Sphenoid Wing Meningioma



In 1614, Felix Plater first described meningiomas at an autopsy. In 1938, Cushing and Eisenhardt first used the term "meningioma" and introduced it as a separate category of extraparenchymal tumors.[1, 2] Meningiomas are believed to arise from the meningothelial cell (arachnoid cap cell) and are usually attached to the inner surface of the dura mater.[3] The parasagittal region, cerebral convexities, skull base, and falx are the most common locations for meningiomas, although they may arise at any location where meninges exist.[4] See the image below.

Meningiomas account for approximately 13%-20% of all brain tumors[5] and 34%-36.4% of all primary brain tumors, making meningiomas the most common primary brain tumors.[6, 7] Meningiomas represent only 4% of all orbital tumors.[8] Of lesions in the supratentorial compartment, sphenoid wing meningiomas represent about 15%-20% of all meningiomas. Sphenoid wing meningiomas are also known as “orbitosphenoid meningiomas,” “meningiomas en plaque of the sphenoid wing,” and “sphenoid wing meningiomas with osseous involvement.”[9] Sphenoid wing meningiomas may be associated with hyperostosis of the sphenoid ridge and may be very invasive, spreading to the dura of the frontal, temporal, and orbital regions.[9, 10, 11, 12] Two different growing patterns of sphenoid wing meningioma have been described: meningioma en masse, forming a nodular space-occupying lesion, and meningioma en plaque, which is flat.

Meningiomas of the anterior skull base are defined as arising anterior to the chiasmatic sulcus that separates the middle cranial fossa from the anterior cranial fossa.[13] Sphenoid wing meningiomas are the most common of the basal meningiomas. Medially, they may expand into the wall of the cavernous sinus, anteriorly into the orbit, and laterally into the temporal bone. Sphenoid wing meningiomas are categorized as lateral, middle, or medial (clinoidal), depending on the origin of the tumor along the sphenoid ridge.[14] Furthermore, medial (clinoidal) meningiomas are further differentiated into 3 subcategories based on their relation to the anterior clinoidal process.

Type I clinoidal meningiomas originate from the inferomedial surface of the clinoidal process proximal to the distal carotid ring. This type is very difficult to resect because of the absence of the arachnoid plane between the tumor and the internal carotid artery.

Type II clinoidal meningiomas originate from the superolateral surface, leading to widening of the sylvian fissure, and are relatively easy to remove.

Type III meningiomas originate at the optic foramen and extend into the optic canal.[15] Other frontal skull base meningiomas can arise from the olfactory groove or planum sphenoidale. Planum sphenoidale meningiomas arise 2 cm posterior to olfactory groove meningiomas, and they may be symmetrical around the midline or may extend to the side. Of olfactory groove meningiomas, about 15%-20% grow into the ethmoid sinuses.[16, 17]  


The most widely known risk factor for meningiomas is ionized radiation exposure.[18, 19, 20, 21, 22] For example, children with tinea capitis who are treated with an average single dose or multiple doses of 1.5 Gy have a relative 9.5% risk of developing meningioma.[23] Dental radiography is a common source of radiation in the United States. The risk of meningioma has been found to double after full-mouth series.[24] In addition, radiation-induced tumors may develop after previous radiation treatment of another lesion. Cahan et al[25] were the first to propose criteria for identifying radiation-induced tumors, and these criteria have been applied to diagnose radiation-induced meningiomas. Radiation-induced tumors were defined as lesions arising after a latency period (4 years in the original article) within a previously irradiated field that have different histology than the radiated tumor.[25] These criteria have been augmented by others over the years with additional features, and the full set of criteria now includes the following:[26, 27, 28]

The most commonly reported radiation-induced tumor is meningioma.[26, 28] The Childhood Cancer Survivor Study in the United States reported a cumulative incidence of 3.1% and a relative risk of 2.7% for meningioma development at 30 years after the primary tumor diagnosis.[21] Radiation-induced meningiomas develop more frequently over the convexities than the skull base, at a ratio of 1.9:1 for both high-dose and low-dose radiation.[28]

Radiation-induced meningiomas more commonly occur as multiples and in a younger age groups than do spontaneous meningiomas.[28] Some authors reported that these tumors exhibit more malignant behavior, as indicated histologically by high cellularity, pleomorphism, multinucleation, and giant cell pseudoinclusions.[29] These findings have not yet been confirmed by others.[28]

There is a wide variation in the literature regarding the latency period for the development of radiation-induced meningioma.[26, 29, 30] It has been suggested that this variation is related to variation in the radiation dose, with a short latency for high doses and long latency for low-dose radiation.[26] The recognized latency period can be as short as 14 months and as long as 63 years, although the average latency period is 30-40 years in most cases.[28, 29, 30]

Aside from radiation, other factors that have been studied as potential causes of meningioma include genetic abnormalities, hormonal factors, and viral infections.

In cytogenetic studies, the most commonly reported genetic abnormality is the loss of NF2 tumor suppressor gene on long arm of chromosome 22 (monosomy 22). This genetic alteration leads to loss of expression of NF2 protein product (neurofibromin) and has been reported in 40%-70% of meningiomas.[31] Other commonly reported genetic alterations in meningioma include deletion of short arm of chromosome 1; loss of chromosomes 6, 10, 14, 18, and 19; and gain of 1q, 9q, 12q, 15q, 17q, and 20q.[31] Abnormalities of chromosome 22 have been associated with type II neurofibromatosis, and 75% of patients with type II neurofibromatosis develop meningioma during their lifetime. Ten percent of these are multiple lesions.[32, 33]

Hormonal factors (eg, estrogen, progesterone, androgen, steroid) have been studied extensively as risk factors for meningiomas because of the striking predominance of meningiomas in women; the female-to-male ratio is 2:1 for intracranial tumors and 10:1 for spinal meningiomas.[31] Other evidence to substantiate the implication of sex-specific hormones comes from data showing increased growth of meningiomas during pregnancy and hormonal replacement therapy.[34] Estrogen receptor (ER) has been found in 30% of meningiomas in one series, predominantly the ER-beta receptor isoform.[35]

The progesterone receptor is the best candidate among the sex-specific factors as a cause for meningiomas. Progesterone receptors have been shown to be expressed in 81% of women and 40% of men with meningiomas.[36, 37] Other studies indicate that progesterone binds to meningiomas in 50%-100% of tested specimens.[36] Although progesterone receptor expression has been observed more frequently in benign meningioma (96%) than the malignant type (40%), no relation has been found between progesterone receptor status and age, sex, location of tumor, or menopausal state.[5, 37] These findings have prompted researchers to develop antiprogesterone medications, such as mifepristone (RU-486), which appears to inhibit tumor growth in vitro and in vivo.[38]

