumors.
 98% of all CNS meningiomas (spinal 2%).
 An annual estimated incidence of 2.3 cases per 100,000 persons.
 Autopsy: 3% of the population over 60 years of age.
 Female preponderance (1.8)
 Peaks age: fourth decade (45yrs)
 Meningiomas are less often seen in the younger age groups.
 Less than 2% occur in childhood and adolescence.
 About 20% of cases seen in adolescents are associated with NF-I.
 Approximately 1% of meningioma patients have neurofibromatosis 2 (NF2).
 May be multiple in up to 8% of cases.
EPIDEMIOLOGY

5.  Ionisation radiation: DNA damage resulting for SS or DS DNA break.
 Atomic bomb (epicenter); low dose scalp IR for ringworm; 10x; Israel (1948-60); Full mouth dental
IR; XRT for IC tumors.
 Hormones:
 Est, Prog, Androgens; Size (+): Luteal/pregnancy; 22q12 related with progesterone expression.
 Progesterone alone: Good : Absence of Prog or Est recep or Presence of estrogen alone: Bad.
 Three Chicago areas hospital: 1987-1992: Protective effect of OCP/HRT.
 OCP/HRT: Interphone group: 1993-2002: Increases risk (OR 1.7 HRT/2.7X OCP)
 Mayo Clinic jacksonville patient database; OR 3X
 Infer Limited statistical evidence of increaed risk.
 BMI: Increased BMI association.
 Head Trauma: Harvey Cushing; Danish study: 228,055 Cohort of head injury: F/u 8yrs; No evidence.
Proinflammatory enzyme COX-2 is upregulated after head trauma: Celecoxib# decreases progression.
 Cell Phone use: 10 studies including Interphone Study ; inconclusive; Small sample size; short f/u.
 Association with breast cancer: Common hormonal risk factor and genetic predisposition; BRCA1
interacting protein 1 (BR1P1) is associated with meningioma risk.*
 Industry/Occupation/Diet/Allergy: Chemical (inconclusive); Diet (no): International Case control study;
Allergic diseases like asthma/eczema associated with glial tumor not evident with meningioma.
 Positive familial history:2X: 1st degree.
 Genetic polymorphism: BR1P1; ATM gene. LOH of chromosome 22 and NF2 gene mutation are
implicated in ~50% of sporadic and 100% of NF2-associated meningiomas.
RISK FACTORS
# Ragel Btet al. Celecoxib inhibits meningioma tumor growth in a mouse xenograft model. Cancer 2007.
*Bethke L et al. Comprehensive analysis of DNA repair gene variants and risk of meningioma. J Natl Cancer Inst 2008.

6. MENINGIOMA TUMORIGENESIS

7. MENINGIOMA TUMOR PROGRESSION

8.  The loss of the long arm of chromosome 22 occurs in 40 to 70% of
meningiomas and is associated with loss of the tumor suppressor gene
(MERLIN) for neurofibromatosis type 2 (NF2), located at 22q12.
 The product of this gene, merlin, is thought to be critical for meningioma
tumorigenesis.
 Merlin belongs to the family of structural proteins that link the
cytoskeleton to several proteins of the cytoplasmic membrane, and some
authors have suggested that merlin may act as a tumor suppressor via its
interactions with the cellular cytoskeleton.
Merlin and Meningioma

9.  It has also been demonstrated that MRI hypointensity on T2-weighted images
is associated with slowed tumor growth, and that MRI hyperintensity on T2-
weighted images is associated significantly with faster tumor growth.
 An annual growth rate of > 1 cm3/year or volume increases > 15% were
considered tumor growth.
 Growth has been defined as a change in tumor size of at least 2 mm,3 5
mm,12 or any measurable change
 Many authors have pointed out that meningiomas without calcification on
imaging are more likely to progress than are calcified meningiomas and no
negative correlation between calcification and slow growth has been
reported.
 Presence of peritumoral edema, ambiguous brain- tumor borders, and
irregular tumor shape are predictor of tumor growth: needs further study.
 Location don’t affects tumor growth.
Tumor growth

10. LOCATION OF MENIGIOMA
GREENBERG 8TH ED
LOCATION OF MENINGIOMA PERCENTAGE
Parasagittal 20.80%
Convexity 15%
Tuberculum sella 13%
Sphenoid wing 12%
Olfactory 10%
Falcine 8%
CPA 6%
Intraventricular 4%
Tentorial 4%
Suprasellar 3%
Middle fossa 3%
Foramen magnum 2%
Orbital 1.20%
Spinal 1.20%
Multiple 0.90%
Pineal 0.50%
Intrasylvian 0.30%
Extracalvarian 0.30%
Others 5%

11. Artist's Composite of Different Potential Locations
of Meningiomas
1. Convexity; 2. olfactory groove: 3. sphenoid ridge; 4. Tuberculum sella: 5. Dorsum sellae; 6. Meckel cave. cranial nerve V:
7. Clivus: 8. Petrosal : 9. Tentorial: 10. Sigmoid sinus: 11. Straight sinus: 12. Transverse sinus: 13. Torcular-supra-infra
tentorial meningioma: 14.Supratentorial interhemispheric meningioma: 15. Falx; 16. superior sagittal sinus.
Nader Tricks and Trade of cranial Neurosurgery

12.  The grading has been done on the basis of histological markers, which
includes,
1. Presence and number of mitotic figures,
2. Overall cellularity,
3. Nuclear to cytoplasmic ratio,
4. Nuclear prominence,
5. The presence of necrosis
 Though the majority of meningiomas are benign Grade I tumors, 23-24% of
the tumors are atypical (Grade II) and 1-3% are found to be anaplastic (Grade
III) under the new WHO classification system.
 Meningiomas with a low risk of recurrence and nonaggressive growth are
classified as grade I, whereas those with a higher likelihood of recurrence and
more aggressive behavior are classified as either grade II or grade III
meningiomas.
CLASSIFICATION

