The management of symptomatic hyperostotic bilateral spheno-orbital meningiomas: patient series

Lauren Harris Department of Neurosurgery, Essex Neuroscience Centre, Queens Hospital, Romford, United Kingdom

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Jarnail S Bal Department of Neurosurgery, Essex Neuroscience Centre, Queens Hospital, Romford, United Kingdom

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Evangelos Drosos Manchester Centre for Clinical Neurosciences, Northern Care Alliance Foundation Trust, Manchester, United Kingdom

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Samir Matloob Department of Neurosurgery, Essex Neuroscience Centre, Queens Hospital, Romford, United Kingdom

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Nicola Y Roberts North West Genomic Laboratory Hub (Manchester), Genomic Diagnostics Laboratory, Manchester Centre for Genomic Medicine, Manchester, United Kingdom

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Charlotte Hammerbeck-Ward Manchester Centre for Clinical Neurosciences, Northern Care Alliance Foundation Trust, Manchester, United Kingdom
Geoffrey Jefferson Brain Research Centre, Manchester, United Kingdom; and

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Omar Pathmanaban Manchester Centre for Clinical Neurosciences, Northern Care Alliance Foundation Trust, Manchester, United Kingdom
Geoffrey Jefferson Brain Research Centre, Manchester, United Kingdom; and

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Gareth Evans Manchester Centre for Genomic Medicine, Manchester Academic Health Science Centre, Division of Evolution Infection and Genomic Medicine, University of Manchester, St Mary’s Hospital, Manchester Universities NHS Foundation Trust, Manchester, United Kingdom

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Andrew T King Manchester Centre for Clinical Neurosciences, Northern Care Alliance Foundation Trust, Manchester, United Kingdom
Geoffrey Jefferson Brain Research Centre, Manchester, United Kingdom; and

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Scott A Rutherford Manchester Centre for Clinical Neurosciences, Northern Care Alliance Foundation Trust, Manchester, United Kingdom
Geoffrey Jefferson Brain Research Centre, Manchester, United Kingdom; and

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Jonathan Pollock Department of Neurosurgery, Essex Neuroscience Centre, Queens Hospital, Romford, United Kingdom

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Alireza Shoakazemi Department of Neurosurgery, Essex Neuroscience Centre, Queens Hospital, Romford, United Kingdom

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BACKGROUND

The occurrence of hyperostotic bilateral spheno-orbital meningiomas (BSOMs) is very rare. Patients present with bilateral symptoms and require bilateral treatment. This series describes 6 patients presenting to 2 UK neurosurgical units and includes a literature review. To the best of the authors’ knowledge, this is the largest series documented.

OBSERVATIONS

This is a retrospective review of patients with BSOMs presenting between 2006 and 2023. Six females, whose mean age was 43 (range: 36–64) years, presented with features of visual disturbance. Bilateral sphen-oorbital meningiomas were identified. All patients underwent bilateral staged resections. The patients had an initial improvement in their symptoms. Extensive genetic testing was performed in 4 patients, with no variants in the NF2, LZTR1, SMARCB1, SMARCE1, and SMARCA4 genes or other variants detected. The mean follow-up was 100.3 (range: 64–186) months. Sixty-seven percent of patients had good long-term visual acuity. The progression rate was 75% and was particularly aggressive in 1 patient. Four patients required radiation therapy, and 2 needed further surgery.

LESSONS

Hyperostotic BSOMs are extensive, challenging tumors causing significant disability. They can recur, with significant patient impact. Multidisciplinary management and indefinite long-term follow-up are essential. The biology of these tumors remains unclear. As molecular testing expands, the understanding of BSOM oncogenesis and potential therapeutic targets is likely to improve.

ABBREVIATIONS

BSOM = bilateral spheno-orbital meningioma; ER = estrogen receptor; MRI = magnetic resonance imaging; PR = progesterone receptor; SOM = spheno-orbital meningioma; USOM = unilateral spheno-orbital meningioma; WHO = World Health Organization

BACKGROUND

The occurrence of hyperostotic bilateral spheno-orbital meningiomas (BSOMs) is very rare. Patients present with bilateral symptoms and require bilateral treatment. This series describes 6 patients presenting to 2 UK neurosurgical units and includes a literature review. To the best of the authors’ knowledge, this is the largest series documented.

OBSERVATIONS

This is a retrospective review of patients with BSOMs presenting between 2006 and 2023. Six females, whose mean age was 43 (range: 36–64) years, presented with features of visual disturbance. Bilateral sphen-oorbital meningiomas were identified. All patients underwent bilateral staged resections. The patients had an initial improvement in their symptoms. Extensive genetic testing was performed in 4 patients, with no variants in the NF2, LZTR1, SMARCB1, SMARCE1, and SMARCA4 genes or other variants detected. The mean follow-up was 100.3 (range: 64–186) months. Sixty-seven percent of patients had good long-term visual acuity. The progression rate was 75% and was particularly aggressive in 1 patient. Four patients required radiation therapy, and 2 needed further surgery.

LESSONS

Hyperostotic BSOMs are extensive, challenging tumors causing significant disability. They can recur, with significant patient impact. Multidisciplinary management and indefinite long-term follow-up are essential. The biology of these tumors remains unclear. As molecular testing expands, the understanding of BSOM oncogenesis and potential therapeutic targets is likely to improve.