Androgen receptors have also been found in approximately 50% of meningiomas, but their receptor expression is variable, making them less likely candidates in the pathophysiology of meningiomas.[39] Similarly, meningiomas vary in expression of receptors for other hormones (eg, vascular endothelial growth factor receptor [VEGFR], epidermal growth factor [EGF], platelet-derived growth factor [PDGF], fibroblast growth factor, insulin-like growth factor-1 [IGF-1]), making them less likely candidates for oncogenesis of meningiomas. It has been suggested that the direct stimulatory effect of EGF on PDGF or PDGF itself may be partially responsible for angiogenesis and even oncogenesis in meningiomas. PDGF is a particularly attractive candidate because it has structural homology with the product of c-sis oncogene on chromosome 22.[33]

Some viruses have been found within meningiomas, including polyoma virus, simian vacuolating virus 40 (SV-40), and adenovirus. A suggested role for these viruses or parts of viruses is related to the proteins involved in the induction or maintenance of tumor growth and transformation.[18] However, this association has not proven.

Among the other potential factors for inducing meningiomas that have not been proven are head trauma and electromagnetic field exposure. Head trauma and skull fractures have been suggested as a risk factor for meningioma development by some authors.[40] However, a large population-based 2014 study from Taiwan found no association between head injury and meningioma development in two cohorts of patient with and without head injury.[41]

Similarly, electromagnetic field exposure, especially with the widespread use of cell phones, has generated interest in relation to the pathophysiology of brain tumors. Many studies suggest that little, if any, evidence supports the implications of cell phone use on meningioma development, although there is generally a lack of well-conducted studies to date and a significant amount of debate in this regard.[5]  


According to the most recently published Central Brain Tumor Registry of the United States (CBTRUS) report, meningioma is the most common nonmalignant brain and central nervous system (CNS) tumor, making up 36.4% of reported tumors (7.86 per 100,000 population). The CBTRUS report also indicates that meningioma is the second most frequently reported brain and CNS tumor overall in adolescents and young adults (age 15-39 years), accounting for 15.9% of tumors. It is the most common tumor in patients aged 35-39 years, accounting for 25.1% of tumors, and is least common in patients aged 15-19 years, accounting for 4.9% of tumors. These numbers increase steadily with age.[42]

The annual incidence of meningiomas can be as low as 0.74 per 100,000 individuals younger than 34 years and as high as 18.86 per 100,000 individuals older than 85 years. It is 2.5 times more common in females than in males and 1.1% more common in blacks than in whites.[6, 43] In children, meningioma accounts for 4.6% of all primary brain tumors.[31, 44] Incidental meningioma is found in 0.52%-0.9% of brain images.[45, 46]  


United States

Meningiomas account for approximately 13%-20% of all brain tumors.


Worldwide, meningiomas account for approximately 13%-20% of all brain tumors.


In a 2016 study of 1549 operated meningiomas, the overall perioperative complication rate was 17.8%-18.8%; of these, the morbidity rate was 1.2%-2.2%.[47]

Among patients with skull base meningiomas, a 2016 study reported the overall mortality rate was 5%, with transient cranial nerve deficits occurring in 32% of cases, definite cranial nerve lesions in 18%, and cerebrospinal fluid (CSF) leak in 14%.[48] Another study reported an overall mortality rate of 5.8%, transient cranial nerve deficit rate of 11.7%, definitive morbidity of 5.8%, and second recurrence rate of 5.8%.[49]

Potential complications include bleeding, deep venous thrombosis and embolism, air embolism, venous infract, wound-healing deficits, paresis, sensory deficits, cranial nerve palsy, aphasia, seizures, brain edema, hygroma, CSF fistula hydrocephalus, ischemia, and pituitary insufficiency. These complications vary depending on preoperative morbid conditions, age, and tumor size and location.


Previous studies reported variability in the prevalence of meningiomas among whites, Africans, African-Americans, and Asians and greater incidence among blacks than whites.[7, 50] However, the 2015 CBTRUS report showed that the rates among whites, blacks, and Hispanics were similar.[42]


The incidence rate of meningioma is higher in females (10.87 per 100,000 population) than in males (4.98 per 100,000 population).[42]

No sexual predilection was found among Africans.[50]


The average age at onset is 63 years. The incidence of meningiomas increases steadily thereafter.[47]


A 1983 study showed that recurrence-free survival rates after complete surgical removal in 114 patients (60% of which were sphenoid wing meningioma) at 5, 10, and 20 years were 80%, 70%, 50%, respectively.[51] The extent of surgical resection and histological grade are very important prognostic factors.

In 1957, Simpson classified meningiomas based on the extent of resection as follows:[52]

The 10-year risk of recurrence for grades I through IV were 9%, 19%, 29%, and 44%, respectively.[52]

The relevance of this system in the current era of microsurgical procedures advancement has been questioned by some authors;[53] however, a 2016 study of 458 patients with World Health Organization (WHO) grade I meningioma indicated that the extent of surgical resection based on Simpson grading is an important predictor of tumor recurrence.[54] The overall tumor recurrence rates for Simpson resection grades I, II, III, and IV were 5%, 22%, 31%, and 35%, respectively.[54] When WHO histological grading of meningiomas is considered regarding survival, a 2016 study of 905 patients demonstrated that the 5-year overall survival rate was 85%-90% for WHO grade I, 75%-78% for WHO grade II, and 30%-35% for WHO grade III tumors.[47] Recurrence rates of tumors graded according to the 2007 WHO classification of tumors of the central nervous system were 7%-25% for WHO grade I, 29%-52% for WHO grade II, and 50%-94% for WHO grade III.[55]

Studies on the prognosis of sphenoid wing meningioma and spheno-orbital meningioma have generally showed good outcomes.