13.  In general, cellular proliferation increases in proportion to grade.
 The mitotic index and Ki-67 proliferation index correlate
approximately with volume growth rate.
 Meningiomas with an KI-67 index of:
 > 4% have an increased risk of recurrence similar to that of atypical
meningioma
 > 20% are associated with death rates analogous to those associated
with anaplastic meningioma.
 Mitotic index: > 4 mitoses per 10 high-power fields: Malignant.
PROLIFERATION

14.  The symptoms and signs are consistent with;
 Localization
 Mass effect
 Increased intracranial pressure due to tumor size.
 Massive intra- cranial hemorrhage and
 Hypoglycemia from tumors that release insulin-like growth factor:
rare.
CLINICAL FEATURE OF MENINGIOMA

15.  The most common clinical features are the following:
• Headaches
• Weakness/paresis
• Altered mental status
 Less commonly, other features noted due to the location of the meningioma are as follows:
• Seizures : Parasagittal/sphenoid wing/convexity
• Hemiplegia : Parasagittal/convexity
• Behavioral changes : Olfactoty groove
• Anosmia : Olfactory groove/ planum sphenoidale
• Foster Kennedy syndrome : Sub-frontal/olfactory groove/Anterior clinoidal
• Visual field defects : Suprasellar/TSM/OGM/Clinoidal
• Proptosis : Orbital/sphenoid wing
• Palpable mass : Convexity/intraosseous
• Stalk effect : TSM, Sellar
• Dizziness, Vertigo, Tinnitus : Cerebellopontine angle meningiomas
• Cranial neuropathies : Suprasellar/medial sphenoid wing/infratentorial
• Hydrocephalus : Intraventricular/pineal region/Infratentorial/TSM
• Parinaud syndrome : Pineal region
CLINICAL FEATURE OF MENINGIOMA

16. WHO grading: 2007

17. Meningioma variants grouped by WHO grade and
biological behavior
2016

18. Donald Simpson's grade:
 Grade I: Macroscopically complete resection of tumor,with excision of dural
attachment and removal of abnormal bone (involved venous sinus is also excised in
relevant cases)
 Grade II: Macroscopically complete resection of tumor with coagulation of dural
attachment
 Grade III: Resection of tumor without coagulation or excision of dural attachment
 Grade IV: Partial debulking of tumor
 Grade V: Biopsy or decompression only
The risks of eventual recurrence after Simpson grades
I, II, III, IV and V were 9%, 16%, 29%, 39%, and 99%.
when the patients survived for 6 months or longer after surgery.
 More recent studies*, however, suggest that recurrence-free survival is not statistically
different between patients undergoing Simpson grade I, II, III, or IV resections.
 Despite this, the Simpson grade of surgical resection should be part of the routine
reporting of surgical results, as it resects more subtle involvement of the dura,
arachnoid, arteries, veins, and nerves that only the surgeon can observe at open
operation and that is not always obvious on routine postoperative magnetic resonance
imaging (MRI).
SIMPSON’S GRADING
*Sughrue ME et al. The relevance of Simpson Grade I and II resection in modern neurosurgical treatment of WHO Grade I
meningiomas. J Neurosurg. 2010.

19. Simpson Classification of Surgical Resection

20.  Lang and coworkers classified them as follows:
Type 1: Purely extracranial
Type II: Purely calvarial
Type III: Calvarial with extracalvarial extension.
Convexity meningioma

21.  Parasagittal meningiomas are classified based on their location along the
superior sagittal sinus into
o Anterior: Between the crista galli and the coronal suture
o Middle: Coronal suture to the lambdoid suture
o Posterior: From the lambdoid suture to the torcula.
They could invade the superior sagittal sinus.
o The sagittal sinus could be ligated when dealing with an anterior
parasagittal meningioma; however, doing the same when dealing with a
more posteriorly placed meningioma could lead to venous infarction as a
result of the substantial number of venous tributaries.
OLFACTORY GROOVE MENINGIOMA (OGM)

22. Type I Tumor is attached to the outer surface of the sinus
Type II Tumor enters the lateral recess of the SSS
Type III Tumor invades one wall of the SSS
Type IV Tumor invades two walls of a still patent sinus
Type V
Tumor spreads over the midline, invades the three
walls, and occludes the SSS
CLASSIFICATION OF PARASAGITAL MENIGNIOMA
Hancq S, Baleriaux D, Brotchi J. Surgical treatment of parasagittal meningiomas. Semin Neurosurg 2003.
Sindou MP, Alvernia JE. Results of attempted radical tumor removal and venous repair in 100 consecutive meningiomas
involving the major dural sinuses. J Neurosurg 2006.
Type I Tumor attaches to the outer surface of the sinus wall
Type II Tumor fragment inside the lateral recess
Type III Tumor invades the ipsilateral wall
Type IV Tumor invades the lateral wall and roof
Type V Complete sinus occlusion with one free wall
Type VI Complete sinus occlusion without any free walls
BROTCHI CLASSIFICATION: 2003 SINDOU CLASSIFICATION: 2006
SINDOU’S CLASS

23.  Classification of meningiomas
according to sinus invasion.
1. Type 1: meningioma attached to
the outer layer of the sinus wall.
2. Type II: Lateral recess Invaded.
3. Type Ill: Ipsilateral wall Invaded
4. Type IV: both Ipsilateral wall
and roof invaded.
5. Type V: sinus totally occluded,
but contralateral wall free of
invasion
6. Type VI: sinus totally invaded
including three walls
Classification of meningioma according to sinus
invasion
SINDOU CLASSIFICATION: 2006

24.  Due to their slow compressive effect on the frontal lobes, they usually
cause behavioral changes or psychiatric symptoms before the onset of
neurologic deficits.
 Foster-Kennedy syndrome, a triad of optic atrophy in the ipsilateral eye,
papilledema in the contralateral eye, and anosmia.
OLFACTORY GROOVE MENINGIOMA

25. COMPARING OGM VS TSM

26.  Patients often present with insidious, progressive visual loss, which is
usually asymmetric. Frequently these tumors are mistaken for pituitary
adenomas, but they are centered on the chiasmatic sulcus of the
tuberculum and grow down the front face of the sella as well as over the
planum
 Pterional, cranioorbital, or unilateral subfrontal: Small to medium-sized
tumors
 Bifrontal extended frontal craniotomy : Larger tumors.

