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Meningioma Treatment & Management

  • Author: Georges Haddad, MD; Chief Editor: Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS  more...
 
Updated: Jan 27, 2016
 

Medical Care

Medical care for meningiomas has been disappointing. It is restricted either to perioperative drugs or to medications that are used after all other means of treatment have failed.[25]

The use of corticosteroids preoperatively and postoperatively has significantly decreased the mortality and morbidity rates associated with surgical resection.

Antiepileptic drugs should be started preoperatively in supratentorial surgery and continued postoperatively for no less than 3 months.

The current experience with chemotherapy is disappointing.

  • This modality of treatment is reserved for malignant cases after failure of surgery and radiotherapy to control the disease.
  • The main drugs studied include temozolomide, which had no effect against recurrent meningiomas in a phase 2 study [26] , and hydroxyurea (ribonucleotide reductase inhibitor); RU-486 (synthetic antiprogestin); and interferon-alpha. The last 3 drugs also showed disappointing results. A recently published prospective phase 2 study of irinotecan (CPT-11) also failed to demonstrate any efficacy.
  • The combination of interferon alpha and 5-fluorouracil synergistically reduces meningioma cell proliferation in culture and warrants further investigation.
  • Some studies have shown a possible role of COX-2 inhibitors in the treatment of recurrent meningiomas. [8]
  • The role of targeted chemotherapy to block the tumorogenic pathways of meningiomas at specific sites is being extensively investigated. [27]
  • Molecules to block specific growth factors or enzymes are being developed. Atypical meningioma (WHO grade II) and anaplastic meningioma (WHO grade III) showed increased fatty acid synthase (FAS) expression. FAS inhibitor (cerulein) decreased meningioma cell survival in vitro. Thus, increased FAS expression in human meningiomas represents a novel therapeutic target for the treatment of unresectable or malignant meningiomas. [28]

Although most meningiomas grow slowly and have a low mitotic rate, clinical benefit has been reported in many case series with either tumor regression or stasis after radiotherapy; however, these results have not been confirmed in randomized trials. Oya et al reported on the natural history of meningiomas.[29] The prospect of benign meningioma growth is an important factor to consider in their proper management. Approximately 40% of 273 meningiomas (in 244 patients) grew within a 4-year period. Lack of calcification, hyperintensity in T2 MRI, and peritumoral edema were predictors of growth in follow up. In addition, age younger than 60 years and tumor size larger than 25 mm (diameter) were also associated with a greater risk.

Radiotherapy is mainly used as adjuvant therapy for incompletely resected, high-grade and/or recurrent tumors. It can also be used as primary treatment in some cases (optic nerve meningiomas[30] and some unresectable tumors).[31, 32]

In general, the ideal treatment of a benign meningioma is surgical resection if possible. Hasegawa et al treated 46 patients with gamma knife radiation (GKR) as the initial treatment modality.[33] The lesions were falcine, convexity, or parasagittal. The study found GKR to be effective. The main caveat was tumor size. Large tumors had the possibility of severe postirradiation edema. This was actually more likely to occur with significant, baseline peritumoral edema. GKR may be selected over surgery in patients with significant medical comorbidities.

Stereotactic radiosurgery has been shown to provide excellent local tumor control with minimal toxicity.[34, 35]

  • It is mainly used for small (< 3 cm in diameter) residual or recurrent lesions when surgery is considered to carry a significantly high risk of morbidity.
  • It has been advocated as an effective management strategy for small meningiomas and for meningiomas involving the skull base or the cavernous sinus.
  • It is used primarily to prevent tumor progression.
  • In a recently published series, the long-term follow up after radiosurgery was reported; a tumor control rate of 94% was found after an average of 103 months.
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Surgical Care

The constant principles in meningioma resection are the following: If possible, all involved or hyperostotic bone should be removed. The dura involved by the tumor as well as a dural rim that is free from tumor should be resected (duraplasty is performed). Dural tails that are apparent on MRI are best removed, even though some may not be involved with the tumor. Make a provision for harvesting a suitable dural substitute (pericranium or fascia lata). The surgeon also can use commercially available dural substitutes. If feasible, always start by coagulating the arterial feeders to the meningioma. See the images below.

Case 1: Surgical view of the tumor. The dura is op Case 1: Surgical view of the tumor. The dura is opened, and the meningioma can be seen extending en plaque over the surface of the brain.
Case 1: Bone flap seen along the removed meningiom Case 1: Bone flap seen along the removed meningioma in toto.
Case 2: Intraoperative view shows the skull involv Case 2: Intraoperative view shows the skull involvement.
Case 2: Bone flap was removed. Note tumoral breach Case 2: Bone flap was removed. Note tumoral breach of the dura. The dura and overlying skull were removed surgically. Duraplasty and cranioplasty were performed
Case 2: Surgical specimen. Complete resection was Case 2: Surgical specimen. Complete resection was achieved.