ABBREVIATIONS

BSOM = bilateral spheno-orbital meningioma; ER = estrogen receptor; MRI = magnetic resonance imaging; PR = progesterone receptor; SOM = spheno-orbital meningioma; USOM = unilateral spheno-orbital meningioma; WHO = World Health Organization

Spheno-orbital meningiomas (SOMs) are benign tumors that can present incidentally or with proptosis and/or visual impairment. Cosmetic impairment explains their early descriptions, including one of the earliest resections by Durante in 1884.1 Visual symptoms include loss of color vision, deficits of acuity or fields from optic nerve or chiasmal compression, papilledema, diplopia, ptosis, and exophthalmos.2–4

The tumors are usually slow-growing and can involve the lesser wing of the sphenoid, orbital wall, or orbital roof, with extension into the superior orbital fissure, optic canal, and anterior clinoid process.5 They are associated with hyperostosis and intraosseous tumor growth and can have an adjacent soft tissue component.6 The soft tissue component is usually directly adjacent to the bony component. An extracranial soft tissue component may be present beneath the temporalis muscle.6 The soft tissue component may be en plaque or may occur as a sessile intradural meningioma. Extension into the cavernous sinus and the paranasal sinuses is common.

Hyperostosis, with histological tumor invasion of the bone, is one of the hallmarks, the cause of which remains unclear.5,7 Suggested mechanisms include overexpression of osteogenic molecules that influence osteoblast and osteoclast activity.8 The hyperostosis can be extensive.

Descriptions of SOM use the terminology of “sphenoid wing meningioma en plaque,” “pterional meningioma en plaque,” and “pterional-orbital meningioma.”5,9 While unilateral SOM (USOM) represents 9%–18% of all skull base meningiomas, bilateral hyperostotic SOMs (BSOMs) are extremely rare.5,9–11

Assessment requires computed tomography and magnetic resonance imaging (MRI). Typical findings include a ground-glass hyperostotic appearance, with avid contrast enhancement.5 Differential diagnosis includes neurosarcoidosis, osteoma, osteoblastic metastasis, Paget’s disease, hyperostosis frontalis interna, tuberculoma, and fibrous dysplasia.12,13

Management options are similar to those for USOM, with the aim of preventing the deterioration of neurological, visual, and cosmetic symptoms. There is the additional risk of bilateral treatment and complexity in prioritizing which side to treat first. Active clinical and radiological surveillance may be appropriate in asymptomatic cases without visual impairment. Surgery with the aim of maximum resection and preservation of function is the mainstay of treatment. Gross-total resection is often not possible because of the involvement of the cavernous sinus and paranasal sinuses.14,15 Radiotherapy and growth-control measures (e.g., hormone antagonists) are applicable in selected cases.

This case series describes 6 patients presenting to 2 tertiary neurosurgical units within the United Kingdom—Essex Neuroscience Centre, Queen’s Hospital and Salford Royal Hospital—between 2006 and 2023. To the best of our knowledge, this is the largest documented case series.

Study Description

Six female patients with a mean age of 43 (range: 36–64) years presented with features of visual impairment or proptosis to 2 neurosurgical units over a 17-year period. The mean follow-up was 100.3 months (range: 64–186).

A summary of their presentations, managements, and outcomes can be seen in Table 1. In each case, the patient was discussed at a dedicated skull base multidisciplinary team meeting. A pterional craniotomy with an extradural and intradural approach, including orbital decompression and anterior clinoidectomy, as described by Couldwell,16 was used. Reconstruction of the orbit with titanium mesh was utilized in unit 1. Four patients had extensive somatic genetic testing (with next-generation sequencing of >200 genes), with no variants in the NF2, LZTR1, SMARCB1, SMARCE1, and SMARCA4 genes or other variants of clinical relevance detected.

TABLE 1

Summary of 6 cases of BSOM

Case No.Age (yrs),* Sex, UnitPresentationPathologySurgeryOrbital ReconstructionHistology, WHO Grade, Ki-67Genetic Test DoneNonsurgical TreatmentTime to ProgressionFU (mos)Visual OutcomeGOS-E at Last FU
1 37, F, 1Bilat papilledema, rt peripheral FD, CN V1 palsy, rt proptosisBSOMRt pterional, lt pterional (27 mos)YesMeningothelial, G1, 4.1%YesRT (36 mos) 50 Gy/30 FLt 27 mos, rt 36 mos84NAD5–lower moderate disability
2 36, F, 2Rt reduced VA, rt central FD, rt disc atrophy, lt papilledemaBSOM rt > ltRt pterional, lt pterional (6 mos), lt pterional (33 mos)NoMeningothelial, G1, < 5%YesRT (37 mos), 40.5 Gy/28 F, mifepristoneLt 33 mos64Rt: VA 1.3, decreased VF; lt: light perception; RAPD, optic atrophy4–upper severe disability
3 64, F, 1Lt proptosis, lt reduced VA, lt temporal quadrantanopiaLt SOM, later rt SOMLt pterional (21 mos), rt pterional (106 mos)YesTransitional, G1, 3%–5%YesRT (27 mos)Lt 14 mos, rt 86 mos186NAD (dry)3–lower severe disability
4 38, F, 2Rt reduced VA, rt papilledema, rt APD, lt ptosisBSOM lt > rtRt pterional, lt pterional (5 mos)NoLt meningothelial, rt myxoid, G1, < 3%NoLt 58 mos70Rt: VA 0.12, lt: VA 0.02, VF NAD5–lower moderate disability
5 43, F, 2Headache, bilat papilledemaBSOMRt pterional, lt pterional (3 wks)NoMeningothelial, G1, 5%–8%NoLt 19 mos91Lt: blurred vision, rt: NAD, VF NAD7–lower good recovery
6 40, F, 1Lt temporal swellingLt SOM, later rt SOMLt pterional, rt pterional (100 mos)Yes (lt)Lt transitional, rt meningothelial, G1, 2%–4%YesLt RT (30 mos) 50.9 Gy/28 F, rt RT (15 mos), 45 Gy/25 FLt 24 mos, rt 93 mos107Lt: hand movement, rt: NAD7–lower good recovery