28. TUBERCULUM SELLAE MENINGIOMA
Origin: region of the chiasmatic sulcus and
tuberculum, usually with a point of origin at the
junction of the optic canal and lateral aspect of the
chiasmatic sulcus.
C.F: Most patients with TSM present with visual
loss; bitemporal visual field loss; Frontal lobe
syndrome.
Displacement:
The optic nerves are usually displaced laterally and
superiorly and the optic chiasm superiorly or
posteriorly. Frequently there is extension down the
medial aspect of one or both optic canals
Significant involvement of the internal carotid, anterior cerebral, or
anterior communicating arteries largely contraindicates the endonasal
approaches.

29.  Optic nerve sheath tumors are a rare form of meningioma that no longer
should be approached surgically unless the entire tumor is confined to the
orbit and the patient has no useful vision.
 Most often these tumors are diagnosed by imaging studies and treated
with fractionated external beam radiotherapy.
 Combined neurosurgical and ophthalmologic approach: FTOZ.
OPTIC NERVE SHEATH MENINGIOMAS

30.  Challenge: They often involve the supraclinoid internal carotid artery and its branches, the
cavernous sinus (CS), and its associated oculomotor nerves and the anterior visual
pathways.
 Middle third meningiomas present with headaches, seizures, and altered mental status.
SPHENOID WING MENIGIOMA

31.  A, En-plaque: Carpet-like dural growth especially located on the sphenoid ridge invades the haversian
canals along the pterion. orbital walls, and zygoma, creating a hyperostotic reaction and the orbital roof,
B, Nodular or Globoid: This variety has been sub-classified into three types:
 Cushing and Eisenhardt distinction: (1) Deep, inner, or clinoidal; (2) Middle or alar; and (3) Lateral,
outer, or pterional.
SPHENOID WING MENIGIOMA:
CLASSIFICATION

32. PIRROTE AND BROTCHI
CLASSIFICATION OF SWM
Roser’s sub- division
A Deep or Clinoidal or sphenocavernous
B Invading en plaque of sphenoid wing
C Invading en masse of sphenoid wing Roser et al further
sub- divided C tumors
into meningiomas en
plaque with and
without cavernous
sinus infiltration, and
purely intraosseous
tumors.
D Middle ridge meningioma
E Pterional or sylvian point
meningiomas.
CLASSIFICATION OF SWM
Group C tumors are thought to combine
features of both group A and B tumors (i.e.,
globular and invasive growth en plaque).

33. 1. Group I arising from the inferior
aspect of the anterior clinoid process
(ACP) proximal to end of carotid
cistern: Anterior clinoidal
meningioma (aka medial SWM) :
Tends to encase ICA without
intervening arachnoid.
2. Group II arising from the superior
and /or lateral aspect of the ACP
separated from the ICA and cranial
nerves by an arachnoidal membrane
of the carotid and sylvian cisterns.
3. Group Ill arising at the level of the
optic foramen extending into canal:
separate from ICA.
CLINOIDAL MENINGIOMAS
Clinoidal meningiomas (CMs) are divided into three groups: Al-Mefty
Some clinoidal meningiomas, however, may grow
into the region of the mesial sphenoid wing and be
confused with medial sphenoid wing meningiomas
Other school of thoughts/Fallacies: Group I tumors are probably rare, and the lack of an arachnoidal dissection plane between the tumor
and the carotid artery may be related to other factors such as repeat surgery. Group III tumors may be more appropriately referred to as
optic foramen, optic sheath, or optic canal meningiomas.

34. ANTERIOR CLINOIDAL MENINGIOMA
6.5% of all meningioma and 25% of Ant fossa Meningiomas
Types of anterior clinoidal meningioma.
Preoperative contrast-enhanced MR images show that the sizes of the tumor on coronal dimensions are <2 cm, 2–
4 cm, and >4 cm, respectively.
Tumors without extradural growth and tumors with extradural growth into the cavernous sinus.
Visual deterioration with ipsilateral nasal hemianopsia, Foster-Kennedy syndrome
Meningothelial >> Transitional are the common variant in ACM.
Pamir combined
coronal diameter in
Al-mefty’s class

35. SPHENOCAVERNOUS MENINGIOMA
“Hirsch criteria for sinus involvement”
Grade Tumor Description
1
Touch or partially encircle the cavernous internal carotid
artery
2
Completely encircle but do not narrow the lumen of the
internal carotid artery
3
Encircle and narrow the lumen of the cavernous internal
carotid artery
Radiological Grade of Cavernous Sinus Tumors as Determined by Magnetic Resonance
Imaging and Angiography According to the Criteria of Hirsch et al

36.  With anterior clinoidal meningiomas, the epicenter of the tumor base is on the anterior clinoid
process and the tumor typically grows upward, forming a small pedicle toward the suprasellar area
and the sylvian fissure. (Fig B upper arrow)
 In contrast, meningiomas of the medial third of the sphenoid wing grow in the direction of the
anterior aspect of the medial temporal lobe. (Fig A and B lower arrow)
 Another characteristic feature of anterior clinoidal meningiomas is the presence of hyperostosis of
the anterior clinoidal process on coronal CT. (Fig C)
CLUE TO DIFFERENTIATE ACM FROM
OTHER SWM
Fig A: Medial sphenoidal wing meningiomas grow in the direction of the anterior aspect of the
medial temporal lobe (lower arrow on A), whereas
Fig B: Anterior clinoidal meningiomas grow upward with a small pedicle (upper arrow on B)
C