Surgical strategies for managing meningiomas in specific locations are discussed in the sections that follow.

Convexity meningioma

Opening the scalp and skull may be bloody because of the hypertrophy of blood vessels originating from the external circulation.

The tumor may breach the sanctity of the dura and the bone, thus appearing subcutaneously.

The dural blood vessels should be coagulated before opening the dura to decrease tumor vascularity.

Usually the tumor is separated from underlying brain parenchyma by an arachnoid layer. This layer may not be complete at the depth of the tumor. In this location, separating the tumor from the brain may be difficult.

Unless the tumor is small and can be removed in 1 piece, the best strategy for excising convexity meningiomas is to find the arachnoidal plane and dissect it gently.

Placing patties circumferentially around the tumor allows quick identification of this crucial plane at a later time.

Coagulate the surface of the tumor, then core it and invaginate the outer layer to allow further circumferential dissection.

Perform dural grafting. (See the video below.)

Surgery on a 46-year-old female with a 2-cm, dural-based enhancing tumor along the left frontal convexity. The lesion was presumed to be a meningioma and showed serial enlargement on MRI, prompting the procedure. Pathology confirmed the tumor to be a WHO grade I meningioma. Video courtesy of Anand I. Rughani, MD, and Jeffrey E. Florman, MD.

Parasagittal meningiomas

These tumors may arise from the convexity and involve the superior sagittal sinus (SSS) by medial extension, or they may arise from the falx and involve the SSS by upward extension. The former subgroup is easier to treat surgically because of its superficial location.

The foremost consideration in surgically treating parasagittal meningiomas is to decide what to do with the SSS. MRV is not yet sensitive enough to confirm unequivocally the complete occlusion of the SSS.

The diagnostic test of choice is still endovascular angiography with late venous images to look for a possible delayed filling of the involved portion of the SSS. If the SSS is completely obliterated by tumor, it can be ligated safely and excised. The surgeon should be careful not to injure the veins that run anteriorly and posteriorly to the tumor. These veins may provide crucial collateral circulation for the venous drainage of the cerebrum and should be preserved at all costs.

If the SSS is only partially involved, the decision of whether to sacrifice it depends on the involved segment.

The anterior third of the SSS can usually be sacrificed with impunity; the middle third, sacrificed at times; and the posterior third, never ligated. In this author's experience, the SSS is never sacrificed beyond the anterior third.

Some surgeons resect a partially involved sinus and reconstruct it later (either with a vein or prosthetic graft).

The author's opinion is that explaining to the patient that some tumor was left behind that may need further resection at a later date is better than taking undue risk of neurological deficit by obliterating more of the SSS. If the sinus is occluded gradually by the tumor, the venous drainage will be diverted over time through parasagittal veins.

Olfactory groove and tuberculum sellae meningiomas

To avoid undue retraction of the frontal lobes, these tumors are best approached through a low craniotomy. This is achieved by removing the supraorbital rim.

A unilateral approach is usually sufficient. The midline burr hole should be placed just above the frontonasal suture. By entering the frontal sinus and removing the orbital rim, a low approach is provided.

To allow adequate visualization, the falx should be sectioned after ligating the most anterior aspect of the SSS. Every attempt should be made to preserve at least one of the olfactory nerves.

These tumors receive their blood supply through various sources: the ethmoidal branches of the ophthalmic arteries, branches from the middle meningeal artery, and the carotid arteries.

These tumors often invade the ethmoid sinuses and, at times, the sphenoid sinus.

Care should be taken to identify and preserve both optic nerves. Note that the usual relationship between the optic nerves and the carotid arteries might not hold true owing to displacement of these vital structures by tumor.

Tumor arterial supply and perforator arteries to the hypothalamus must be differentiated because both arise from the anterior circulation. (See the video below.)

Meningioma resection in the tuberculum sellae. Video courtesy of Anand I. Rughani, MD, and Jeffrey E. Florman, MD.

Sphenoid-wing meningiomas

Sphenoid-wing meningiomas present either as en plaque meningiomas or as globular masses.

Removing the zygoma and the orbital rim allows wider exposure of the sphenoid wing, the middle cranial fossa, the anterior cranial fossa, and the anterior clinoid.

Medial tumors may extend within the cavernous sinus.

Tentorial and torcular meningiomas

Tentorial meningiomas may be supplied by a multitude of vessels that arise from the tentorial leaf. These should be coagulated thoroughly before one attempts to remove the tumor.

A major supply may be the Bernasconi-Cassinari artery, which arises from the cavernous portion of the carotid artery and runs posteriorly to supply the tentorium.