The results of a retrospective study of 25 patients who underwent surgical resection and orbital reconstruction with an average of 5 years of follow-up showed that a gross-total resection was achieved in 70% of patients, with surgery limited by the superior orbital fissure and the cavernous sinus. Proptosis improved in 96% of patients, with 87% improvement in visual function. Ocular paresis improved in 68%, although 20% of patients experienced temporary ocular paresis postoperatively. Overall, 95% of patients reported an improved functional orbit. There were no perioperative deaths or morbidity related to the surgical approach or reconstruction. Tumor recurrence occurred in 8% of patients.[56]

In another series of 67 patients with sphenoorbital meningioma who underwent surgical resection with orbital wall reconstruction, a total removal was achieved in 14 cases (82.3%), with only one recurrence (7.1%) over a mean follow-up period of 36 months. Proptosis was corrected in all cases, and visual acuity improved in 7 (70%) of 10 cases. Radical resection was followed by cranio-orbital reconstruction to prevent enophthalmos and to obtain good cosmetic results. No deaths or serious complications occurred in association with surgery. Revision of the orbital reconstruction was required because of postoperative enophthalmos (two cases) or restricted postoperative ocular movement (one case).[57]

A 2016 series of 33 patients with spheno-orbital meningioma who underwent resection without formal orbital wall reconstruction (mean follow-up, 4.5 years) showed improved proptosis in all patients, and only 2 patients had tumor recurrence at the orbit that required surgery.[9]

The authors of these studies emphasize aggressive removal of the hyperostotic bone to achieve satisfactory results and to decrease the risk of recurrence. For example, a study of 47 patients with spheno-orbital meningioma who underwent surgery via the frontotemporal approach without orbital wall reconstruction showed that complete resection was achieved in 51% of cases. At a mean follow-up of 52 months, proptosis normalized in 90.9% and improved in the remaining patients, visual acuity normalized in 20.8% and improved in 45.8% patients, and cranial nerve deficit subsided in all but two cases. The recurrence rate was 29.7%.[58] According to the authors, the high recurrence rate in this study was likely related to the incomplete removal of the invaded bone to minimize perioperative morbidity. 

Patient Education

Some useful information is provided by the American Brain Tumor Association.


The classic triad of sphenoid (spheno-orbital) wing meningioma is proptosis (86%), which may be painless; visual impairment (78%); and ocular paresis (20%).[56, 57] Headache is also a common manifestation[57] , in addition to ptosis.

Slowly growing scalp masses have been reported.

Transient ischemic attack–like presentation has been reported.[59]

Variants of the clinical syndrome include the following:


Sphenoid wing meningiomas can be associated with various cranial nerve dysfunction due to superior orbital fissure involvement and foraminal encroachment of cranial nerves located at the skull base.[63] Swelling of the sphenoid bone and exophthalmos are common examination findings.


An increased incidence of meningiomas has been reported in patients with neurofibromatosis type II and in those with abnormalities of chromosome 22, as follows:[31, 32, 33]

Various viruses that have been described in association with primary brain tumors, including SV-40, adenovirus, and papovavirus, have been identified in meningiomas.[18]

Hormonal factors, namely estrogen and progesterone, have been implicated in the pathophysiology of meningiomas. Both estrogen and progesterone receptors have been reported in a large majority of meningiomas, with a greater percentage of meningiomas expressing active progesterone receptors than estrogen receptors.[31, 35, 37]

The beta-receptor beta subtype of PDGF was identified in 100% of meningiomas in one study.[33]

In vitro, PDGF appears to enhance cell proliferation of meningioma cells. The medium in which meningioma cells are grown in vitro has been shown to contain PDGF, and supplementary addition of PDGF to cultured meningioma cells appears to stimulate their growth.[33]

Vascular endothelial growth factor also seems to play a role in the biology of meningiomas. The degree of peritumoral edema on T2-weighted MRI has been correlated directly with the degree of staining intensity of the meningioma in vitro.[33]

Epidermal growth factor has been described in large percentage of meningiomas in tissue culture.[64]

Head trauma was suggested as a possible etiology for meningiomas, but recent prospective studies have shown no increased incidence of meningiomas in patients with head trauma. 


The complexity of skull base approaches, proximity of the cranial nerves, poor accessibility, dural attachments, and involvement of the extracranial compartment, especially the nasal sinuses for skull base meningiomas, makes the complication frequency for these lesions higher than with other locations.[92]

Depending on the exact location of the meningioma, a different subset of neural structures may become involved.

For medial sphenoid wing meningiomas, visual loss and abnormalities of cranial nerves III, IV, VI, V1, and V2 may occur because the meningioma may have some degree of encasement of these structures as they pass through the cavernous sinus.

Seizures, paresis, and sensory loss may occur, depending on potential damage to adjacent brain parenchyma among patients with lateral sphenoid wing meningiomas. 

Laboratory Studies

Laboratory studies may be indicated to rule out other differential diagnoses (eg, metabolic panel including calcium, bone-specific alkaline phosphatase, urine hydroxyproline).

Imaging Studies

Plain radiography of the skull

Abnormalities have been found in 30%-60% of patients with sphenoid wing meningioma. Hyperostosis, thinning of bone, and irregular foci of calcification can be seen.[70]

CT scanning of the bone window

CT scanning of the bone window typically shows thick, hyperdense, intradiploic lesion expanding the calvaria and destroying the cortical layers of the skull. The bony expansion and ground-glass appearance of sphenoid wing meningioma complicates differentiation from fibrous dysplasia;[71] however, the inner table of the skull looks smooth in fibrous dysplasia, whereas sphenoid wing meningiomas often demonstrate irregularity of the inner table associated with a dural reaction. Clinically, fibrous dysplasia usually presents in younger individuals and stops growing after puberty, in contrast to meningioma, which typically develops in older individuals. Among sphenoid wing meningiomas, 59% are osteoblastic, 10%-35% are osteolytic, and 6% are a mixed picture of both osteolytic and hyperostosis.[67, 72]

View Image

CT scan brain bone window showing intraosseous meningioma involving left sphenoid wing, lateral orbital, superior orbital fissure, and the anterior pa....


MRI allows better delineation of the soft tissue component of the tumor and dural involvement, as well as delineation of intraorbital extension or growth. There might be no dural tail in sphenoid wing meningioma, especially the en plaque variant.[71]

View Image

MRI brain T2W (left) and T1W Fat-Sat (right) sequences showing involvement of the left sphenoid wing associated with dural thickening and the periorbi....