37.  Challenging tumors
 Occurs in relatively young patient (life expectancy of at least 15 years),
 Surgery is indicated at the time of detection, regardless of the size or the
presence of symptoms.
 Various skull-base approaches with or without intra- or extradural removal of
anterior clinoid.
 Pterional and subfrontal approaches
 Al-Mefty exclusively used the orbitocranial approach: shortest distance to
tumor, suitability for surgical attack via multiple routes, and early
interception of the tumor’s blood supply through the sphenoid ridge.
 Lee and colleagues 2011: Modified Dolenc cranial base approach: involves
extradural clinoidectomy, removal of the roof of the optic canal, and
opening of the optic nerve sheath.
 Oculomotor morbidity is extremely high after a direct approach to this region
ANTERIOR CLINOIDAL MENINGIOMA:
SURGERY

38. Surgical approach

39. Extent of Tumor Removal: A Grading System According to De Monte et al.
Grade Tumor Description
1 Complete microscopic removal of tumor and its dural attachment with any abnormal bone
2
Complete microscopic removal of tumor with diathermy coagulation of its dural
attachment
3a
Complete microscopic removal of intra- and extradural tumor without resection or
coagulation of its dural attachment
3b
Complete microscopic removal of intradural tumor without resection or coagulation of its
dural attachment or any extradural tumor
4a
Intentional subtotal removal to preserve cranial nerves or blood vessels; complete
microscopic removal of tumor dural attachment
4b Partial removal leaving tumor <10% in volume
5 Partial removal leaving >10% in volume or decompression with or without biopsy
CAVERNOUS SINUS MENINGIOMA

40. Series (Ref. No.) No. of Cases
No. of Total Resections
(%)
Follow-up (mo)
Cioffi et al., 1987 (6) 12 1 (8.3) 24
De Monte et al., 1994 (9)a 41 31 (76) 45
Dolenc et al., 1987 (12) 40 Unknown Unknown
Hakuba et al., 1989 (16) 4 Unknown Unknown
Kawase et al., 1987 (20) 9 7 (77.8) Unknown
Lesoin and Jomin, 1987 (25) 16 0 Unknown
Risi et al., 1994 (31) 15 4 (26.7) Unknown
Sekhar et al., 1992 (36)a 70 61 (87.1) 36
Sepehrnia et al., 1991 (38) 36 18 (50)
Von Wild and Eskinja, 1989 (44) 9 4 (44.4) 10
O'Sullivan et al. (present study) 39 8 (20.5) 24
Reported Cases of Meningiomas of the Cavernous
Sinus

41.  The resectability of meningiomas of the cavernous sinus depends on the
degree of internal carotid artery involvement;
 Total excision of cavernous sinus meningiomas is possible but rarely
achieved in holocavernous meningiomas;
 Cranial nerve morbidity is significant; and
 Subtotal excision with or without postoperative radiotherapy is an
effective short-term oncological strategy.
SURGERY

42.  Optic nerve sheath meningiomas (ONSMs) involve the optic nerve and the anterior visual pathways.
 They usually arise from the arachnoidal membrane of the intraorbital nerve and extend through the optic
canal to the anterior fossa.
 Without treatment, slowly but progressive growth often results in unremitting visual loss.
 Axial CECT: Tram track sign: Hyperdense encasement of optic sheath surrounding the hypodense optic
nerve.
 XRT: EBRT: 50-55Gy: 75% improvement in VA, 33% complication; while SRS or SCRT: Visual
improvement 80%, 4% complication.
OPTIC NERVE SHEATH MENINGIOMA
SCHICK AND COLLEAGUES CLASSIFIICATION Treatment (SCHICK)
Type I: Intraorbital
lesions
IA Flat extension around the optic nerve XRT without biopsy
IB Bulbiform mass around the optic nerve XRT, if painful with no useful vision: surgery
IC Exophytic tumor around the optic nerve Surgery
Type II: : Intraorbital
tumors with intracranial
extension through the
optic canal or superior
orbital fissure
IIA Intraorbital growth through the optic canal Intradural exploration with Optic canal and SOF
decompression = STR ff XRT.
IIB Growth through the superior orbital fissure or
cavernous sinus)
Cavernous sinus involvement be treated with XRT
Type III: Intraorbital
tumors with widespread
intracranial tumor
extension
IIIA Extension to chiasm Preventive surgery to avoid involvement of
chiasma and contralateral optic nerve.
IIIB Extension to chiasm, contralateral optic nerve, and
planum sphenoidale

43.  Apart from the cavernous sinus, they could also arise from the posterior
aspect of the sphenoid wing, clivus, petrous bone or from the middle
cranial fossa floor.
 These meningiomas are usually closely associated with the cavernous
sinus and present a challenge to the neurosurgeon as surgical resection
could result in a cranial neuropathy.
 Approaches: sub-temporal, middle fossa or supra petrosal approaches.
MIDDLE FOSSA MENINGIOMA

44.  1% of all intracranial meningiomas.
 10-15% of CP tumor (80-90% of VS in CPA region)
 Desgeorges and colleagues classified these meningiomas into three groups based on their
proximity to the internal acoustic canal (lAC):
 I : Meningiomas anterior to the lAC.
II : Meningiomas centered at the lAC, (Sometime not used this class)
III : Meningiomas posterior to the lAC.
 CPA meningioma vs Vestibular Schawannoma
 Widening of the lAC when there is a vestibular schwannoma.
 Hyperostosis, intratumoral calcification, broad tumor base on the tentorium, and a dural
tail all favor the diagnosis of a meningioma.
 T2-weighted gradient echo sequences: microhemorrhages of VS
 Angle with petrous bone: 81% vestibular schwannoma will form an acute angle, while
a meningioma will form an obtuse angle.
 Retrosigmoid and trans-labyrinthine approaches
CEREBELLOPONTINE ANGLE (CPA)
MENINGIOMAS