This artery is usually not apparent on normal angiograms but may be conspicuous in angiograms of tentorial meningiomas.

A definite attempt should be made at recognizing the Bernasconi-Cassinari artery during surgery and coagulating it to decrease tumor vascularity.

Tentorial meningiomas often grow in both the infratentorial and supratentorial compartments and should be approached accordingly.

Studying the preoperative angiogram is imperative in cases of torcular meningiomas to delineate the patency of the different sinuses and the available collateral circulation. Removing these tumors completely is often impossible because of partial involvement of the venous sinuses.

Cerebellopontine angle meningiomas

In acoustic neuromas, the facial nerve usually lies anterosuperiorly to the tumor and is encountered late in surgery. This relationship is lost in cerebellopontine angle meningiomas, because the facial nerve may lie along the posterior tumor edge and can be injured early in surgery (unless care is taken to identify it).

Before attempting to remove the tumor, the surgeon should first diminish its blood supply by coagulating its supplying arteries from the dura. To do so, the interface of the tumor and the petrous bone should be followed. A partial cerebellar resection may be necessary to avoid undue retraction of the brain.

Meningiomas involving the cavernous sinus

The issue of meningiomas involving the cavernous sinus is currently an area of intense interest in neurosurgery. No one doubts that, in experienced hands, such meningiomas can be treated successfully.

The debate centers on 2 points: when to operate and how aggressive the resection should be. The following opinion is a personal reflection on the matter, and diverging views may be found in the literature.

  • Asymptomatic cavernous sinus meningiomas should not be operated but should be monitored carefully by means of repeated physical examination and serial MRI.
  • Symptomatic meningiomas in otherwise healthy patients should be resected by neurosurgeons who are trained for such procedures.

Avoid injuring the cranial nerves or the carotid artery. This author does not believe in the benefit of bypassing and resecting the cavernous carotid artery in these cases.

The surgeon should remember that a multitude of processes may affect the cavernous sinus and mimic a meningioma, including sarcoidosis and infection/inflammation that lead to the Tolosa-Hunt syndrome.

Gamma knife may be a good treatment option in parasellar meningiomas.[36]  Large tumors can be partially resected and treated with gamma knife after resection. In a report by Jensen et al, a good outcome was obtained, with an impressive 69% local tumor growth control.

Clival and petroclival meningiomas

These tumors represent some of the greatest challenges in neurosurgery; although partial resection is relatively straightforward, complete resection remains a daunting task.

Partial resection usually does not translate into any benefit for the patient and only renders further surgeries more difficult; therefore, every attempt should be made to complete the resection. If surgery has to be interrupted for logistical reasons, the second operation should be scheduled the earliest possible opportunity.

A multitude of approaches has been devised for these tumors. The traditional approaches such as the suboccipital or the subtemporal are usually insufficient to allow complete removal. More extensive approaches, such as the petrosal approach, are needed. This approach consists of combined supratentorial and infratentorial craniotomies, associated with a simple mastoidectomy down to the solid angle (ie, the bone encasing the inner ear). After the tentorium is split, the petroclival meningioma can be visualized in its entirety.

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Consultations

If the patient has neurofibromatosis, the neurosurgeon may want to refer the patient for genetic counseling and for audiometric testing.

If the radiologic diagnosis is not clear cut, a detailed discussion with the radiologist should attempt to rule out other pathologic entities, such as neurofibromas or sarcomas.

In specific cases, consulting a radiation oncologist may be appropriate.

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Diet

No dietary restrictions are necessary in patients with meningiomas. If the patient is on perioperative steroids, a low-salt diet is appropriate.

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Activity

Patients with a meningioma who undergo surgery can resume their normal activities after an adequate period of postoperative rest (1-3 mo).

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Contributor Information and Disclosures
Author

Georges Haddad, MD Clinical Assistant Professor, Department of Medicine, Division of Vascular Surgery, American University of Beirut, Lebanon

Georges Haddad, MD is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Coauthor(s)

Ali Turkmani, MD Staff Physician, Department of Neurosurgery, American University Hospital

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Jorge C Kattah, MD Head, Associate Program Director, Professor, Department of Neurology, University of Illinois College of Medicine at Peoria

Jorge C Kattah, MD is a member of the following medical societies: American Academy of Neurology, American Neurological Association, New York Academy of Sciences

Disclosure: Nothing to disclose.