Angiography is not necessary in sphenoid wing meningioma. When performed, it usually shows tumor blush of the en masse component and tortuous external carotid artery feeders.[71]

C-PiB and F-FDG positron-emission tomography scanning

Two patients who had undergone contrast-enhanced MRI scans that revealed extra-axial tumors next to the sphenoid wing were examined using C-PiB and F-FDG positron-emission tomography (PET) scanning. The researchers concluded that C-PiB could be used as a meningioma marker.[73]  

Other Tests

Other tests may include the following:

Histologic Findings

According to the WHO, in 2007 and 2016, 3 types of meningiomas exist based on malignant behavior, as follows:[55, 75, 76]

Malignant transformation is rare. Originally, malignancy was seen in anaplastic tumors, but they may arise from any of the meningioma variants or atypical meningiomas. Papillary histopathology is associated with local aggressiveness and an increased incidence of late distant metastasis. The papillary type is considered malignant by definition and is encountered more frequently in children.[77]

Earlier classification schemes used the term angioblastic meningioma for what is now considered to be a hemangiopericytoma. This neoplasm is distinctly separate from a meningioma, and it shows extremely high propensity for recurrence and metastasis. Hemangiopericytoma is a sarcoma in the new WHO classification.[76, 78]

Meningiomas are generally slow growing. Growth patterns of meningioma in a 2011 series of incidentally diagnosed meningioma included no growth, linear growth, or exponential growth. The presence of calcification, T2-weighted MRI tumor hypointensity, and older age at onset were associated with slower growth rate.[79]

In a large series of 603 asymptomatic meningiomas, 63% did not increase in size, and only 6% of patients eventually experienced symptoms over a mean follow-up of 3.9 years.[80]

Another series of 273 incidental meningiomas in 244 patients with a mean follow-up period of 3.8 years observed a 2 mm or greater increase in maximum diameter in 120 tumors (44% of the cases).[81]

True metastases are extremely uncommon, and dissemination is usually believed to occur hematogenously, with the lungs as the most common site.[82]

Bony invasion is not evidence of malignancy in meningiomas, and invasion of mesenchymal components (eg, bone, muscle, dura) can occur with benign meningiomas.[83]  

Surgical Care

Total microsurgical resection of sphenoid wing meningioma is usually curative. A recurrence risk approaching 30% has been reported when incomplete removal is attempted.[58, 84] Depending on the bony involvement and the soft tissue component of the tumor, the principles of resecting a sphenoid wing en plaque meningioma are complete removal of all the involved bone, including the sphenoid wing, orbital roof, and orbital lateral wall. Decompression of optic nerve, superior orbital fissure, and maxillary branch of the trigeminal nerve posteriorly to foramen rotundum should be accomplished.

The skin incision is made 0.5-1 cm anterior to the tragus at the level of the zygomatic arch and extended behind the hairline toward the widow peak. It can be curved back across the midline toward the contralateral superior temporal line, if needed. Care must be taken not to injure the temporal branch to the frontalis muscle or the facial nerve that passes anterior to it. The temporalis muscle, along with the superficial and the deep fascial layers, are incised in similar fashion from the skin down to the bone. The musculocutaneous flap is reflected anteriorly using a periosteal elevator. Avoid cauterizing the blood supply and innervation to the temporalis muscle to prevent future muscle atrophy.

Once the muscle is elevated and reflected anteriorly, lateral sphenoid wing hyperostosis is usually apparent, and any noticed during elevation of the temporal muscle is excised.

Multiple bur holes are then made around the invaded or hyperostotic bone to prevent excessive bleeding and dural tear. The drill is then used to connect the bur holes and to remove the invaded bone. This process continues until all hyperostotic tissue is removed from the sphenoid wing down to the meningo-orbital band.

The meningo-orbital band is then coagulated and cut sharply, followed by dural stripping from the superior orbital fissure and the anterior part of the lateral wall of the cavernous sinus, exposing the middle fossa floor laterally to the foramen spinosum and posteriorly to the foramen rotundum. Hyperostotic tissue is then removed in a similar manner from the orbital roof and lateral walls of the orbit.

The superior orbital fissure is completely decompressed. The optic nerve in the canal is unroofed, and anterior clinoidectomy is performed.

Once the bone removal is complete, attention is focused on resecting the intradural portion of the tumor, and the dura is resected beyond the enhanced dural tail. The intraorbital extension with involvement of the periorbita and extraocular muscles should also be removed.

Abdominal fat or temporalis fascia with or without pericranial flap can be used to repair the frontal, maxillary, and ethmoid sinuses if they have been opened to prevent postoperative development of a CSF leak and rhinorrhea. A duraplasty is performed using a dural substitute.

There is no clear consensus in the literature regarding whether to reconstruct the orbit. Orbital wall reconstruction has been recommended whenever the orbital floor or more than one wall has been resected or the periorbita was resected to prevent occurrence of pulsatile enophthalmos postoperatively.[85] However, studies have concluded that this complication is uncommon and that orbital reconstruction is unnecessary except in rare occasions when the orbital rim is resected.[9, 86, 87]

When orbital reconstruction is needed, the area can be reconstructed using mesh, dural substitute, or split bone if only the superior and lateral walls of the orbit have been removed. The cranial flap is placed back if it was not involved by the tumor, or a piece of Medpor can be used to cover the cranial defect, making sure to cover the keyhole area. The temporal muscle is then reattached, and the skin is closed in two layers. 

Medical Care

Anecdotal reports have described using antihormonal agents in the treatment of meningiomas. Medical treatment is reserved for atypical and malignant meningiomas as an adjunct to surgery.

Medication Summary

Tamoxifen, an antiestrogen hormone, inhibits the effects of estrogen by competitively binding to estrogen receptor, producing a nuclear complex that decreases DNA synthesis and inhibits estrogen effects. Its use has been reported in small series of patients with refractory or unresectable meningiomas; in one study, 19 patients were included in a phase II trial. Results showed partial MRI response in 3 patients, 6 patients remained stable for a median duration of 31 months, and 10 patients had progression.[88]

Mifepristone, RU-486 (Mifeprex), is an antiprogesterone agent. A 2015 systematic review of all studies reporting on this medication did not provide any evidence for benefit beyond preclinical uses.[89]

Hydroxyurea is a chemotherapeutic agent that selectively inhibits ribonucleoside diphosphate reductase and induces apoptosis. Small case series of patients with recurrent grade II and III meningiomas have been published. Some of the these studies suggest clinical stabilization of the disease with radiological response except in one patient.[90]

Sunitinib is a tyrosine kinase inhibitor that targets VEGFR and PDGF receptor. A prospective, multicenter, single-arm phase II trial of 36 patients with recurrent WHO II and III meningioma found 42% progression-free survival at 6 months, with 5.2 months median progression-free survival and 24.6 months median overall survival. This study demonstrated that expression of VEGFR2 predicted progression-free survival of a median of 1.4 months in VEGFR2-negative patients versus 6.4 months in VEGFR2-positive patients, suggesting that VEGFR2 might be an important prognosticator in WHO II/III meningioma.[91]

Other systemic therapies have been evaluated for recurrent meningioma including cytotoxic chemotherapies (temozolomide, irinotecan, and combination therapy with cyclophosphamide, doxorubicin, and vincristine), biologics (interferon alfa-2b), and targeted therapies (erlotinib, gefitinib, somatostatin analogs, sunitinib, valatinib, imatinib, bevacizumab).

Tamoxifen (Soltamox)

Clinical Context:  Competitively binds to estrogen receptor, producing a nuclear complex that decreases DNA synthesis and inhibits estrogen effects.

