meningioma presentation

1. MENINGIOMA
PRESENTED BY : DR. ABHIJEET KAMBLE
JUNIOR RESIDENT II
H.P. GOVERNMENT DENTAL COLLEGE, SHIMLA
DEPARTMENT OF MAXILLOFACIAL AND ORAL SURGERY

2. “Winning is overrated. The only time it is really important is in
surgery and war.” ~ Al McGuire
GOOD AFTERNOON

3. CONTENTS
1. HISTORY
2. INTRODUCTION
3. EPIDEMIOLOGY
4. RISK FACTORS
5. CAUSES
6. CLINICAL FEATURES
7. IMAGING AND MANAGEMENT

4. HISTORY
 The term meningioma was first coined by Harvey Cushing during his Cavendish lecture in
Cambridge in (1922).

5. HISTORY

6. INTRODUCTION
 Refers to set of tumors that arise contiguously to the meningies.
 Meningiomas are benign tumors of the meninges and arise from
arachnoidal cap cells, which reside in the arachnoid layer
covering of the brain. They represent 15% of all primary brain
neoplasms.
 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.
 Meningiomas may occur intracranially or within the spinal canal.
 Meningiomas can also occur in an intraventricular or intraosseous
location (rare).

7. EPIDEMIOLOGY
 Meningiomas constitute 13–25% of primary intracranial neoplasms.
 2 – 10 cases per 100,000 individuals.
 Accounts for approximately 20% of all primary intracranial neoplasms.
- majority are benign, with about 1%-3% classified as malignant
- 98% are intracranial but may arise anywhere in central nervous system
 2.3% of individuals have undiagnosed asymptotic meningioma on autopsy.
 Meningiomas show a higher incidence among women as compared to men in most ethnic groups. (1:1.4 to
1:2.8)
- 8.4-4.6 for women vs 2.2-3.8 for men per 100,000.
 In a population-based study performed in Los Angeles County, African Americans showed a higher incidence

8. PATHOPHYSIOLOGY

10. RISK FACTORS
 Likely
- First degree relative.
- NF2 gene – Chromosome 22q12.2
• Merlin Protein ( thought to be involved
in cell-to-cell contact and motility )
• Lower expression in meningioma and
loss of Merlin protein lead to
development of benign meningioma.
 Exposure to ionizing radiation.
- use of radiation therapy to head and
neck for neoplastic conditions has been
shown to be associated with an increase in
the incidence of meningiomas.

11. RISK FACTORS
 Possible
 HRT
 Obesity, Increased BMI
 Intrathecal Methotrexate.
 Oral Contraceptive
- Current or past hormone replacement therapy associated with increased risk of
meningioma.
- Increased with any estradiol-only therapy
- Increased with use of estradiol-only for =/> 3 years
- Not significantly affected by use of estradiol plus progestin.
- Obesity associated with increased risk of meningioma compared to normal
weight.

12. ASSOCIATED SYNDROMES
 Hereditary syndromes associated with meningioma include
 Li-Fraumeni syndrome – AD, TP53, Sarcoma, breast, leukemia and
adrenal gland (SBLA) syndrome.
 Gardener – Cr5q21, APC, AD
 Von Hippel-Lindau – Cr3p25, AD, VHL suppressor gene.
 Cowden – PTEN tumor suppressor
 Gorlin – Cr9q22 PTCH tumor suppressor
 Multiple endocrine neoplasia type I – pituitary, parathyroid, and
pancreas.

13. CAUSES
 Unknown
 NF2 gene – Familial cases.

14. CLINICAL FEATURES

16. IMAGING
 Modalities
- X ray
- CT
- MRI
- MRS
- octreotide scintigraphy
- Positron Emission Tomography PET – CT SCAN

17. IMAGING
 X Ray
- X Ray no longer have a role in the diagnosis or management of
meningiomas.
- Hyperostosis or lytic lesion.
- Calcification.

18. COMPUTERIZED TOMOGRAPHY
 CT is often the first modality employed to investigate neurological signs or symptoms, and often is
the modality which detects an incidental lesion.
 Specificity of Typical Imaging Features of Meningioma :
 Hyperdensity
 Calcification
 Hyperostosis
 “Dural Tail” Sign
 Angiographic Vascular Pattern (Radial “Sunburst” and Prolonged Blush)

19. HYPERDENSITY
 About two thirds of meningiomas are radiographically hyperdense,
explained by increased cellularity and diffuse microcalcification.
 These are suggestive but not very specific features.

20. CALCIFICATION
 About 25–30% of meningiomas are fully
calcified on CT, and the forms of
calcification include
psammomatous/sand-like, focal,
diffuse, and rim calcifications.
 Hyperostosis
An extra-axial mass with skull hyperostosis is
highly suggestive of a meningioma, but reactive
or invasive changes can be seen with other
tumors, such as lymphoma or metastases, in
addition to more benign osseous defects such as
fibrous dysplasia.