BSOM = bilateral hyperostotic spheno-orbital meningioma; CN = cranial nerve; F = fractions; FD = field defect; FU = follow-up; G = grade; GOS-E = Extended Glasgow Coma Outcome Scale; NAD = no abnormality detected; RAPD = relative afferent pupillary defect; RT = radiotherapy; SOM = spheno-orbital meningioma; VA = visual acuity; VF = visual field; WHO = World Health Organization.

Age at presentation.

Includes testing for variants in NF2, LZTR1, SMARCB1, SMARCE1, and SMARCA4 genes and others of clinical relevance; no variants detected.

Case 1

A 37-year-old female presented with bilateral papilledema, worse on the right, with a right-sided peripheral scotoma, proptosis, and abducens nerve palsy. She did not work, lived with her family, was a nondrinker, a smoker, and a nondriver.

Imaging identified BSOMs (Fig. 1). She underwent a right-sided resection, with residual in the cavernous sinus, the pterygopalatine fossa, and the sphenoid sinus. Postoperatively, her symptoms resolved. Histological analysis showed a meningothelial meningioma World Health Organization (WHO) grade 1, Ki-67 4.1%, 75% positive for progesterone receptor (PR), and negative for estrogen receptor (ER). On somatic genetic testing, no variants of clinical relevance were detected.

FIG. 1
FIG. 1

Case 1. Contrast T1-weighted magnetic resonance imaging (MRI) scans. A: Preoperative imaging showing the right spheno-orbital meningioma (SOM) enhancing homogeneously and extending into the right orbit. B: Postoperative scan obtained after a right-sided operation. The extent of excision can be seen on the right side. The growing SOM on the left side is clearly identified compared to the previous scan, with extension into the orbit. C: The most recent scan showing bilateral resection. Reconstruction mesh can be identified on the left side.

On serial imaging, there was progression of the left-sided SOM, with mild proptosis. Twenty-seven months later she underwent a left-sided resection. Histological analysis was the same, with 100% PR.

Imaging at 36 months showed a gradual increase in the right-sided lesion. She underwent fractionated radiotherapy (50 Gy in 30 fractions), with stable imaging at 50 months.

At 84 months, she remained well with no visual deficit and stable residual. She developed premature menopause, attributed to the radiotherapy. She has not resumed work and continues to smoke.

Case 2

A 36-year-old female presented with reduced right-sided visual acuity, a right central visual field deficit, right optic disc atrophy, and left papilledema. She worked as an executive assistant to an investment director, lived with her husband, was a social drinker, a nonsmoker, and a driver.

Imaging demonstrated an extensive right SOM, a large left SOM, a tectal plate–enhancing abnormality, and 2 smaller posterior parasagittal suspected meningiomas (Fig. 2). Right-sided subtotal resection was performed. She had improvement in her right-sided visual acuity (from log of minimum angle of resolution [logMAR] of 0.56 to 0.10) and a reduction in the field deficit. Histological analysis showed a meningothelial meningioma WHO grade 1 and Ki-67 4.1%. Postoperatively, she developed a pulmonary embolism and had focal seizures.

FIG. 2
FIG. 2

Case 2. Preoperative imaging. A: Computed tomography (CT) head scan showing extensive hyperostosis at the skull base. B: Contrast T1-weighted MRI scan showing the soft-tissue component and compression of the optic nerves. C: Contrast T1-weighted MRI scan showing other abnormalities in the pineal and posterior parasagittal regions.

The left SOM was resected 6 months later. She developed a transient left-sided abduction failure. Histological analysis showed a meningothelial meningioma WHO grade 1 and Ki-67 < 5%. On somatic genetic testing, no variants of clinical relevance were detected. Loss of heterozygosity was identified, representing the activating “hits” in the tumor.

On serial imaging, there was significant regrowth in the bony component. Clinically, she had progressive periorbital swelling with a reduction in visual acuity and visual fields bilaterally and congested optic nerve heads. At 33 months, she underwent left-sided revisional surgery, including optic nerve decompression (joint with the maxillofacial team). She had a complete left oculomotor palsy postoperatively, hypoesthesia in the left V2 region, and improved papilledema.

She underwent radiation to the skull base (40.5 Gy in 28 fractions) at 37 months. Immunohistochemistry for PR showed dense positive staining in 100% of cells, so she was started on mifepristone 200 mg daily at 43 months. She started denosumab and zoledronic acid to stabilize the hyperostosis at 48 months.

Her posterior parasagittal meningioma demonstrated serial growth and was treated with linear accelerator (LINAC) Cyberknife (Accuray) stereotactic radiosurgery (25 Gy in 5 fractions) at 44 months.

At 64 months, imaging appeared stable (Supplementary Fig. 1). She has been medically retired because of her visual impairment, and she no longer drives. She remains independent in all activities, with lifestyle modifications, including the use of a walking cane.

Case 3

A 64-year-old female presented with a left-sided, 7-mm proptosis, reduced visual acuity (6/9), and an inferior quadrantanopia. She was retired, lived with her husband, and was a social drinker, a nonsmoker, and a nondriver.