45.  Foramen magnum meningiomas present with variable symptoms.
 Most patients have a history of neck or sub-occipital pain, and motor sensory
symptoms develop, usually in one arm, and then in the contralateral leg.
 Because of the lower cranial nerve morbidity associated with surgical resection of
these tumors, incidentally discovered tumors in this location can initially be followed.
 Class: Anterior, Lateral and Posterior
 The standard approach for these tumors is the far lateral sub-occipital approach with
the patient in the three-quarter prone position.
 The posterior one third of the occipital condyle is removed to improve access to the
ventral dura.
 Once the dura is opened, the vertebral artery can be identified and is usually not
directly invaded by meningioma.
 With Meninigoma below VA, Ther lower CNs are displaced superiorly while tumor
above VA, the position is unpredictable. avid
 Sharp dissection of the arachnoid plane is key to preserving the rootlets of cranial
nerves IX, X, XI, and XII.
 The patient should be warned that for the larger tumors such dissections could result in
transient and possibly permanent problems with dysphasia and dysphonia.
FORAMEN MAGNUM MENINGIOMAS

46.  Arise from arachnoidal cap cells in the region of the torcular Herophili.
 Meningiomas invading the torcular region can be categorized into two main subtypes based on predominant site of
invasion:
 1. Torcular (T)
 2. Transverse sinus (TS): Cerebellar convexity ( medial, Lateral or superior) and tentorial origin
(Medial, Lateral and falcotentorial)
 Torcular Meningiomas
 • Frequently, torcular meningiomas present with neurologic signs indicative of intracranial
hypertension.
 • All of the patients in the Cushing and Eisenhardt series exhibited papilledema, while in half of them a
homonymous field deficit was round Infratentorial extension may result in cerebellar signs, including
ataxia, dysmetria, hypotonia, and nystagmus.
 Transverse Sinus Meningiomas
 These are typically placed into two categories: those arising from the cerebellar convexity or from the
tentorium
 Cerebellar Convexity/Superior origin
 These are divided into medial, lateral, or superior, with the superior type most likely to invade the TS.
Symptoms are relatively few and nonspecific: headache, cerebellar signs, symptoms of increased
intracranial pressure, and hydrocephalus.
 Tentorial Origin
 These are divided into medial, lateral, or falcotentorial types based on assessment of tumor origin at
surgery.
 Medial and lateral types are further classified as anterior, middle, or posterior.
 Most tumors of tentorial origin affecting the sinus grow infratentorially and produce characteristic
symptoms of headache and truncal ataxia.
TORCULAR MENINGIOMA Diagnosis and Imaging
Patients must undergo CT
scaning and MRI with
gadolinium including an MR
venogram (MRV) to establish
the dimensions, degree of
bone invasion, presence of
surrounding edema,
relationships of the tumor
with the surrounding
structures, and degree of
venous sinus involvement.
Digital subtraction
angiography (DSA) to
determine variants of
circulation in the torcular and
lateral sinuses is critical
before surgical intervention
can be established.
Nader’s classification about
degree of the meningioma's sinus
invasion:
As parasagital menigioma
Type I - attachment to outer
surface of a sinus wall,
Type II - fragment inside a lateral
recess,
Type III - invasion of one wall,
Type IV - invasion of two walls,
Types V and VI - complete sinus
occlusion, with or without one
wall free,

47.  Surgery usually is the preferred treatment modality for patients with torcular
and peritorcular meningiomas.
 The debate lies in the decision of the surgeon to restore venous circulation by
way of bypass or to rely on collateral circulation after tumor re- section.
 Various surgical interventions have been established depending on the type of
sinus invasion as well as patient-specific factors of the case, such as age and
preoperative symptoms of the patient.
 Anatomic variants of the dural sinuses should be anticipated through imaging
as they will affect the surgeon's decision to restore venous.
 the external jugular vein for short grafting (< 10 em) or the internal
saphenous vein for larger grafts.
 In the eventuality of "inoperable" tumors, radiosurgery such as gamma knife
treatment and hypo fractionated stereotactic radiotherapy (hFSRT) have
emerged as means of effectively reducing neurologic deficits with relatively
limited morbidity.
Treatment

48.  Yasargil’s classification of tentorial meningiomas (TMs)
defines eight types of tumors according to their location
on the cerebellar tentorium.
 They were subsequently regrouped as follows: 5
TENTORIAL MENINGIOMA
3-6%
Group Characteristics
I Anteromedial, arising from the apex of the tentorial margin
II Anterolateral, arising from the lateral aspect of the tentorial incisural
margin
III Intermediate, arising from the intermediate aspect of the tentorium remote
from the incisura and the dural sinuses
IV Posteromedial, arising from posteromedial aspect of the tentorium close
to straight sinus or venous confluence at the torcula; this group also
includes the falcotentorial and torcular meningiomas.
V Posterolateral, arising from the posterolateral aspect of the tentorium
close to the sigmoid sinus
The most frequent benign meningomas in these locations are fibroblastic and meningothelial

49. AL-MEFTY’S MENINGIOMA

50.  Occipital Interhemispheric Approach: I II, III
 Transtentorial access : I, II, and IV.
 Subtentorial: II
 Bioccipital-Suboccipital Approach: IV
 Midline Supracerebellar Infratentorial Approach: I, IV
 Paramedian Supracerebellar Infratentorial Retrosigmoid Approach: II, III,
and V meningiomas
APPROACH
Transzygomatic approach: Medial
tentorial meningiomas

