Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Meningioma Workup

  • 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
 

Laboratory Studies

No specific laboratory tests are used to screen for meningioma.

Next

Imaging Studies

Imaging studies are the mainstay of diagnosis. See images below for representative radiologic views of various subtypes.

Plain skull radiograph may reveal hyperostosis and increased vascular markings of the skull, as well as intracranial calcifications.

On plain head CT scans, meningiomas are usually dural-based tumors that are isoattenuating to slightly hyperattenuating.

  • They enhance homogeneously and intensely after the injection of iodinated contrast material.
  • Perilesional edema may be extensive. Hyperostosis and intratumoral calcifications may be present.
  • The tumor compresses the brain without invading it.
  • Multiple meningiomas may be difficult to differentiate from metastasis.

On T1- and T2-weighted MRIs, the tumors have variable signal intensity. If a meningioma is suspected, obtaining an enhanced MRI is imperative.

  • Meningiomas enhance intensely and homogeneously after injection of gadolinium gadopentetate.
  • The edema may be more apparent on MRI than on CT scanning.
  • An enhancing tail involving the dura may be apparent on MRI.

Cystic meningiomas may exhibit intratumoral or peritumoral cysts. The peritumoral cysts may actually represent a gliotic response and may not necessitate surgical extirpation.

Endovascular angiography allows the surgeon to preoperatively determine the vascularization of the tumor and its encroachment on vital vascular structures.

Late venous images are important to determine the patency of the involved dural sinuses.

Angiographic features of meningiomas include the following:

  • Supply from the external circulation
  • Mother-in-law blush (which comes early and leaves late)
  • Sunburst or radial appearance of the feeding arteries

Although magnetic resonance arteriography (MRA) and magnetic resonance venography (MRV) have decreased the role of classical angiography, the latter remains a powerful tool for planning surgery.

Angiography is still indispensable if embolization of the tumor is deemed necessary.

New research tools such as positron emission tomography (PET), including octreotide-PET, or magnetic resonance spectroscopy (MRS) have been used to predict in vivo the aggressiveness of meningiomas.[16] See the images below.

Case 1: MRI of a meningioma on plaque. Case 1: MRI of a meningioma on plaque.
Case 1: Bone-window CT reveals calcification of th Case 1: Bone-window CT reveals calcification of the meningioma.
Case 2: Gadolinium-enhanced MRI of a meningioma in 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 invo Case 2: Bone-window CT scan reveals the skull involvement. Note the absence of tumoral calcification.
Case 3: Tentorial meningioma. A, Contrast-enhanced 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 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 s 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, Pati 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 th 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 ab 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 super 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.
This is an extra-axial tumor. Glioblastoma multifo 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.
Previous
Next

Procedures

Preoperative endovascular embolization of the vascular feeders from the external circulation may be beneficial in extremely vascular meningiomas.[17] If this is the case, resection should be performed shortly after embolization to decrease the likelihood of tumor revascularization.

Previous
Next

Histologic Findings

Meningiomas are usually globular, well-demarcated neoplasms. They have a wide dural attachment and become invaginated into the underlying brain without invading it. Their cut surface is either translucent pale or homogeneously reddish brown. It may be gritty on cutting. Some meningiomas occur as a sheetlike extension that covers the dura but does not invaginate the parenchyma; this variant is called meningioma en plaque. The last morphologic variant is the cavernous sinus meningioma that infiltrates the cavernous sinus and becomes interdigitated with its contents. The 3 most common histologic subtypes of meningiomas are the meningothelial (syncytial), transitional, and fibroblastic meningiomas. See images below for representative pathologic views of various subtypes.

Pathology slides (hematoxylin-eosin; original magn 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, origi 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).

Meningothelial meningiomas reveal densely packed cells that are arranged in sheets with no clearly discernible cytoplasmic borders. Although not prominent, whorls are present (calcified whorls are termed psammoma bodies). Nuclei show intranuclear vacuoles.

Fibroblastic (fibrous) meningiomas reveal sheets of interlacing spindle cells. The intercellular stroma is composed of reticulin and collagen. The transitional variety reveals features common to both the meningothelial and fibroblastic varieties; others include angiomatous, microcystic, secretory,[18] clear cell, choroid, lymphoplasmacyte-rich, papillary, and metaplastic variants.

Meningiomas may be associated with hyperostosis.[4] The exact nature of the cause of this hyperostosis is controversial (ie, reactive versus tumoral infiltration).

Immunohistochemistry

Immunohistochemistry can help diagnose meningiomas, which are positive for epithelial membrane antigen (EMA) in 80% of cases. They stain negative for anti-Leu 7 antibodies (positive in schwannomas) and for glial fibrillary acidic protein (GFAP). Progesterone receptors can be demonstrated in the cytosol of meningiomas; the presence of other sex hormone receptors is much less consistent. Somatostatin receptors also have been demonstrated consistently in meningiomas.[19]

Malignancy

The notion of malignancy in meningiomas is still vague.[20] Some histologic variants, such as papillary meningioma, undoubtedly carry a less favorable prognosis than other histologic types.[21] Two features are considered clear signs of malignancy: cortical invasion by the tumor and distal metastasis. Of note, in the 2007 WHO grading scheme, brain invasion is considered a criterion for atypia.

Several stains have been used to help predict the behavior of meningiomas. These stains quantify the mitotic rate of these tumors. Bromodeoxyuridine (BudR) labeling requires an intravenous (IV) injection before tumor removal. On the other hand, immunohistologic staining for proliferating cell nuclear antigen (PCNA) can be performed on fixed specimens. Some have attempted to correlate the pathology and behavior of meningiomas to the loss of specific genetic material.

The World Health Organization classification of meningiomas is presented in Table 2.

Table. Summary of the 2007 WHO Grading Scheme for Meningiomas (Open Table in a new window)

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

 

The expression levels of E- cadherin and beta-catenin were found to be inversely correlated with peritumoral edema, aggressiveness of meningiomas, and probability of recurrence.[23]

In a review of 21 pediatric meningiomas operated on over a period of 24 years, 24% were WHO grade II and 24% where associated with a large cystic component.[24]

Previous
 
 
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].

 
Previous
Next
 
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
Previous
Next
 
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.