An extensive hyperostotic left-sided SOM was identified (Fig. 3). A left-sided resection was performed, with improvement in the ptosis and quadrantanopia. Residual tumor was left in the cavernous sinus, superior and inferior orbital fissures, pterygopalatine, and infratemporal fossa and extending into the planum.

FIG. 3
FIG. 3

Case 3. Contrast T1-weighted MRI scans. A: Preoperative imaging. The left SOM is identified with involvement of the lateral wall of the orbit, cavernous sinus, optic foramen, and posterior ethmoid region. There is no right-sided lesion. B: Eighty-six-month follow-up scan showing the growing right SOM extending into the superior orbital fissure and cavernous sinus, with an extraosseous soft-tissue component in the lateral orbit and middle fossa. C: Most recent scan showing the bilateral extent of resection.

At 14 months, there was a recurrence of the temporal hemianopia. Tumor recurrence was seen on imaging and required reoperation at 21 months, with postoperative radiotherapy at 27 months (28 fractions). She had no new deficit with a persistent field deficit.

On serial imaging, at 86 months, a progressive right SOM was visible. Mild proptosis was evident. At 102 months, she developed a right-sided abducens nerve palsy. At 106 months, she underwent a right-sided resection. Postoperatively, there was resolution of the abducens palsy and no significant intraorbital residual. Histological analysis showed a WHO grade 1 transitional meningioma, Ki-67 3%–5%. On genetic testing, no variants of relevance were detected.

At the 186-month follow-up, she reported dry eyes with normal vision.

Case 4

A 38-year-old right-handed female presented with right-sided visual deterioration, papilledema, an afferent pupillary defect, with left-sided ptosis. She worked as a youth worker, lived with her son, and was a nondrinker, an ex-smoker, and a driver.

Imaging demonstrated BSOMs (Supplementary Fig. 2). She underwent right-sided resection, and her vision improved postoperatively. Histological analysis showed a WHO grade 1 meningothelial meningioma. Due to the serial growth of the left-sided lesion, she underwent a left pterional craniotomy 5 months later. Histological analysis showed a WHO grade 1 myxoid (metaplastic) meningioma, Ki-67 < 3%. Postoperatively she developed a transient right-sided weakness, expressive dysphasia, and short-term memory loss.

A small residual remains under radiological surveillance at 70 months. This is enlarging on serial imaging, with radiation under consideration. Her vision is intact. She stopped working and continues to drive.

Case 5

A 43-year-old female presented with occipital headaches and an irregular obscuration in her sight. She had bilateral papilledema. She worked as a human resources manager, lived with her husband, was a social drinker, a nonsmoker, and a driver.

Imaging (Supplementary Fig. 3) demonstrated BSOMs, larger on the right. She underwent a right-sided resection, with a small residual in proximity to the internal carotid artery. Histological analysis showed a meningothelial meningioma WHO grade 1, Ki-67 5%–8%. Three weeks later, she had a complete resection of the left SOM. Histology was also a WHO grade 1 meningothelial meningioma. She made a good recovery with no deficit.

A 19 months, MRI suggested a recurrence of the intraosseous and soft tissue component of the left SOM, in close proximity to the optic foramen and superior orbital fissure. Serial imaging suggested a growth rate of 3 mm/year.

Over time, a minor degree of left proptosis has become evident, with no visual deficit. At 91 months, she remains well, under active surveillance. Her vision is blurred in the left eye, and she wears reading glasses. She continues to work and drive and has mild short-term memory loss.

Case 6

A 40-year-old female presented with 9 months of painless swelling of the left temporal region. She had a left vestibular schwannoma resected 5 years previously, with residual facial nerve palsy. She worked as a medical secretary, lived with her family, was a nonsmoker, social drinker, and nondriver.

Imaging (Fig. 4) showed a left SOM, with no obvious right SOM. She underwent a left subtotal resection, with a residual at the middle fossa floor. Histology was consistent with a transitional meningioma, WHO grade 1. On genetic testing, there were no variants of relevance detected.

FIG. 4
FIG. 4

Case 6. Contrast T1-weighted MRI scans with CT. A: Preoperative imaging. The left SOM was identified, involving the lateral sphenoid wing and the roof, floor, and lateral wall of the orbit, with extensive hyperostosis along the lateral orbital wall, orbital roof, and temporal bone. There was a suspicion of dural enhancement along the right greater wing of the sphenoid, but no tumor was confidently identified. B: Postoperative 93-month follow-up scans showing the growing right SOM. Sphenoid and lateral orbital wall hyperostosis can be identified on the right side. Reconstruction material as well as residual hyperostosis can be seen on the left side. C: Most recent scan showing the bilateral extent of resection.

At 24 months, there was a recurrence. This was treated with fractionated radiotherapy, after which she experienced vision deterioration (hand movement perception at 6 months postradiotherapy).

At 93 months, a right SOM was identified, which was resected. Histology revealed a meningothelial meningioma, WHO grade 1. Immunohistochemistry for PR showed positive staining in 100% of tumor cells and negative for ER. Postoperative scanning confirmed near-total excision, and her vision was preserved. MRI at 105 months confirmed progression of the residual, and lower-dose fractionated radiotherapy was administered.

At 107 months, MRI showed stability of the right lesion and only minor progression of the left, with the patient under active surveillance. She has retained her functioning vision in the right eye, and her vision remains stable on the left. She continues working full time.