Chief Editor

Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS Professor Emeritus of Neurology and Psychiatry, Clinical Professor of Medicine, Clinical Professor of Family Medicine, Clinical Professor of Neurosurgery, State University of New York Upstate Medical University; Neuroscience Director, Department of Neurology, Crouse Irving Memorial Hospital

Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS is a member of the following medical societies: American College of International Physicians, American Heart Association, American Stroke Association, American Academy of Neurology, American Academy of Pain Medicine, American College of Forensic Examiners Institute, National Association of Managed Care Physicians, American College of Physicians, Royal College of Physicians, Royal College of Physicians and Surgeons of Canada, Royal College of Surgeons of England, Royal Society of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Frederick M Vincent, Sr, MD Clinical Professor, Department of Neurology and Ophthalmology, Michigan State University Colleges of Human and Osteopathic Medicine

Frederick M Vincent, Sr, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Forensic Examiners Institute, American College of Legal Medicine, American College of Physicians

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous coauthors Tarafa Baghdadi, MD and Roukoz B Chamoun, MD to the development and writing of this article.

References
  1. Evans DG. Neurofibromatosis type 2: genetic and clinical features. Ear Nose Throat J. 1999 Feb. 78(2):97-100. [Medline].

  2. Ibebuike K, Ouma J, Gopal R. Meningiomas among intracranial neoplasms in Johannesburg, South Africa: prevalence, clinical observations and review of the literature. Afr Health Sci. 2013 Mar. 13(1):118-21. [Medline].

  3. Sughrue ME, Rutkowski MJ, Aranda D, Barani IJ, McDermott MW, Parsa AT. Treatment decision making based on the published natural history and growth rate of small meningiomas. J Neurosurg. 2010 Apr 30. [Medline].

  4. Pieper DR, Al-Mefty O, Hanada Y, Buechner D. Hyperostosis associated with meningioma of the cranial base: secondary changes or tumor invasion. Neurosurgery. 1999 Apr. 44(4):742-6; discussion 746-7. [Medline].

  5. Hallinan JT, Hegde AN, Lim WE. Dilemmas and diagnostic difficulties in meningioma. Clin Radiol. 2013 Aug. 68(8):837-44. [Medline].

  6. Majchrzak K, Tymowski M. Surgical treatment of the tentorial and falco-tentorial junction meningiomas. Minim Invasive Neurosurg. 2009 Apr. 52(2):93-7. [Medline].

  7. Arima T, Natsume A, Hatano H, et al. Intraventricular chordoid meningioma presenting with Castleman disease due to overproduction of interleukin-6. Case report. J Neurosurg. 2005 Apr. 102(4):733-7. [Medline].

  8. Ragel BT, Jensen RL, Couldwell WT. Inflammatory response and meningioma tumorigenesis and the effect of cyclooxygenase-2 inhibitors. Neurosurg Focus. 2007. 23(4):E7. [Medline].

  9. Kim JH, Lee SH, Rhee CH, et al. Loss of heterozygosity on chromosome 22q and 17p correlates with aggressiveness of meningiomas. J Neurooncol. 1998 Nov. 40(2):101-6. [Medline].

  10. Albrecht S, Goodman JC, Rajagopolan S, Levy M, Cech DA, Cooley LD. Malignant meningioma in Gorlin's syndrome: cytogenetic and p53 gene analysis. Case report. J Neurosurg. 1994 Sep. 81(3):466-71. [Medline].

  11. Verstegen MJ, van den Munckhof P, Troost D, Bouma GJ. Multiple meningiomas in a patient with Rubinstein-Taybi syndrome. Case report. J Neurosurg. 2005 Jan. 102(1):167-8. [Medline].

  12. Hao S, Smith TW, Chu PG, et al. The oncofetal protein IMP3: a novel molecular marker to predict aggressive meningioma. Arch Pathol Lab Med. 2011 Aug. 135(8):1032-6. [Medline].

  13. Niedermaier T, Behrens G, Schmid D, Schlecht I, Fischer B, Leitzmann MF. Body mass index, physical activity, and risk of adult meningioma and glioma: A meta-analysis. Neurology. 2015 Oct 13. 85 (15):1342-50. [Medline].

  14. Hughes, S. Overweight and Lack of Exercise Linked to Meningioma. Medscape Medical News. Available at http://www.medscape.com/viewarticle/851300. September 22, 2015; Accessed: December 7, 2015.

  15. Milham S. Meningioma and mobile phone use. Int J Epidemiol. 2010 Aug. 39(4):1117; author reply 1119. [Medline].

  16. Lee JW, Kang KW, Park SH, et al. 18F-FDG PET in the assessment of tumor grade and prediction of tumor recurrence in intracranial meningioma. Eur J Nucl Med Mol Imaging. 2009 Oct. 36(10):1574-82. [Medline].

  17. Abdel Kerim A, Bonneville F, Jean B, Cornu P, LeJean L, Chiras J. Balloon-assisted embolization of skull base meningioma with liquid embolic agent. J Neurosurg. 2010 Jan. 112(1):70-2. [Medline].

  18. Zielinski G, Grala B, Koziarski A, Kozlowski W. Skull base secretory meningioma. Value of histological and immunohistochemical findings for peritumoral brain edema formation. Neuro Endocrinol Lett. 2013 Apr 5. 34(2):111-117. [Medline].