51.  5% of all intracranial meningiomas.
 The most common location is the atrium of the lateral ventricle. (80%), 3rd (15%), 4th (5%)
 They may arise either from the stroma of the choroid plexus or from rests of arachnoid tissue inside it.
 A patient usually presents with symptoms related to obstructive hydrocephalus such as headaches,
nausea, and vomiting.
 Intraventricular and subarachnoid hemorrhage
 Weakness of upper limb progressing to contralateral leg.
 Seizures can occur with large tumors in either hemisphere, and speech disturbance can occur for left-
sided lesions.
 Approach
 Lateral ventricle tumors: anterior transcallosal or parietooccipital approach.
 Trigone: Non-dominant: Temporal parietal craniotomy; dominant hemisphere: superior parietal
lobule approach..
 Anterior third ventricle : anterior transcallosal approach.
 Posterior third ventricle: Posterior transcallosal or supra- cerebellar infratentorial trajectory.
 Fourth ventricle : Medial sub-occipital approach.
INTRAVENTRICULAR MENINGIOMAS
2%

52. GROUP CHARACTERISTICS
A Pure convexity meningiomas arising from the dura over the posterior convexity of the
cerebellum
B Inferior peritorcular meningiomas arising from or invading the inferior wall of the torcular
herophili or the medial transverse sinus
C Parasinus meningiomas arising in the angle between petrous and convexity dura, including the
wall of the sigmoid and transverse sinuses
D Meningiomas with secondary invasion of cerebellar convexity/fossa.
CEREBELLAR CONVEXITY MENINGIOMA
Midline or paramedial suboccipital infratentorial trajectory.

53.  SMs arise at the junction of the spinal arachnoids and the dura of the
nerve root sheath.
 Approximately 83% to 94% have an intradural component, 5% to 14%
are extradural, and 10% may grow in both compartments.
 Thoracic spine: 73%, cervical: 16% and lumbar region : 5%.
 C.F: sensitive motor deficit, Myelopathy, BSS, autonomic symptoms.
 MC: psammomatous subtype
 Somatosensory and motor evoked potentials are generally used.
SPINAL MENINGIOMAS
7.5%-12%
Review: Sandalcioglu and co-workers: 137 SM

54. WORK-UP

55.  Appear as homogeneous, densely enhancing mass with broad base of attachment
along dural border.
 60-70HU : calcifications.
 Cerebral edema, Mild or marked: white matter of the entire hemisphere.
 Intraventricular meningiomas: 50% produce extra ventricular edema. On
angiogram, these may falsely appear malignant.
CT SCAN

56.  Occasionally may be isointense with brain on T1WI and T2WI, but most
enhance with gadolinium.
 Brain edema may or may not be present.
 Calcifications appear as signal voids on MRI.
 Gives information regarding patency of dural venous sinuses (accuracy in
predicting sinus involvement is ≈ 90%).
 Dural tail is a common finding. (60%).
MRI

57.  DWI/ADC: atypical and malignant subtypes may show greater than expected
restricted diffusion although recent work suggests that this is not useful in
prospectively predicting histological grade.
 MR spectroscopy: usually it does not play a significant role in diagnosis but
can help distinguish meningiomas from mimics.
 Features include:
 Increase in alanine (1.3-1.5 ppm)
 Increased gluatamine/glutamate
 Increased choline (CHO): cellular tumour
 Absent or significantly reduced N-acetylaspartate (NAA): non-
neuronal origin
 absent or significantly reduced creatine (Cr)
 MR perfusion: good correlation between volume transfer constatn (K-
trans) and histological grade
Typical V/S Atypical/Malignant

58.  CSF vascular cleft sign : extra-axial; invasion: grade II and grade III
 Dural tail is seen in 60-72% (note that a dural tail is also seen in other
processes)
 Sunbrust or spokewheel appearance of the vessels.
 Arterial narrowing
 Typically seen in meningiomas which encase arteries.
 Useful sign in parasellar tumours, in distinguishing a meningioma
from a pituitary macroadenoma; the latter typically does not narrow
vessels.

59.  Meningiomas characteristically have external carotid artery feeders.
 Exceptions: OGM: ICA (ethmoidal branches of the ophthalmic
artery), Suprasellar meningiomas :ophthalmic arteries, Parasellar
meningiomas : ICA.
 Secondary vascular supply may be derived from pial branches of the
anterior, middle, and posterior cerebral arteries.
 Artery of Bernasconi & Cassinari AKA artery of tentorium (a branch of
the meningohypophyseal trunk) AKA the “Italian” artery: enlarged in
lesions involving tentorium (e.g. tentorial meningiomas).
 Angiography also gives information about occlusion of dural venous
sinuses, especially for para-sagittal/falx meningiomas.
 Oblique views are often best for evaluating patency of the superior
sagittal sinus (SSS).
CT Angiogram

60.  The "Mother-in-Law" sign is commonly seen when there is a
meningioma, as the tumor contrast blush "comes early (in the arterial
phase), stays late (beyond the venous phase), and is very dense."
 Angiography can also help confirm diagnosis by the distinctive
prolonged homogeneous tumor blush.
 Angiography also provides an opportunity for pre-op embolization.
DIGITAL SUBTRACTION ANGIOGRAMS (DSA)