Class Summary

Inhibit effects of estrogen by competitively binding to estrogen receptor.

Mifepristone, RU-486 (Korlym, Mifeprex)

Clinical Context:  Experimental antiprogesterone agent. Used in patients with recurrent benign meningiomas; in one study of 14 patients, tumor regression was reported in 5 of 14 patients.

Class Summary

RU-486 has been used experimentally in the treatment of this medical condition.

Sunitinib (Sutent)

Clinical Context:  This agent shows antitumor and antiangiogenic effects. May inhibit multiple-receptor tyrosine kinases, including platelet-derived growth factors, vascular endothelial growth factors, FMS-like tyrosine kinase-3, colony-stimulating factor type 1, and glial cell-line–derived neurotrophic factor receptor. Studies have shown that VEGFR2-positive patients may achieve progression-free survival of up to 6.4 months.

Class Summary

Agents in this class inhibit cell growth and proliferation and exhibit antiangiogenic properties.


Bhupendra C K Patel, MD, FRCS, Professor of Ophthalmic Plastic and Facial Cosmetic Surgery, Department of Ophthalmology and Visual Sciences, John A Moran Eye Center, University of Utah School of Medicine

Disclosure: Nothing to disclose.


Gmaan Ali M Alzhrani , MBBS, MA, Fellow in Skull Base and Vascular Surgery, Clinical Neuroscience Center, University of Utah School of Medicine

Disclosure: Nothing to disclose.

William T Couldwell, MD, PhD, Professor of Neurosurgery (Adult Neurosurgery) and Joseph J Yager Chair, Department of Neurosurgery, Adjunct Professor of Surgery (Otolaryngology-Head and Neck Surgery), University of Utah School of Medicine; Attending Neurosurgeon, University of Utah Hospital

Disclosure: Nothing to disclose.

Specialty Editors

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.

Chief Editor

Hampton Roy, Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Disclosure: Nothing to disclose.

Additional Contributors

Andrew W Lawton, MD, Neuro-Ophthalmology, Ochsner Health Services

Disclosure: Nothing to disclose.

Sally B Zachariah, MD, Associate Professor, Department of Neurology, University of South Florida College of Medicine; Director, Department of Neurology, Division of Strokes, Veteran Affairs Medical Center of Bay Pines

Disclosure: Partner received none from none for none.


Suzan Khoromi, MD Fellow, Pain and Neurosensory Mechanisms Branch, National Institute of Dental and Cranial Research, National Institutes of Health

Suzan Khoromi, MD is a member of the following medical societies: American Academy of Neurology, American Pain Society, and International Association for the Study of Pain

Disclosure: Nothing to disclose.

Brian R Younge, MD Professor of Ophthalmology, Mayo Clinic School of Medicine

Brian R Younge, MD is a member of the following medical societies: American Medical Association, American Ophthalmological Society, and North American Neuro-Ophthalmology Society

Disclosure: Nothing to disclose.