  19. Wang S, Yang W, Deng J, Zhang J, Ma F, Wang J. Correlation between 99mTc-HYNIC-octreotide SPECT/CT somatostatin receptor scintigraphy and pathological grading of meningioma. J Neurooncol. 2013 Jul. 113(3):519-26. [Medline].

  20. Rosenberg LA, Prayson RA, Lee J, Reddy C, Chao ST, Barnett GH, et al. Long-term experience with World Health Organization grade III (malignant) meningiomas at a single institution. Int J Radiat Oncol Biol Phys. 2009 Jun 1. 74(2):427-32. [Medline].

  21. Wang DJ, Zheng MZ, Gong Y, et al. Papillary meningioma: clinical and histopathological observations. Int J Clin Exp Pathol. 2013. 6(5):878-88. [Medline]. [Full Text].

  22. Dutta D, Lee HN, Munshi A, et al. Intracerebral cystic rhabdoid meningioma. J Clin Neurosci. 2009 Aug. 16(8):1073-4. [Medline].

  23. Zhou K, Wang G, Wang Y, Jin H, Yang S, Liu C. The potential involvement of E-cadherin and beta-catenins in meningioma. PLoS One. 2010. 5(6):e11231. [Medline].

  24. Lakhdar F, Arkha Y, El Ouahabi A, et al. Intracranial meningioma in children: different from adult forms? A series of 21 cases. Neurochirurgie. 2010 Aug. 56(4):309-14. [Medline].

  25. Norden AD, Drappatz J, Wen PY. Advances in meningioma therapy. Curr Neurol Neurosci Rep. 2009 May. 9(3):231-40. [Medline].

  26. Chamberlain MC, Tsao-Wei DD, Groshen S. Temozolomide for treatment-resistant recurrent meningioma. Neurology. 2004 Apr 13. 62(7):1210-2. [Medline].

  27. Milker-Zabel S, Huber P, Schlegel W, Debus J, Zabel-du Bois A. Fractionated stereotactic radiation therapy in the management of primary optic nerve sheath meningiomas. J Neurooncol. 2009 Sep. 94(3):419-24. [Medline].

  28. Haase D, Schmidl S, Ewald C, Kalff R, Huebner C, Firsching R, et al. Fatty acid synthase as a novel target for meningioma therapy. Neuro Oncol. 2010 Aug. 12(8):844-54. [Medline].

  29. Oya S, Kim SH, Sade B, Lee JH. The natural history of intracranial meningiomas. J Neurosurg. 2011 May. 114(5):1250-6. [Medline].

  30. Smith JL, Vuksanovic MM, Yates BM, Bienfang DC. Radiation therapy for primary optic nerve meninigiomas. J Clin Neuroph. 1981. 1:85-99. [Medline].

  31. Mirimanoff RO. New radiotherapy technologies for meningiomas: 3D conformal radiotherapy? Radiosurgery? Stereotactic radiotherapy? Intensity-modulated radiotherapy? Proton beam radiotherapy? Spot scanning proton radiation therapy. . or nothing at all?. Radiother Oncol. 2004 Jun. 71(3):247-9. [Medline].

  32. Nutting C, Brada M, Brazil L, et al. Radiotherapy in the treatment of benign meningioma of the skull base. J Neurosurg. 1999 May. 90(5):823-7. [Medline].

  33. Hasegawa T, Kida Y, Yoshimoto M, Iizuka H, Ishii D, Yoshida K. Gamma Knife surgery for convexity, parasagittal, and falcine meningiomas. J Neurosurg. 2011 May. 114(5):1392-8. [Medline].

  34. Kondziolka D, Levy EI, Niranjan A, et al. Long-term outcomes after meningioma radiosurgery: physician and patient perspectives. J Neurosurg. 1999 Jul. 91(1):44-50. [Medline].

  35. Kondziolka D, Niranjan A, Lunsford LD, Flickinger JC. Stereotactic radiosurgery for meningiomas. Neurosurg Clin N Am. 1999 Apr. 10(2):317-25. [Medline].

  36. Williams BJ, Yen CP, Starke RM, et al. Gamma Knife surgery for parasellar meningiomas: long-term results including complications, predictive factors, and progression-free survival. J Neurosurg. 2011 Jun. 114(6):1571-7. [Medline].

  37. Strassner C, Buhl R, Mehdorn HM. Recurrence of intracranial meningiomas: did better methods of diagnosis and surgical treatment change the outcome in the last 30 years?. Neurol Res. 2009 Jun. 31(5):478-82. [Medline].