61. LOCATION EXTRADURAL VESSELS INTRADURAL VESSELS
Convexity MMA -
Parasagittal MMA -
Falcine MMA, Ant falx artery -
Sphenoid Wing/ACM MMA -
OGM Ant br. MMA Cavernous ICA, Ethmoid br. of ophthalmic a.
TSM Post Ethmodal br of ophthalmic a.
Supra sellar/ Parasellar Ophthalmic a./ ICA respectively
Tentorial MMA Marginal tentorial br of SCA, Bernasconi &
Cassinari artery
Tentorial/ Clivus MMA Cavernous ICA, Davidoff & Schecter
Petroclival MMA, IMA, APA MHT, ILT
Post. Fossa (PM) M br of VA, PMA -
Post Fossa (Lateral) - Transmastoid br OA
Intraventricular - Choroidal a.
Foramen magnum Mening. br APA, OA, VA, PICA, and PSA
Abbreviation: OGM: Olfactory groove meningioma; MMA: Middle meningeal artery; OA: Occipital artery; MHT: meningohypophyseal trunk;
ILT: the anterior branch of the inferolateral trunk; APA: Asc. Pharyngeal a; PSA: Post spinal a.
Note secondary supply may be derived from pial br of ACA, MCA or PCA.
ARTERIAL FEEDER OF MENINGIOMAS

62.  Calcifications within the tumor (in ≈10%).
 Hyperostosis or blistering of the skull (including floor of frontal fossa
with olfactory groove meningiomas).
 Enlargement of vascular grooves (especially middle meningeal artery).
PLAIN X-RAYS

63.  Manelfe and associates, in 1973, first described the microcatheter
technique of meningioma embolization.
 Preoperative embolization can be an important adjuvant treatment
modality.
 Embolizing materials could be liquid or particulate agents.
 The liquid agents :
1. N-butyl cyanoacrylate (NBCA),
2. ONYX (ethylene vinyl alcohol polymer dissolved in dimethyl
sulfoxide), and
3. Fibrin glue
 Particulate agents: PVA particles and microspheres .
PRE-OP PLANNING
EMBOLIZATION

64. Indications:
1. Surgeons’ preference
institutional practices,
2. Large tumor size,
3. Extensive tumor vascularity,
4. Skull base meningiomas with
difficult-to-access arterial
supply
EMBOLIZATION
Benefits:
1. Reduced operative blood loss,
2. Easier tumor resection, and
3. Shortened surgical time).

65. 1. Hemorrhage ( Intratumoral and SAH)
2. Cranial nerve deficits (usually transient)
3. Stroke from embolization through ICA or VA anastomoses
4. Scalp necrosis
5. Retinal embolus, and
6. Potentially dangerous tumor swelling.
7. Some meningiomas (e.g. olfactory groove) are less amenable to
embolization due to risk of blindness.
Complication of embolisation

66.  Pre-op embolization: Reduces the vascularity of these often bloody
tumors, facilitating surgical removal.
 Timing of subsequent surgery is controversial. Some advocate waiting 7–
10 days to permit tumor necrosis which simplifies resection.

67.  Antiepileptic medication should naturally be continued during the
perioperative period in patients with a known history of seizures. For
meningioma patients with no history of seizures.
 However, a meta-analysis of five randomized controlled trials in patients
with primary brain neoplasms found no effect of prophylactic
antiepileptic medication on seizure control.
 The American Academy of Neurology does not recommend the use of
antiepileptic medications in brain tumor patients with no history of
seizures.
PREOPERATIVE SEIZURE PROPHYLAXIS
Sirven JI et al. Seizure prophylaxis in patients with brain tumors: a meta- analysis. Mayo Clin Proc 2004.

68.  Meningioma resection improves seizure control in patients with
preoperative epilepsy.
 ~5 to 20% of patients may develop new postoperative seizures.1,2
 The use of postoperative antiepileptic medications such as phenytoin
after intracranial neurosurgical procedures has been shown to reduce
early postoperative seizures by ~40 to 50%.
 Recent studies comparing levitiracetam to phenytoin have also shown no
difference in postoperative seizure rates in glioma patients.
 The American Academy of Neurology currently recommends
discontinuing postoperative seizure prophylaxis after 1 week in patients
with no history of seizures. 3
POSTOPERATIVE SEIZURE PROPHYLAXIS
1. Chozick BS et al. Incidence of seizures after surgery for supratentorial meningiomas: a modern analysis. J Neurosurg 1996.
2. Lieu AS et al. Intracranial meningiomas and epilepsy: incidence, prognosis and influencing factors. Epilepsy Res 2000.
3. Glantz MJ et al; Anticonvulsant prophylaxis in patients with newly diagnosed brain tumors. Neurology 2000.

69.  Intraoperative monitoring including,
 Brainstem Evoked Potentials
 Somatosensory Evoked Potentials (SSEPS)
 Neuronavigation
 Microscopic Magnification
 Ultrasonic Aspirator
 Microsurgical instruments:
 A lumbar drain may be necessary to reduce brain turgor intra- operatively.
 The abdomen and/or thigh should be prepared for possible fat or fascial
graft harvesting.
 Perioperative antibiotics, steroids, and anticonvulsants are given.
 Central line and arterial lines are placed.
Preoperative Planning and Special Equipment

70.  Every meningioma patient is unique and deserves a tailored approach.
 Surgeons approaching these lesions should have mastered all cranial
approaches including the ones to the skull base. as the choice of the
proper approach should always be based on what is best for the patient
and what carries the least amount of risk leading to deficits and
complications while providing a high chance of success.