Discussion

Observations

Bilateral hyperostotic SOMs are extremely rare, with no documented prevalence. We report 6 cases of BSOMs from 2 units, over a 17-year interval. With bilateral disease, patients are at risk of bilateral visual impairment. The previous literature consists of only 3 patients in a series by Luetjens and 3 in Ringel’s cohort of 63.5,17

In this series, 2 cases had different histopathological classifications bilaterally, 2 had evidence of only 1 SOM at presentation, 5 had tumors that were not in continuity on imaging, and the rate of growth (and recurrence) was not equal bilaterally. This suggests that BSOMs are separate entities and are not continuous over the midline with en plaque growth (except perhaps in case 2). It is unclear whether the biological behavior of BSOMs differs from their unilateral counterparts. Because of the scarce literature, information was extrapolated from USOM cases.

While, historically, SOMs have been managed conservatively, there has been a shift toward surgery given the successful improvement in visual symptoms. In a 2021 meta-analysis of 1486 patients, surgery improved visual acuity in 91%, visual fields in 87%, proptosis is 96%, and diplopia and ophthalmoplegia in 96%.2

Radical resection of SOMs remains challenging, with a high risk of complications.18,19 The extent of resection is directly related to the recurrence rate.9,20 Tumor growth along the sphenoid wing, temporal base, cavernous sinus, superior orbital fissure, optic apparatus, and orbit, with extensive dural involvement and extracranial extension, can limit gross-total resection.13–15,21 In 1 case, the disease involved the bone and dura in a continuous area of the whole, bilateral, anterior skull base, completely precluded curative surgical treatment, and mandated additional therapy with radiotherapy and hormonal antagonists.

In BSOMs, the extent of tumor growth precludes surgical treatment of both sides in 1 operation. The need for 2 operations duplicates the discomfort, inconvenience, and risk. The decision about which side to operate on first is made by selecting the most symptomatic side, to optimize visual function. This is regardless of the relative lesion size.

Opinions differ on whether orbit reconstruction is required. Couldwell16 published persuasive evidence against reconstruction, demonstrating the superior improvement in proptosis by omitting this step and the lack of pulsatile enophthalmos.11,13 Arguments in favor include possible reduction in meningocele formation, diplopia from muscle fibrosis, orbital pain, pulsating enophthalmos, and restrictive ptosis.5,22,23 It has been advocated when more than 1 wall is resected.5,24 A variety of techniques and materials for reconstruction have been suggested.2,22,25–27

Postoperative complications are well documented after SOM surgery. There is a risk of thermal injury to nerves. Resulting symptoms may include trigeminal hypesthesia (19%), ptosis (17%), diplopia (17%), ophthalmoplegia (16%) due to cranial nerve or extraocular muscle involvement, impaired frontalis function, pseudomeningocele, and cerebrospinal fluid leak.2,13,14,24,28 In our series, 67% had good visual acuity on long-term follow-up, consistent with the SOM literature.17

Recurrent SOMs are a known challenge to treat, as seen in our series.11 Information on recurrence rates is available from the literature on USOMs. Recurrence rates of 5%–56.2% are reported in USOMs, depending on the extent of resection and length of follow-up.4,9,21,28,29 In our series, the progression rate was 75%, and the aggressive recurrence in 1 patient may suggest that BSOMs behave more aggressively than a USOM. Long-term clinical and radiological surveillance is essential. The relatively young age of patients with SOM, compared with other patients with meningioma, makes recurrence especially important in the long term. While the rate of growth of these tumors is often slow (0.3 cm3/yr), more rapid growth has been reported in younger patients with USOM, with a large initial tumor volume.30

Radiation therapy and stereotactic radiosurgery have been shown to effectively control growth.31 At present, there are no guidelines in SOMs. It has been advocated for residual tumor if it is WHO grade 2 or 3 or after subtotal resection if there is growth or recurrence.28 In 1 series, none of the 42 patients who had received radiation therapy for SOM experienced a recurrence over 4.2 years.32 Some preoperatively plan to use radiotherapy for inoperable locations.19,33 Radiotherapy should ensure a maximum dose of 10 Gy to the optic nerve.34 In our series, 4 patients were treated with radiation, and 1 patient will likely receive it in the future. The extensive meningioma in case 2 was a challenge for radiation target planning.

Lessons

For BSOMs, coincidental SOM tumors of this rarity seem unlikely. The possibility of a genetic or molecular causation is suggested, despite no known mutations being identified. It is well known that patients with NF2-related schwannomatosis with pathogenic variants in the NF2 gene (loss of function in the tumor-suppressor protein schwannomin) develop multiple meningiomas.35 Approximately 60% of sporadic meningiomas display genetic alterations of the NF2 gene on 22q12.2.36–38 They tend to exhibit a mesenchymal phenotype, such as fibrous or transitional, rather than meningothelial histology.36 Two patients had transitional histology but no evidence of NF2 variations.36 It would also be expected that patients with germline pathogenic variants in NF2 would have developed vestibular schwannomas by the age of presentation with BSOMs. In case 6, despite a history of a vestibular schwannoma and 1 SOM demonstrating transitional histopathology, no mutation was identified.

Given the lack of a germline variant in NF2 or identifiable variants, a non-NF2 cause is likely. A number of recurrent genetic alterations in NF2-nonmutated meningiomas have been identified, including TRAF7, KLF4, AKT1, SMO, PIK3CA, and RNA polymerase II subunit A (POLR2A).36 These somatic mutations are usually found in grade 1 meningiomas and mostly do not coexist with NF2 mutations. Meninges of the skull base originate from mesoderm, often meningothelial variants, whereas the meninges of the convexity originate from the neural crest, often fibrous variants.36 This is in keeping with the histology in our series, which was predominantly meningothelial. The NF2 gene alterations are preferentially found in the convexity, and most others are found in the skull base.36 Despite extensive testing, however, no mutations were identified.