21. “DURAL TAIL” SIGN
 The “Dural tail” or “flair” sign is not specific to meningiomas as it has been described with a
variety of other lesions such as metastases, glioma, acoustic neuroma, sarcoidosis.
 About 60% of meningiomas manifest a Dural tail sign. A broad Dural attachment of a tumor
with an adjacent Dural tail is highly suggestive of a meningioma.
 Goldsher et al. [14] characterized the “Dural tail” in meningiomas by three imaging features:
tapered appearance, greater Dural enhancement than the tumor, and visualization on two
consecutive slices.
reflect either tumor
infiltration or
elicited
inflammation in the
adjacent dura

22. “MRS”
 MR Spectroscopic Profile
 Though not specific, the spectroscopic profile in
combination with conventional MR features of
meningiomas can be helpful in select difficult cases
(e.g., schwannoma versus meningioma.).
 N-Acetylaspartate (NAA) and creatine (Cr) are neuronal
markers which, not surprisingly, are significantly
reduced in nonneuronal tumors such as a meningioma.
But, as with other notably cellular neoplasms, choline
(Cho) is increased. Relative specific markers for
meningioma are alanine (Ala) and glutamine/glutamate
(Glx), which are consistently increased in meningiomas
compared to gliomas, schwanommas, and metastases.
Meningiomas also show nonspecific peaks of lipids.

23. MRI
 MRI is the investigation of choice for
the diagnosis and characterization
of meningiomas.
 Typically appear as extra-axial
masses with a broad Dural base.
They are usually homogenous and
well circumscribed.

24. PET – CT SCAN
 There is no established role of PET -CT Scan

25. WORLD HEALTH ORGANIZATION (WHO) MENINGIOMA
CLASSIFICATIONS
Types and Classification

26. TREATMENT
 Depends upon the size and location, and on the patients age, symptoms,
comorbidities, health status.

27. OBSERVATION
 Observation over a period of time for patients meeting the following criteria:
1. Patients with few symptoms and little or no swelling in the adjacent brain areas.
2. Patient with mild or minimal symptoms who have a long history of tumors
without much negative effect on their quality of life.
3. Older patients with very slow – progressing symptoms.
4. Patients for whom treatment carries a significant risk.
5. Patients who choose not to have surgery after being offered alternate treatment
options.

28. RADIOTHERAPY
 Fractionated Stereotactic Radiotherapy: Fractionated stereotactic radiotherapy (FSRT) combines the precision of
stereotactic positioning with the radiobiologic advantages of fractionation, allowing higher total doses and safe
target coverage.
 Intensity-Modulated Radiation Therapy:
 Proton Beam Radiation Therapy: used to precisely deliver dose to the intracranial target volume while sparing
normal brain tissue
 Gamma Knife Surgery:

29. TREATMENT
 Depends upon the size and location, and on the patients age, symptoms,
comorbidities, health status.

30. TREATMENT

31. TREATMENT

32. SURGICAL APPROACHES

33. SURGICAL APPROACHES
 The extra – cranial meningiomas can be approached either anteriorly ( from
front through the face or through inside the mouth ), laterally ( from the side
of the face near ear ), or inferiorly ( from below the lower jaw at the side).

34. SURGICAL APPROACHES
 FTOZ

35. SURGICAL APPROACHES

36. SURGICAL APPROACHES
Sub temporal-preauricular infratemporal fossa approach

37. SURGICAL APPROACHES

38. SURGICAL APPROACHES

39. SURGICAL APPROACHES

40. ANTEROLATERAL CORRIDOR APPROACH TO THE
INFRATEMPORAL FOSSA

41. ANTEROLATERAL CORRIDOR APPROACH TO THE
INFRATEMPORAL FOSSA

42. 2 WAY APPROACH
 1st approach: Preauricular trans zygomatic approach to approach
the infratemporal fossa, done to access tumor from the side. Using
a semicoronal incision, followed by a zygomatic arch osteotomy.

43. 2 WAY APPROACH
 2nd approach: by a transoral approach, via a superior gingivolabial sulcus
approach to retrieve the excised lesion

44. LATERAL APPROACHES
The division of infratemporal approaches into
subtypes is based on the work of Fisch et al.,
who classified infratemporal fossa approaches as
Type A,
Type B, and
Type C.

45. APPROACH
 The Type A approach is suitable for lesions of the jugular foramen and of the posterior
infratemporal and mandibular fossae.
 In the Type B approach, a zygomatic osteotomy permits more extensive drilling of the
horizontal portion of the petrous ICA so that the petrous apex and clivus can be approached
extradurally.
 The Type C approach is an anterior extension of the Type B approach.3,4,6 It is useful for
gaining exposure of the more medial infratemporal fossa, pterygopalatine fossa, and
nasopharynx

46. THANK YOU