  1. Cushing H, Eisenhardt L, Thomas C, eds. Meningiomas: Their Classification, Regional Behaviour, Life History, and Surgical End Results. Springfield, Ill: Charles C Thomas; 1938.
  2. Rockhill J, Mrugala M, Chamberlain MC. Intracranial meningiomas: an overview of diagnosis and treatment. Neurosurg Focus. 2007. 23 (4):E1. [View Abstract]
  3. Bright R. Reports of Medical Cases, Selected With a View of Illustrating the Symptoms and Cure of Diseases by a Reference to Morbid Anatomy. London: Longman, Rees, Orme, Brown & Green; 1827.
  4. Yamashita J, Handa H, Iwaki K, Abe M. Recurrence of intracranial meningiomas, with special reference to radiotherapy. Surg Neurol. 1980 Jul. 14 (1):33-40. [View Abstract]
  5. Claus EB, Bondy ML, Schildkraut JM, Wiemels JL, Wrensch M, Black PM. Epidemiology of intracranial meningioma. Neurosurgery. 2005 Dec. 57 (6):1088-95; discussion 1088-95. [View Abstract]
  6. Ostrom QT, Gittleman H, de Blank PM, Finlay JL, Gurney JG, McKean-Cowdin R, et al. American Brain Tumor Association Adolescent and Young Adult Primary Brain and Central Nervous System Tumors Diagnosed in the United States in 2008-2012. Neuro Oncol. 2016 Jan. 18 Suppl 1:i1-i50. [View Abstract]
  7. Ibebuike K, Ouma J. Demographic profile of patients diagnosed with intracranial meningiomas in two academic hospitals in Johannesburg, South Africa: a 12-month prospective study. Afr Health Sci. 2014 Dec. 14 (4):939-45. [View Abstract]
  8. Bonavolontà G, Strianese D, Grassi P, Comune C, Tranfa F, Uccello G, et al. An analysis of 2,480 space-occupying lesions of the orbit from 1976 to 2011. Ophthal Plast Reconstr Surg. 2013 Mar-Apr. 29 (2):79-86. [View Abstract]
  9. Bowers CA, Sorour M, Patel BC, Couldwell WT. Outcomes after surgical treatment of meningioma-associated proptosis. J Neurosurg. 2016 Sep. 125 (3):544-50. [View Abstract]
  10. Sughrue ME, Rutkowski MJ, Chen CJ, Shangari G, Kane AJ, Parsa AT, et al. Modern surgical outcomes following surgery for sphenoid wing meningiomas. J Neurosurg. 2013 Jul. 119 (1):86-93. [View Abstract]
  11. Nakamura M, Roser F, Jacobs C, Vorkapic P, Samii M. Medial sphenoid wing meningiomas: clinical outcome and recurrence rate. Neurosurgery. 2006 Apr. 58 (4):626-39, discussion 626-39. [View Abstract]
  12. Scarone P, Leclerq D, Héran F, Robert G. Long-term results with exophthalmos in a surgical series of 30 sphenoorbital meningiomas. Clinical article. J Neurosurg. 2009 Nov. 111 (5):1069-77. [View Abstract]
  13. Rhoton AL Jr. The anterior and middle cranial base. Neurosurgery. 2002 Oct. 51 (4 Suppl):S273-302. [View Abstract]
  14. MacCarty CS. Meningiomas of the sphenoidal ridge. J Neurosurg. 1972 Jan. 36 (1):114-20. [View Abstract]
  15. al-Mefty O, Ayoubi S. Clinoidal meningiomas. Acta Neurochir Suppl (Wien). 1991. 53:92-7. [View Abstract]
  16. Liu JK, Christiano LD, Patel SK, Tubbs RS, Eloy JA. Surgical nuances for removal of olfactory groove meningiomas using the endoscopic endonasal transcribriform approach. Neurosurg Focus. 2011 May. 30 (5):E3. [View Abstract]
  17. Hentschel SJ, DeMonte F. Olfactory groove meningiomas. Neurosurg Focus. 2003 Jun 15. 14 (6):e4. [View Abstract]
  18. Bondy M, Ligon BL. Epidemiology and etiology of intracranial meningiomas: a review. J Neurooncol. 1996 Sep. 29 (3):197-205. [View Abstract]
  19. Busch D. Genetic susceptibility to radiation and chemotherapy injury: diagnosis and management. Int J Radiat Oncol Biol Phys. 1994 Nov 15. 30 (4):997-1002. [View Abstract]
  20. Morgenstern PF, Shah K, Dunkel IJ, Reiner AS, Khakoo Y, Rosenblum MK, et al. Meningioma after radiotherapy for malignancy. J Clin Neurosci. 2016 Aug. 30:93-7. [View Abstract]
  21. Friedman DL, Whitton J, Leisenring W, Mertens AC, Hammond S, Stovall M, et al. Subsequent neoplasms in 5-year survivors of childhood cancer: the Childhood Cancer Survivor Study. J Natl Cancer Inst. 2010 Jul 21. 102 (14):1083-95. [View Abstract]
  22. Taylor AJ, Little MP, Winter DL, Sugden E, Ellison DW, Stiller CA, et al. Population-based risks of CNS tumors in survivors of childhood cancer: the British Childhood Cancer Survivor Study. J Clin Oncol. 2010 Dec 20. 28 (36):5287-93. [View Abstract]
  23. Sadetzki S, Flint-Richter P, Ben-Tal T, Nass D. Radiation-induced meningioma: a descriptive study of 253 cases. J Neurosurg. 2002 Nov. 97 (5):1078-82. [View Abstract]
  24. Longstreth WT Jr, Phillips LE, Drangsholt M, Koepsell TD, Custer BS, Gehrels JA, et al. Dental X-rays and the risk of intracranial meningioma: a population-based case-control study. Cancer. 2004 Mar 1. 100 (5):1026-34. [View Abstract]
  25. CAHAN WG, WOODARD HQ. Sarcoma arising in irradiated bone; report of 11 cases. Cancer. 1948 May. 1 (1):3-29. [View Abstract]
  26. Al-Mefty O, Topsakal C, Pravdenkova S, Sawyer JR, Harrison MJ. Radiation-induced meningiomas: clinical, pathological, cytokinetic, and cytogenetic characteristics. J Neurosurg. 2004 Jun. 100 (6):1002-13. [View Abstract]
  27. Shenoy SN, Munish KG, Raja A. High dose radiation induced meningioma. Br J Neurosurg. 2004 Dec. 18 (6):617-21. [View Abstract]
  28. Godlewski B, Drummond KJ, Kaye AH. Radiation-induced meningiomas after high-dose cranial irradiation. J Clin Neurosci. 2012 Dec. 19 (12):1627-35. [View Abstract]
  29. Choudhary A, Pradhan S, Huda MF, Mohanty S, Kumar M. Radiation induced meningioma with a short latent period following high dose cranial irradiation - case report and literature review. J Neurooncol. 2006 Mar. 77 (1):73-7. [View Abstract]
  30. Boljesíková E, Chorváth M, Hurta P, Steno J, Bízik I. Radiation-induced meningioma with a long latency period: a case report. Pediatr Radiol. 2001 Sep. 31 (9):607-9. [View Abstract]
  31. Pećina-Šlaus N, Kafka A, Lechpammer M. Molecular Genetics of Intracranial Meningiomas with Emphasis on Canonical Wnt Signalling. Cancers (Basel). 2016 Jul 15. 8 (7):[View Abstract]
  32. Mawrin C, Chung C, Preusser M. Biology and clinical management challenges in meningioma. Am Soc Clin Oncol Educ Book. 2015. e106-15. [View Abstract]
  33. Hilton DA, Shivane A, Kirk L, Bassiri K, Enki DG, Hanemann CO. Activation of multiple growth factor signalling pathways is frequent in meningiomas. Neuropathology. 2016 Jun. 36 (3):250-61. [View Abstract]
  34. Benson VS, Kirichek O, Beral V, Green J. Menopausal hormone therapy and central nervous system tumor risk: large UK prospective study and meta-analysis. Int J Cancer. 2015 May 15. 136 (10):2369-77. [View Abstract]
  35. Carroll RS, Zhang J, Black PM. Expression of estrogen receptors alpha and beta in human meningiomas. J Neurooncol. 1999 Apr. 42 (2):109-16. [View Abstract]
  36. Carroll RS, Glowacka D, Dashner K, Black PM. Progesterone receptor expression in meningiomas. Cancer Res. 1993 Mar 15. 53 (6):1312-6. [View Abstract]
  37. Hsu DW, Efird JT, Hedley-Whyte ET. Progesterone and estrogen receptors in meningiomas: prognostic considerations. J Neurosurg. 1997 Jan. 86 (1):113-20. [View Abstract]
  38. Olson JJ, Beck DW, Schlechte JA, Loh PM. Effect of the antiprogesterone RU-38486 on meningioma implanted into nude mice. J Neurosurg. 1987 Apr. 66 (4):584-7. [View Abstract]
  39. Chen J, Chen G. Expression of androgen receptor in meningiomas. J Tongji Med Univ. 2001. 21 (2):140-2. [View Abstract]
  40. Preston-Martin S. Descriptive epidemiology of primary tumors of the brain, cranial nerves and cranial meninges in Los Angeles County. Neuroepidemiology. 1989. 8 (6):283-95. [View Abstract]
  41. Kuan AS, Chen YT, Teng CJ, Wang SJ, Chen MT. Risk of meningioma in patients with head injury: a nationwide population-based study. J Chin Med Assoc. 2014 Sep. 77 (9):457-62. [View Abstract]
  42. Ostrom QT, Gittleman H, Fulop J, Liu M, Blanda R, Kromer C, et al. CBTRUS Statistical Report: Primary Brain and Central Nervous System Tumors Diagnosed in the United States in 2008-2012. Neuro Oncol. 2015 Oct. 17 Suppl 4:iv1-iv62. [View Abstract]
  43. Wiemels J, Wrensch M, Claus EB. Epidemiology and etiology of meningioma. J Neurooncol. 2010 Sep. 99 (3):307-14. [View Abstract]
  44. Mehta N, Bhagwati S, Parulekar G. Meningiomas in children: A study of 18 cases. J Pediatr Neurosci. 2009 Jul. 4 (2):61-5. [View Abstract]
  45. Yue NC, Longstreth WT Jr, Elster AD, Jungreis CA, O'Leary DH, Poirier VC. Clinically serious abnormalities found incidentally at MR imaging of the brain: data from the Cardiovascular Health Study. Radiology. 1997 Jan. 202 (1):41-6. [View Abstract]
  46. Vernooij MW, Ikram MA, Tanghe HL, Vincent AJ, Hofman A, Krestin GP, et al. Incidental findings on brain MRI in the general population. N Engl J Med. 2007 Nov 1. 357 (18):1821-8. [View Abstract]