  38. Agarwal V, Babu R, Grier J, et al. Cerebellopontine angle meningiomas: postoperative outcomes in a modern cohort. Neurosurg Focus. 2013 Dec. 35(6):E10. [Medline].

  39. Al-Mefty O, Smith R. Clival and petroclival meningiomas. Al-Mefty O, ed. Meningiomas. New York, NY: Raven; 1991.

  40. Alexiou GA, Vartholomatos G, Tsiouris S, et al. Evaluation of meningioma aggressiveness by (99m)Tc-Tetrofosmin SPECT. Clin Neurol Neurosurg. 2008 Jul. 110(7):645-8. [Medline].

  41. Black P, Kathiresan S, Chung W. Meningioma surgery in the elderly: a case-control study assessing morbidity and mortality. Acta Neurochir (Wien). 1998. 140(10):1013-6; discussion 1016-7. [Medline].

  42. Cappabianca P, Cirillo S, Alfieri A, et al. Pituitary macroadenoma and diaphragma sellae meningioma: differential diagnosis on MRI. Neuroradiology. 1999 Jan. 41(1):22-6. [Medline].

  43. De Monte F, Al-Mefty O. Meningiomas. Kaye AH, Laws ER, eds. Brain Tumors: An Encyclopedic Approach. Ediburgh, Scotland: Churchill Livingstone; 1995: 675-704.

  44. Drummond KJ, Zhu JJ, Black PM. Meningiomas: updating basic science, management, and outcome. Neurologist. 2004 May. 10(3):113-30. [Medline].

  45. Feldman RP, Marcovici A, Suarez M, Goodrich JT. Foreign body granuloma mimicking intracranial meningioma: case report and review of the literature. Neurosurgery. 1999 Apr. 44(4):855-8. [Medline].

  46. Haddad GF, Al-Mefty O. Approaches to petroclival tumors. Wilkins RH, Rengachary SS, eds. Neurosurgery. 2nd ed. New York, NY: McGraw-Hill; 1996. Vol 2: 1695-706.

  47. Haddad GF, Al-Mefty O. Meningiomas: an overview. Wilkins RH, Rengachary SS, eds. Neurosurgery. 2nd ed. New York, NY: McGraw-Hill; 1996. Vol 1: 833-42.

  48. Haddad GF, Al-Mefty O. The road less traveled: transtemporal access to the CPA. Clinical Neurosurgery. 1994. 41:150-167.

  49. Iwai Y, Yamanaka K, Yasui T, et al. Gamma knife surgery for skull base meningiomas. The effectiveness of low-dose treatment. Surg Neurol. 1999 Jul. 52(1):40-4; discussion 44-5. [Medline].

  50. Jaffrain-Rea ML, Minniti G, Santoro A, et al. Visual improvement during octreotide therapy in a case of episellar meningioma. Clin Neurol Neurosurg. 1998 Mar. 100(1):40-3. [Medline].

  51. Kleihues P, Cavanee W. World Health Organization Classification of Tumours: Pathology and Genetics: Tumours of the Nervous System. Lyon, France: IARC; 2000.

  52. Klutmann S, Bohuslavizki KH, Tietje N, et al. Clinical value of 24-hour delayed imaging in somatostatin receptor scintigraphy for meningioma. J Nucl Med. 1999 Aug. 40(8):1246-51. [Medline].

  53. Kotzen RM, Swanson RM, Milhorat TH, Boockvar JA. Post-traumatic meningioma: case report and historical perspective. J Neurol Neurosurg Psychiatry. 1999 Jun. 66(6):796, 798. [Medline].

  54. Larner AJ, Ball JA, Howard RS. Sarcoid tumour: continuing diagnostic problems in the MRI era. J Neurol Neurosurg Psychiatry. 1999 Apr. 66(4):510-2. [Medline].

  55. Lee GK, Coel M, Ko J, Tom B. Two meningiomas detected incidentally by Tc-99m HDP bone scintigraphy during a work-up for breast cancer. Clin Nucl Med. 1999 Jul. 24(7):525-6. [Medline].

  56. Liu M, Liu Y, Li X, Zhu S, Wu C. Cystic meninigioma. J Clin Neurosci. 2007 Sep. 14(9):856-9. [Medline].

  57. Lusis E, Gutmann DH. Meningioma: an update. Curr Opin Neurol. 2004 Dec. 17(6):687-92. [Medline].

  58. Nakasu S, Nakasu Y, Nakajima M, et al. Preoperative identification of meningiomas that are highly likely to recur. J Neurosurg. 1999 Mar. 90(3):455-62. [Medline].

  59. Norden AD, Drappatz J, Wen PY. Targeted drug therapy for meningiomas. Neurosurg Focus. 2007. 23(4):E12. [Medline].

  60. Perry A, et al. Meningiomas. Louis DN, Ohgaki H, Wiestler OD, Cavenee WK, Burger PC, Jouvet A, et al. World Health Organization Classification of Tumours of the Central Nervous System. 4th ed. Lyon: IARC; 164-172.