There are a number of limitations to this work. It is a 2-center study, and given the rare nature of these lesions, the sample size is small. It is currently unclear whether the biological behavior of these BSOMs is different from other meningiomas or from USOMs. Only 4 of the 6 patients had molecular testing, and no mutations were identified. Because of the length of the follow-up, histological analysis was performed a number of years ago. This means that the DNA methylation status of these tumors is unknown, which is likely to be important in future classifications and outcome predictions.39 The number of genetic alterations is also rapidly expanding with improved genetic sequencing approaches.37 This is likely to help our understanding of meningioma oncogenesis, including BSOMs, and potential therapeutic targets.40

Bilateral hyperostotic SOMs are extremely rare and these 6 patients represent the largest documented case series to date. For the patients, these tumors can be life changing, with a bilateral threat to vision and the need for extensive surgery and indefinite monitoring. These are extensive and technically challenging tumors. While maximal safe resection with the aim to improve visual function is recommended, the extensive bony involvement makes this difficult. This tumor subgroup has the potential to behave in an aggressive manner, despite the lack of atypical histology in this series. Long-term follow-up of these cases will be undertaken to better understand the full clinical implications.

Acknowledgments

Gareth Evans reports support from the National Institute for Health and Care Research (NIHR), Manchester Biomedical Research Center (grant no. IS-BRC-1215-20007; funder ID: 100014653).

Author Contributions

Conception and design: Harris, Bal, Evans, Rutherford, Pollock, Shoakazemi. Acquisition of data: Harris, Bal, Drosos, Hammerbeck-Ward, Evans, King, Pollock, Shoakazemi. Analysis and interpretation of data: Harris, Bal, Roberts, Hammerbeck-Ward, Pathmanaban, Evans. Drafting of the article: Harris, Bal, Drosos, Evans, Shoakazemi. Critically revising the article: Harris, Bal, Matloob, Hammerbeck-Ward, Pathmanaban, Evans, King, Rutherford, Pollock, Shoakazemi. Reviewed submitted version of the manuscript: Harris, Bal, Drosos, Hammerbeck-Ward, Pathmanaban, Evans, King, Rutherford, Pollock, Shoakazemi. Approved the final version of the manuscript on behalf of all authors: Harris. Administrative/technical/material support: Harris, Shoakazemi. Study supervision: Bal, Matloob.

Supplemental Information

Online Only Content

Supplemental material is available with the online version of the article.

Supplementary Figs. 1–3. https://thejns.org/doi/suppl/10.3171/CASE23179.

Previous Presentations

Some of the cases were presented orally at the annual British Skull Base Society Meeting held in Liverpool, United Kingdom, January 25–26, 2018.

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    Saeed P, van Furth WR, Tanck M, et al. Surgical treatment of sphenoorbital meningiomas. Br J Ophthalmol. 2011;95(7):9961000.

  • 4

    Shrivastava RK, Sen C, Costantino PD, Della Rocca R. Sphenoorbital meningiomas: surgical limitations and lessons learned in their long-term management. J Neurosurg. 2005;103(3):491497.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 5

    Luetjens G, Krauss JK, Brandis A, Nakamura M. Bilateral sphenoorbital hyperostotic meningiomas with proptosis and visual impairment: a therapeutic challenge. Report of three patients and review of the literature. Clin Neurol Neurosurg. 2011;113(10):859863.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 6

    Almeida JP, Omay SB, Shetty SR, et al. Transorbital endoscopic eyelid approach for resection of sphenoorbital meningiomas with predominant hyperostosis: report of 2 cases. J Neurosurg. 2018;128(6):18851895.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 7

    Pieper DR, Al-Mefty O, Hanada Y, Buechner D. Hyperostosis associated with meningioma of the cranial base: secondary changes or tumor invasion. Neurosurgery. 1999;44(4):742747.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 8

    Di Cristofori A, Del Bene M, Locatelli M, et al. Meningioma and bone hyperostosis: expression of bone stimulating factors and review of the literature. World Neurosurg. 2018;115:e774e781.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 9

    Alzhrani G, Couldwell W. Bony hyperostosis recurrence after complete resection of sphenoorbital meningioma. Cureus. 2017;9(8):e1540.

  • 10

    Bowers CA, Sorour M, Patel BC, Couldwell WT. Outcomes after surgical treatment of meningioma-associated proptosis. J Neurosurg. 2016;125(3):544550.

  • 11

    Maroon JC, Kennerdell JS, Vidovich DV, Abla A, Sternau L. Recurrent spheno-orbital meningioma. J Neurosurg. 1994;80(2):202208.

  • 12

    Al-Shyal GH, Mohamed MS, Eissa MF. Surgical management of sphenoid ridge meningioma en plaque (spheno-orbital meningioma). Al-Azhar Assiut Med J. 2020;18(3):295.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 13

    Schick U, Bleyen J, Bani A, Hassler W. Management of meningiomas en plaque of the sphenoid wing. J Neurosurg. 2006;104(2):208214.

  • 14

    Oya S, Sade B, Lee JH. Sphenoorbital meningioma: surgical technique and outcome. J Neurosurg. 2011;114(5):12411249.

  • 15

    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;111(5):10691077.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 16

    Couldwell W. Sphenoid wing meningioma treatment & management: surgical care, medical care. Medscape. 2019. Accessed June 12, 2022. https://emedicine.medscape.com/article/1215752-treatment.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 17

    Ringel F, Cedzich C, Schramm J. Microsurgical technique and results of a series of 63 spheno-orbital meningiomas. Neurosurgery. 2007;60(4 suppl 2):214222.