71.  Four critical HPE variables
1. Grade: WHO I, II, III
2. Histological subtype: Meningothelial, clear cell, rhabdoid, etc.
3. Proliferative indices: Mean KI-67 index
4. Brain invasion: Increases the likelihood of recurrence to level
similar to atypical meningioma (not anaplastic).
 But it is not an indicator of malignant grade.
PATHOLOGY

72.  Multiple menigioma: suggest NF2
 Pleomorphic xanthoastrocytoma: Peripherally located/dural tail.
 Rosai-Dorfman disease: Connective tissue Dz, Sinus histocytosis and
massive pain less lymphadenopathy/ Dural tail. CD68 and S-100 (+):
XRT.
DIFFERENTIAL DIAGNOSIS

73.  Immunohistochemical markers of proliferation potential such as Ki-67,
MIB-1, and proliferating cell nuclear antigen (PCNA) indices have also
been correlated with risk of recurrence.
 Oya and colleagues indicated that an MIB-1value of 3% or higher was
associated with a greater recurrence rate of World Health Organization
(WHO) grade I meningiomas surgically treated by Simpson grade II or
III resection.
 Ideally, pathological grade and histology, Simpson surgical grade,
and a marker of proliferation index should be included in the
reporting/analysis of operative meningioma specimens.
RECURRENCE

74. Meningioma Recurrence Remarks
OGM 5-41% Obeid and Almefty’s series
Parasagittal 9,19,29,40% Simpson’s 10 year F/U
Recurrence
Description and WHO
grade
Mean KI-67 index Recurrence rate
WHO I 0.7% 9%
WHO II 2.1% 29%
WHO III 11% 50%

75. TREATMENT ALGORITHM FOR
MANAGEMENT OF MENINGIOMA

76.  Subfrontal approach: large and giant olfactory groove meningiomas.
 FTOZ: Large OGM
 Supraorbital craniotomy : small unilateral olfactory groove meningiomas.
 Pterional approach : sphenoid wing, OGM or temporal meningiomas.
 Middle fossa, retrosigmoid, translabyrinthine, transcochlear, infratemporal fossa
and retrolabyrinthine approaches
 For skull base meningiomas (petroclival/lpetrous ridge, tentorium, sigmoid,
internal auditory canal and jugular foramen regions).
 TSM: Bifrontal, FT, FL, Expanded endonasal.
 Endoscopic sellar surgery: pioneered (Jankowski in 1992) : Planum sphenoidale
meningiomas and other meningiomas in the sellar/parasellar region.
 FM meningiomas: Anterior and Lateral: Posterolateral/transcondylar app
*Posterior: Posterior suboccipital approach.
Surgical approach

77.  Radiotherapy treatment has proved to be effective in controlling tumor growth,
particularly for residual tumor following resection of skull base meningiomas.
 Value of XRT:
1. Partially resected meningiomas.
2. Inaccessible meningiomas,
3. Inoperable meningiomas,
4. Post-resection cavity for grade iii meningiomas.
5. Remnants that have demonstrated confirmed growth..
 High dose of about 55-60 Gy could be beneficial.
 Alternatively, one can follow these patients with CT or MRI and use XRT for
documented progression.
XRT
Barbaro NM et al. Radiation Therapy in the Treatment of Partially Resected Meningiomas. Neurosurgery.
1987.
Barbaro et al. Option Recurrence
UCSF series of 135 non malignant
meningoma F/u 5-15 years
Total resection 4%
PR with XRT 32%
PR without XRT 60%
PR: Partial resection: Extracted from Greenberg 8th
Mean time to recurrence was longer in the XRT group (125 mos) than in the non-XRT group (66 mos).

78. RADIOTHERAPY
For small to medium-size tumors less than 30 mm, or less than 8 cc, at sites
not associated with critical structures such as optic nerves, chiasm, or
brainstem, radiosurgery is a powerful technique as either a primary form of
therapy, for residual
disease, or for treatment of recurrence
Case report of malignant Astrocytoma developing after XRT used to treat
meningioma.

79.  Lars Leksell: 1960s,
 It is considered most effective for tumors less than 3 cm in diameter or 10
cm3 in volume.
 Influence factor: clear tumor-brain interphase, proximity to areas of
functionally important brain or nerves, and other critical structures.
 Excellent tumor control for WHO; grade I meningiomas is usually
achieved with 12 to 16 Gy. (Ganz et al)
 No improvement with marginal doses greater than 15 Gy (Kondziolka et)
STEREOTACTIC RADIOSURGERY

80.  PBT delivers protons instead of radiotherapy photons.
 Protons are more conformal and homogeneous than photons and their use
decreases the dose in surrounding tissue compared to photon beam
therapy.
 However, the treatment results of PBT appear to be similar to those for
IMRT.
PROTON BEAM THERAPY

81.  Many modalities have been tested including cytotoxic drugs,
immunomodulation, molecular agents, and hormonal therapy.
 No effective chemotherapy till date
 Promise: Interferon alpha-2b and hydroxyurea.
 Hydroxyurea suggested for treatment of unresectable and recurrent
meningiomas: arrests meningioma cell growth in the S phase DNA
synthesis inhibitionapoptosis
 Conventional combined chemotherapy— cyclophosphamide, adriamycin,
and vincristine—showed a modest activity against malignant
meningiomas and may improve the median survival time.
 Treatment with interferon alpha-2b has presented some success in
preventing meningioma growth.
CHEMOTHERAPY

82.  Ki-67, MIB-1, and proliferating cell nuclear antigen (PCNA)
are predictors increased recurrence, while CDKN2A
deletion, along with a 9p21 deletion, is a predictor of
malignant progression, increased recurrence, and poor
survival.
PROGNOSTIC MARKERS

83. Criteria:
Radiation-Induced Meningioma
1. Tumor must arise in the irradiated field
2. Histological features must differ from those of any previous neoplasm
3. A sufficient latency or induction period following radiation must elapse before
meningioma is diagnosed (usually > 5 years)
4. No family history of phacomatosis.
5. Tumor must not be recurrent or metastatic
6. Tumor must not be present before radiation therapy

84. Thank you

MENINGIOMA
DR. SURESH BISHOKARMA
MCH NEUROSURGERY ®
UPENDRA DEVKOTA MEMORIAL NATIONAL INSTITUTE OF
NEUROLOGICAL AND ALLIED SCIENCES
BANSBARI, NEPAL