  47. Linsler S, Keller C, Urbschat S, Ketter R, Oertel J. Prognosis of meningiomas in the early 1970s and today. Clin Neurol Neurosurg. 2016 Oct. 149:98-103. [View Abstract]
  48. da Silva CE, de Freitas PE. Large and giant skull base meningiomas: The role of radical surgical removal. Surg Neurol Int. 2015 Jun 29. 6:113. [View Abstract]
  49. da Silva CE, Peixoto de Freitas PE. Recurrence of Skull Base Meningiomas: The Role of Aggressive Removal in Surgical Treatment. J Neurol Surg B Skull Base. 2016 Jun. 77 (3):219-25. [View Abstract]
  50. Ohaegbulam SC. Geographical neurosurgery. Neurol Res. 1999 Mar. 21 (2):161-70. [View Abstract]
  51. Adegbite AB, Khan MI, Paine KW, Tan LK. The recurrence of intracranial meningiomas after surgical treatment. J Neurosurg. 1983 Jan. 58 (1):51-6. [View Abstract]
  52. SIMPSON D. The recurrence of intracranial meningiomas after surgical treatment. J Neurol Neurosurg Psychiatry. 1957 Feb. 20 (1):22-39. [View Abstract]
  53. Sughrue ME, Kane AJ, Shangari G, Rutkowski MJ, McDermott MW, Berger MS, et al. The relevance of Simpson Grade I and II resection in modern neurosurgical treatment of World Health Organization Grade I meningiomas. J Neurosurg. 2010 Nov. 113 (5):1029-35. [View Abstract]
  54. Nanda A, Bir SC, Maiti TK, Konar SK, Missios S, Guthikonda B. Relevance of Simpson grading system and recurrence-free survival after surgery for World Health Organization Grade I meningioma. J Neurosurg. 2016 Apr 8. 1-11. [View Abstract]
  55. Louis DN, Ohgaki H, Wiestler OD, Cavenee WK, Burger PC, Jouvet A, et al. The 2007 WHO classification of tumours of the central nervous system. Acta Neuropathol. 2007 Aug. 114 (2):97-109. [View Abstract]
  56. Shrivastava RK, Sen C, Costantino PD, Della Rocca R. Sphenoorbital meningiomas: surgical limitations and lessons learned in their long-term management. J Neurosurg. 2005 Sep. 103 (3):491-7. [View Abstract]
  57. Bikmaz K, Mrak R, Al-Mefty O. Management of bone-invasive, hyperostotic sphenoid wing meningiomas. J Neurosurg. 2007 Nov. 107 (5):905-12. [View Abstract]
  58. Talacchi A, De Carlo A, D'Agostino A, Nocini P. Surgical management of ocular symptoms in spheno-orbital meningiomas. Is orbital reconstruction really necessary?. Neurosurg Rev. 2014 Apr. 37 (2):301-9; discussion 309-10. [View Abstract]
  59. Oluigbo CO, Choudhari KA, Flynn P, McConnell RS. Meningioma presenting with transient ischaemic attacks. Br J Neurosurg. 2004 Dec. 18 (6):635-7. [View Abstract]
  60. Rodríguez-Colón G, Bratton EM, Serracino H, Bennett JL, Hink EM. Sphenoid Wing Meningioma with Extraocular Muscle Involvement Mimicking Idiopathic Orbital Inflammation. Ophthal Plast Reconstr Surg. 2016 Feb 12. [View Abstract]
  61. Walia HS, Grumbine FL, Sawhney GK, Risner DS, Palejwala NV, Emanuel ME, et al. An aggressive sphenoid wing meningioma causing foster kennedy syndrome. Case Rep Ophthalmol Med. 2012. 2012:102365. [View Abstract]
  62. Frič R, Hald JK, Antal EA. Benign Sphenoid Wing Meningioma Presenting with an Acute Intracerebral Hemorrhage - A Case Report. J Cent Nerv Syst Dis. 2016 Apr 21. 8:1-4. [View Abstract]
  63. Yang J, Ma SC, Liu YH, Wei L, Zhang CY, Qi JF, et al. Large and giant medial sphenoid wing meningiomas involving vascular structures: clinical features and management experience in 53 patients. Chin Med J (Engl). 2013 Dec. 126 (23):4470-6. [View Abstract]
  64. Narla S, Uppin MS, Saradhi MV, Sahu BP, Purohit AK, Sundaram C. Assessment of expression of epidermal growth factor receptor and p53 in meningiomas. Neurol India. 2014 Jan-Feb. 62 (1):37-41. [View Abstract]
  65. Daffner RH, Yakulis R, Maroon JC. Intraosseous meningioma. Skeletal Radiol. 1998 Feb. 27 (2):108-11. [View Abstract]
  66. Jayaraj K, Martinez S, Freeman A, Lyles KW. Intraosseous meningioma--a mimicry of Paget's disease?. J Bone Miner Res. 2001 Jun. 16 (6):1154-6. [View Abstract]
  67. Agrawal V, Ludwig N, Agrawal A, Bulsara KR. Intraosseous intracranial meningioma. AJNR Am J Neuroradiol. 2007 Feb. 28 (2):314-5. [View Abstract]
  68. Tokgoz N, Oner YA, Kaymaz M, Ucar M, Yilmaz G, Tali TE. Primary intraosseous meningioma: CT and MRI appearance. AJNR Am J Neuroradiol. 2005 Sep. 26 (8):2053-6. [View Abstract]
  69. Rosahl SK, Mirzayan MJ, Samii M. Osteolytic intra-osseous meningiomas: illustrated review. Acta Neurochir (Wien). 2004 Nov. 146 (11):1245-9. [View Abstract]
  70. Changhong L, Naiyin C, Yuehuan G, Lianzhong Z. Primary intraosseous meningiomas of the skull. Clin Radiol. 1997 Jul. 52 (7):546-9. [View Abstract]
  71. Chen TC. Primary Intraosseous Meningioma. Neurosurg Clin N Am. 2016 Apr. 27 (2):189-93. [View Abstract]
  72. Crawford TS, Kleinschmidt-DeMasters BK, Lillehei KO. Primary intraosseous meningioma. Case report. J Neurosurg. 1995 Nov. 83 (5):912-5. [View Abstract]
  73. Chaves H, Bergamo Y, Paz S, Sanchez F, Vazquez S. Sphenoid wing meningioma behavior on 11C-PiB and 18F-FDG PET. Clin Nucl Med. 2015 Jan. 40 (1):e81-2. [View Abstract]
  74. Gay E, Vuillez JP, Palombi O, Brard PY, Bessou P, Passagia JG. Intraoperative and postoperative gamma detection of somatostatin receptors in bone-invasive en plaque meningiomas. Neurosurgery. 2005 Jul. 57 (1 Suppl):107-13; discussion 107-13. [View Abstract]
  75. Backer-Grøndahl T, Moen BH, Torp SH. The histopathological spectrum of human meningiomas. Int J Clin Exp Pathol. 2012. 5 (3):231-42. [View Abstract]
  76. Louis DN, Perry A, Reifenberger G, von Deimling A, Figarella-Branger D, Cavenee WK, et al. The 2016 World Health Organization Classification of Tumors of the Central Nervous System: a summary. Acta Neuropathol. 2016 Jun. 131 (6):803-20. [View Abstract]
  77. Ludwin SK, Rubinstein LJ, Russell DS. Papillary meningioma: a malignant variant of meningioma. Cancer. 1975 Oct. 36 (4):1363-73. [View Abstract]
  78. Winek RR, Scheithauer BW, Wick MR. Meningioma, meningeal hemangiopericytoma (angioblastic meningioma), peripheral hemangiopericytoma, and acoustic schwannoma. A comparative immunohistochemical study. Am J Surg Pathol. 1989 Apr. 13 (4):251-61. [View Abstract]
  79. Chamoun R, Krisht KM, Couldwell WT. Incidental meningiomas. Neurosurg Focus. 2011 Dec. 31 (6):E19. [View Abstract]
  80. Yano S, Kuratsu J, Kumamoto Brain Tumor Research Group. Indications for surgery in patients with asymptomatic meningiomas based on an extensive experience. J Neurosurg. 2006 Oct. 105 (4):538-43. [View Abstract]
  81. Oya S, Kim SH, Sade B, Lee JH. The natural history of intracranial meningiomas. J Neurosurg. 2011 May. 114 (5):1250-6. [View Abstract]
  82. Adlakha A, Rao K, Adlakha H, Perry A, Crotty TB, Scheithauer BW, et al. Meningioma metastatic to the lung. Mayo Clin Proc. 1999 Nov. 74 (11):1129-33. [View Abstract]
  83. Velnar T, Pregelj R, Limbaeck-Stokin C. Brain meningioma invading and destructing the skull bone: replacement of the missing bone in vivo. Radiol Oncol. 2011 Dec. 45 (4):304-9. [View Abstract]
  84. Simas NM, Farias JP. Sphenoid Wing en plaque meningiomas: Surgical results and recurrence rates. Surg Neurol Int. 2013 Jul 9. 4:86. [View Abstract]
  85. DeMonte F, Tabrizi P, Culpepper SA, Suki D, Soparkar CN, Patrinely JR. Ophthalmological outcome after orbital entry during anterior and anterolateral skull base surgery. J Neurosurg. 2002 Oct. 97 (4):851-6. [View Abstract]
  86. Ringel F, Cedzich C, Schramm J. Microsurgical technique and results of a series of 63 spheno-orbital meningiomas. Neurosurgery. 2007 Apr. 60 (4 Suppl 2):214-21; discussion 221-2. [View Abstract]
  87. Saeed P, van Furth WR, Tanck M, Freling N, van der Sprenkel JW, Stalpers LJ, et al. Surgical treatment of sphenoorbital meningiomas. Br J Ophthalmol. 2011 Jul. 95 (7):996-1000. [View Abstract]
  88. Goodwin JW, Crowley J, Eyre HJ, Stafford B, Jaeckle KA, Townsend JJ. A phase II evaluation of tamoxifen in unresectable or refractory meningiomas: a Southwest Oncology Group study. J Neurooncol. 1993 Jan. 15 (1):75-7. [View Abstract]
  89. Cossu G, Levivier M, Daniel RT, Messerer M. The Role of Mifepristone in Meningiomas Management: A Systematic Review of the Literature. Biomed Res Int. 2015. 2015:267831. [View Abstract]
  90. Gurberg J, Bouganim N, Shenouda G, Zeitouni A. A case of recurrent anaplastic meningioma of the skull base with radiologic response to hydroxyurea. J Neurol Surg Rep. 2014 Aug. 75 (1):e52-5. [View Abstract]
  91. Kaley TJ, Wen P, Schiff D, Ligon K, Haidar S, Karimi S, et al. Phase II trial of sunitinib for recurrent and progressive atypical and anaplastic meningioma. Neuro Oncol. 2015 Jan. 17 (1):116-21. [View Abstract]
  92. Kotecha RS, Jacoby P, Cole CH, Gottardo NG. Morbidity in survivors of child and adolescent meningioma. Cancer. 2013 Dec 15. 119 (24):4350-7. [View Abstract]