  • 18

    Matsuda M, Akutsu H, Tanaka S, Matsumura A. Combined simultaneous transcranial and endoscopic endonasal resection of sphenoorbital meningioma extending into the sphenoid sinus, pterygopalatine fossa, and infratemporal fossa. Surg Neurol Int. 2017;8(1):185.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 19

    Gonen L, Nov E, Shimony N, Shofty B, Margalit N. Sphenoorbital meningioma: surgical series and design of an intraoperative management algorithm. Neurosurg Rev. 2018;41(1):291301.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 20

    Masalha W, Heiland DH, Steiert C, et al. Progression-free survival, prognostic factors, and surgical outcome of spheno-orbital meningiomas. Front Oncol. 2021;11:672228.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 21

    Dalle Ore CL, Magill ST, Rodriguez Rubio R, et al. Hyperostosing sphenoid wing meningiomas: surgical outcomes and strategy for bone resection and multidisciplinary orbital reconstruction. J Neurosurg. 2020;134(3):711720.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 22

    Pritz MB, Burgett RA. Spheno-orbital reconstruction after meningioma resection. Skull Base. 2009;19(2):163170.

  • 23

    Artru F, Jourdan C, Convert J, et al. An effacement score for basal cisterns to predict ICP level and outcome after closed head injury. Intracranial Press VII. 1989;29(4):273279.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 24

    Honeybul S, Neil-Dwyer G, Lang DA, Evans BT, Ellison DW. Sphenoid wing meningioma en plaque: a clinical review. Acta Neurochir (Wien). 2001;143(8):749758.

  • 25

    Pace ST, Koreen IV, Wilson JA, Yeatts RP. Orbital reconstruction via deformable titanium mesh following spheno-orbital meningioma resection: ophthalmic presentation and outcomes. Ophthal Plast Reconstr Surg. 2020;36(1):8993.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 26

    Bassi M, Antonelli V, Tomassini A, et al. Synchronized “one-step” resection and cranio-orbital reconstruction for spheno-orbital lesions with custom made implant. J Craniofac Surg. 2021;32(5):18701873.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 27

    Chambless LB, Mawn LA, Forbes JA, Thompson RC. Porous polyethylene implant reconstruction of the orbit after resection of spheno-orbital meningiomas: a novel technique. J Craniomaxillofac Surg. 2012;40(1):e28e32.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 28

    Terrier LM, Bernard F, Fournier HD, et al. Spheno-orbital meningiomas surgery: multicenter management study for complex extensive tumors. World Neurosurg. 2018;112:e145e156.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 29

    Sandalcioglu IE, Gasser T, Mohr C, Stolke D, Wiedemayer H. Spheno-orbital meningiomas: interdisciplinary surgical approach, resectability and long-term results. J Craniomaxillofac Surg. 2005;33(4):260266.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 30

    Saeed P, van Furth WR, Tanck M, et al. Natural history of spheno-orbital meningiomas. Acta Neurochir (Wien). 2011;153(2):395402.

  • 31

    Stafford SL, Pollock BE, Foote RL, et al. Meningioma radiosurgery: tumor control, outcomes, and complications among 190 consecutive patients. Neurosurgery. 2001;49(5):10291038.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 32

    Peele KA, Kennerdell JS, Maroon JC, et al. The role of postoperative irradiation in the management of sphenoid wing meningiomas. A preliminary report. Ophthalmology. 1996;103(11):17611767.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 33

    Boari N, Gagliardi F, Spina A, Bailo M, Franzin A, Mortini P. Management of spheno-orbital en plaque meningiomas: clinical outcome in a consecutive series of 40 patients. Br J Neurosurg. 2013;27(1):8490.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 34

    Stafford SL, Pollock BE, Leavitt JA, et al. A study on the radiation tolerance of the optic nerves and chiasm after stereotactic radiosurgery. Int J Radiat Oncol Biol Phys. 2003;55(5):11771181.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 35

    Bachir S, Shah S, Shapiro S, et al. Neurofibromatosis type 2 (NF2) and the implications for vestibular schwannoma and meningioma pathogenesis. Int J Mol Sci. 2021;22(2):112.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 36

    Lee YS, Lee YS. Molecular characteristics of meningiomas. J Pathol Transl Med. 2020;54(1):4563.

  • 37

    Birzu C, Peyre M, Sahm F. Molecular alterations in meningioma: prognostic and therapeutic perspectives. Curr Opin Oncol. 2020;32(6):613622.

  • 38

    Lee S, Karas PJ, Hadley CC, et al. The role of Merlin/NF2 loss in meningioma biology. Cancers (Basel). 2019;11(11):1633.

  • 39

    Maas SLN, Stichel D, Hielscher T, et al. Integrated molecular-morphologic meningioma classification: a multicenter retrospective analysis, retrospectively and prospectively validated. J Clin Oncol. 2021;39(34):38393852.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 40

    Venur VA, Santagata S, Galanis E, Brastianos PK. New molecular targets in meningiomas: the present and the future. Curr Opin Neurol. 2018;31(6):740746.

Supplementary Materials

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  • Expand
  • FIG. 1

    Case 1. Contrast T1-weighted magnetic resonance imaging (MRI) scans. A: Preoperative imaging showing the right spheno-orbital meningioma (SOM) enhancing homogeneously and extending into the right orbit. B: Postoperative scan obtained after a right-sided operation. The extent of excision can be seen on the right side. The growing SOM on the left side is clearly identified compared to the previous scan, with extension into the orbit. C: The most recent scan showing bilateral resection. Reconstruction mesh can be identified on the left side.