  61. Rempel SA, Ge S, Gutierrez JA. SPARC: a potential diagnostic marker of invasive meningiomas. Clin Cancer Res. 1999 Feb. 5(2):237-41. [Medline].

  62. Runzi MW, Jaspers C, Windeck R. Successful treatment of meningioma with octreotide [letter]. Lancet. 1989 May 13. 1(8646):1074. [Medline].

  63. Sharif S, Brennan P, Rawluk D. Non-surgical treatment of meningioma: a case report and review. Br J Neurosurg. 1998 Aug. 12(4):369-72. [Medline].

  64. Vaicys C, Schulder M, Wolansky LJ, Fromowitz FB. Falcotentorial plasmacytoma: case report. J Neurosurg. 1999 Jul. 91(1):132-5. [Medline].

  65. Whittle IR, Smith C, Navoo P, Collie D. Meningiomas. Lancet. 2004 May 8. 363(9420):1535-43. [Medline].

 
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Case 1: MRI of a meningioma on plaque.
Case 1: Bone-window CT reveals calcification of the meningioma.
Case 1: Surgical view of the tumor. The dura is opened, and the meningioma can be seen extending en plaque over the surface of the brain.
Case 1: Bone flap seen along the removed meningioma in toto.
Case 2: Gadolinium-enhanced MRI of a meningioma invading the overlying dura and bone. Compare with appearance in Case 1.
Case 2: Bone-window CT scan reveals the skull involvement. Note the absence of tumoral calcification.
Case 2: Intraoperative view shows the skull involvement.
Case 2: Bone flap was removed. Note tumoral breach of the dura. The dura and overlying skull were removed surgically. Duraplasty and cranioplasty were performed
Case 2: Surgical specimen. Complete resection was achieved.
Case 3: Tentorial meningioma. A, Contrast-enhanced CT scan shows the enhancing meningioma. Transverse T1-weighted MRIs shows isointensity of the tumor compared with the surrounding brain (B) and its homogenous enhancement (C). Coronal (D), coronal enhanced (E), and sagittal enhanced (F) T1-weighted MRIs. Posterior circulation angiograms show tumoral blush (arrow in G) and the Bernasconi-Cassinari artery (arrow in H).
Case 3: Tentorial meningioma. Gadolinium-enhanced T1-weighted MRI immediately (A) and 2 years after surgery (B-D). Transverse images show posterior (arrow in B) and anterior (arrow in C) recurrence involving the tentorium. Sagittal images show posterior (D) and anterior (E) recurrence involving the tentorium. Lower vignette reveals complete excision of the recurrence after a second operation.
Case 3: Tentorial meningioma A, Pathology showed syncytial meningioma. Note hypercellularity and minimal whorling (hematoxylin-eosin, original magnification X400). B, MRI performed 4 years after the first operation reveals a recurrence over the posterior tentorium. C, Two-dimensional planning for stereotactic radiosurgery. Three recurrences lie in the plane of the tentorium on a single line. D, Three-dimensional planning for stereotactic radiosurgery. Three arcs were used to irradiate the largest recurrence.
Case 4: Recurrent subcutaneous meningioma. A, Patient underwent surgery for a parieto-occipital meningioma in 1978. She was lost to follow-up until 1996, when this transverse T2-weighted MRI was obtained. Arrow indicates surgical bed of the resected meningioma. B, Although the initial surgical bed is tumor-free, sagittal T2-weighted MRI shows a large subcutaneous recurrence. C, Lower transverse section also shows recurrence. Note variegated appearance of the tumor. D, Transverse section at a lower level. Postoperative sagittal (E) and transverse (F, G) enhanced T1-weighted MRI shows gross total removal of the tumor. H and I, Tumoral recurrence 3 months after surgery, at the same level as in G and F, respectively. Patient received repeat surgery for subtotal removal of the tumor; a pediculated subcutaneous flap was used to close the surgical defect. After surgery, patient received conventional radiotherapy.
Case 5: Bilateral olfactory meningioma invading the facial sinuses. Coronal (A), transverse (B), and sagittal (C) gadolinium-enhanced T1-weighted MRI shows bilateral olfactory meningiomas, and the falx dividing the tumor in 2. Arrow indicates tumor invasion of the sinuses. D, Postoperative enhanced T1-weighted MRI shows that the tumor was completely removed by means of craniotomy and a transfacial approach. E, Tumor was first approached intracranially. Enhanced T1-weighted MRI reveals complete excision of the intracranial component. Arrow indicates residual in the sinuses. F, Residual was completely excised by means a transfacial approach performed with the otolaryngology team.