CT scan brain bone window showing intraosseous meningioma involving left sphenoid wing, lateral orbital, superior orbital fissure, and the anterior part of the middle fossa floor.

MRI brain T2W (left) and T1W Fat-Sat (right) sequences showing involvement of the left sphenoid wing associated with dural thickening and the periorbita. Notice proptosis of the left globe secondary to left orbital wall thickening.

Coronal T1-weighted MRI with gadolinium enhancement of a sphenoid wing meningioma with some degree of encasement of bilateral cavernous sinuses.

T1-weighted MRI with gadolinium (coronal section) of same patient with sphenoid wing meningioma. A better visualization of en plaque growth of the meningioma along the convexity of the cerebral hemisphere on the left side is seen, in addition to better illustration of intracavernous carotid arteries bilaterally and en plaque growth of meningioma inferiorly and laterally around both temporal lobes.

T1-weighted gadolinium enhanced (sagittal section) of same patient with meningioma of the sphenoid wing.

CT scan brain bone window showing intraosseous meningioma involving left sphenoid wing, lateral orbital, superior orbital fissure, and the anterior part of the middle fossa floor.

MRI brain T2W (left) and T1W Fat-Sat (right) sequences showing involvement of the left sphenoid wing associated with dural thickening and the periorbita. Notice proptosis of the left globe secondary to left orbital wall thickening.