Case 6: Subfrontal meningioma in a patient with abnormal behavior. A, Contrast-enhanced CT scan clearly shows bilateral subfrontal meningioma. B, Transverse T1-weighted MRI of same lesion. C, Intense gadolinium enhancement of the tumor. Coronal (D) and sagittal (E) gadolinium-enhanced T1-weighted MRIs. F, Anterior circulation angiogram reveals posterior displacement of the anterior cerebral artery by tumor. G, Postoperative MRI shows complete removal of the tumor. H-I, Pathology slides (hematoxylin-eosin; original magnification X100 in H, X400 in I) show syncytial meningioma with well-identified whorls and no psammoma bodies.
Case 7: Parasagittal meningioma invading the superior sagittal sinus (SSS). A, Sagittal T1-weighted MRI shows a meningioma (arrow). B, T2-weighted MRI. Note midline shift and tumoral invasion of the skull (arrow). C, Transverse T2-weighted MRI. D, Angiogram shows invasion of the SSS, which remains patent. Sagittal (E, G), transverse (F) postoperative T1-weighted MRI. H, Gadolinium-enhanced postoperative T1-weighted MRI shows residual tumor, which was intentionally left to preserve patency of the SSS. I, Pathology slide (hematoxylin-eosin, original magnification X100) shows a highly vascular syncytial meningioma.
Pathology slides (hematoxylin-eosin; original magnification X400 in A-B, X100 in C-D). A, Fibroblastic meningioma (arrowheads) abutting the dura (arrow). B, Psammomatous meningioma (arrow indicates psammoma body). C, Meningothelial meningioma, tumor in case 4. E, Meningioma with marked vascularity (arrowheads indicate meningioma cluster; arrow, vessel wall).
Case 4: Pathology slides (hematoxylin-eosin, original magnification X400). A, Meningioma with malignant features, as evinced by prominent nucleoli (yellow dot) and mitoses (arrows). B, Intranuclear cytoplasmic intrusion (pseudoinclusion).
This is an extra-axial tumor. Glioblastoma multiforme (GBM) and astrocytoma are intraparenchymal tumors, and GBM enhances in a variegated fashion. Acoustic schwannomas are seen in the posterior fossa but not in this location. Fibrous dysplasia involves the skull but does not cause this amount of compression.
Surgery on a 46-year-old female with a 2-cm, dural-based enhancing tumor along the left frontal convexity. The lesion was presumed to be a meningioma and showed serial enlargement on MRI, prompting the procedure. Pathology confirmed the tumor to be a WHO grade I meningioma. Video courtesy of Anand I. Rughani, MD, and Jeffrey E. Florman, MD.
Meningioma resection in the tuberculum sellae. Video courtesy of Anand I. Rughani, MD, and Jeffrey E. Florman, MD.
Table.
Location Symptoms
Parasagittal Monoparesis of the contralateral leg
Subfrontal Change in mentation, apathy or disinhibited behavior, urinary incontinence
Olfactory groove Anosmia with possible ipsilateral optic atrophy and contralateral papilledema (this triad termed Kennedy-Foster syndrome)
Cavernous sinus Multiple cranial nerve deficits (II, III, IV, V, VI), leading to decreased vision and diplopia with associated facial numbness
Occipital lobe Contralateral hemianopsia
Cerebellopontine angle Decreased hearing with possible facial weakness and facial numbness
Spinal cord Localized spinal pain, Brown-Sequard (hemispinal cord) syndrome
Optic nerve Exophthalmos, monocular loss of vision or blindness, ipsilateral dilated pupil that does not react to direct light stimulation but might contract on consensual light stimulation; often, monocular optic nerve swelling with optociliary shunt vessels
Sphenoid wing Seizures; multiple cranial nerve palsies if the superior orbital fissure involved
Tentorial May protrude within supratentorial and infratentorial compartments, producing symptoms by compressing specific structures within these 2 compartments[6]
Foramen magnum Paraparesis, sphincteric troubles, tongue atrophy associated with fasciculation
Table. Summary of the 2007 WHO Grading Scheme for Meningiomas
WHO Grade Histological Subtype Histological Features
I Meningothelial, fibroblastic, transitional, angiomatous, microcystic, secretory, lymphoplasmacytic metaplastic, psammomatous Does not fulfill criteria for grade II or III
II (Atypical) Chordoid, clear cell 4 or more mitotic cells per 10 hpf and/or 3 or more of the following: increased cellularity, small cells, necrosis, prominent nucleoli, sheeting, and/or brain invasion in an otherwise Grade I tumor
III (Anaplastic) Papillary, rhabdoid[22] 20 or more mitoses per 10 hpf and/or obviously malignant cytological characteristics such that tumor cell resembles carcinoma, sarcoma, or melanoma
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