  • FIG. 2

    Case 2. Preoperative imaging. A: Computed tomography (CT) head scan showing extensive hyperostosis at the skull base. B: Contrast T1-weighted MRI scan showing the soft-tissue component and compression of the optic nerves. C: Contrast T1-weighted MRI scan showing other abnormalities in the pineal and posterior parasagittal regions.

  • FIG. 3

    Case 3. Contrast T1-weighted MRI scans. A: Preoperative imaging. The left SOM is identified with involvement of the lateral wall of the orbit, cavernous sinus, optic foramen, and posterior ethmoid region. There is no right-sided lesion. B: Eighty-six-month follow-up scan showing the growing right SOM extending into the superior orbital fissure and cavernous sinus, with an extraosseous soft-tissue component in the lateral orbit and middle fossa. C: Most recent scan showing the bilateral extent of resection.

  • FIG. 4

    Case 6. Contrast T1-weighted MRI scans with CT. A: Preoperative imaging. The left SOM was identified, involving the lateral sphenoid wing and the roof, floor, and lateral wall of the orbit, with extensive hyperostosis along the lateral orbital wall, orbital roof, and temporal bone. There was a suspicion of dural enhancement along the right greater wing of the sphenoid, but no tumor was confidently identified. B: Postoperative 93-month follow-up scans showing the growing right SOM. Sphenoid and lateral orbital wall hyperostosis can be identified on the right side. Reconstruction material as well as residual hyperostosis can be seen on the left side. C: Most recent scan showing the bilateral extent of resection.

  • 1

    Durante F. Contribution to endocranial surgery. Lancet. 1887;130(3344):654655.

  • 2

    Fisher FL, Zamanipoor Najafabadi AH, Schoones JW, Genders SW, van Furth WR. Surgery as a safe and effective treatment option for spheno-orbital meningioma: a systematic review and meta-analysis of surgical techniques and outcomes. Acta Ophthalmol. 2021;99(1):2636.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 3

    Saeed P, van Furth WR, Tanck M, et al. Surgical treatment of sphenoorbital meningiomas. Br J Ophthalmol. 2011;95(7):9961000.

  • 4

    Shrivastava RK, Sen C, Costantino PD, Della Rocca R. Sphenoorbital meningiomas: surgical limitations and lessons learned in their long-term management. J Neurosurg. 2005;103(3):491497.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 5

    Luetjens G, Krauss JK, Brandis A, Nakamura M. Bilateral sphenoorbital hyperostotic meningiomas with proptosis and visual impairment: a therapeutic challenge. Report of three patients and review of the literature. Clin Neurol Neurosurg. 2011;113(10):859863.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 6

    Almeida JP, Omay SB, Shetty SR, et al. Transorbital endoscopic eyelid approach for resection of sphenoorbital meningiomas with predominant hyperostosis: report of 2 cases. J Neurosurg. 2018;128(6):18851895.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 7

    Pieper DR, Al-Mefty O, Hanada Y, Buechner D. Hyperostosis associated with meningioma of the cranial base: secondary changes or tumor invasion. Neurosurgery. 1999;44(4):742747.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 8

    Di Cristofori A, Del Bene M, Locatelli M, et al. Meningioma and bone hyperostosis: expression of bone stimulating factors and review of the literature. World Neurosurg. 2018;115:e774e781.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 9

    Alzhrani G, Couldwell W. Bony hyperostosis recurrence after complete resection of sphenoorbital meningioma. Cureus. 2017;9(8):e1540.

  • 10

    Bowers CA, Sorour M, Patel BC, Couldwell WT. Outcomes after surgical treatment of meningioma-associated proptosis. J Neurosurg. 2016;125(3):544550.

  • 11

    Maroon JC, Kennerdell JS, Vidovich DV, Abla A, Sternau L. Recurrent spheno-orbital meningioma. J Neurosurg. 1994;80(2):202208.

  • 12

    Al-Shyal GH, Mohamed MS, Eissa MF. Surgical management of sphenoid ridge meningioma en plaque (spheno-orbital meningioma). Al-Azhar Assiut Med J. 2020;18(3):295.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 13

    Schick U, Bleyen J, Bani A, Hassler W. Management of meningiomas en plaque of the sphenoid wing. J Neurosurg. 2006;104(2):208214.

  • 14

    Oya S, Sade B, Lee JH. Sphenoorbital meningioma: surgical technique and outcome. J Neurosurg. 2011;114(5):12411249.

  • 15

    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;111(5):10691077.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 16

    Couldwell W. Sphenoid wing meningioma treatment & management: surgical care, medical care. Medscape. 2019. Accessed June 12, 2022. https://emedicine.medscape.com/article/1215752-treatment.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 17

    Ringel F, Cedzich C, Schramm J. Microsurgical technique and results of a series of 63 spheno-orbital meningiomas. Neurosurgery. 2007;60(4 suppl 2):214222.

  • 18

    Matsuda M, Akutsu H, Tanaka S, Matsumura A. Combined simultaneous transcranial and endoscopic endonasal resection of sphenoorbital meningioma extending into the sphenoid sinus, pterygopalatine fossa, and infratemporal fossa. Surg Neurol Int. 2017;8(1):185.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 19

    Gonen L, Nov E, Shimony N, Shofty B, Margalit N. Sphenoorbital meningioma: surgical series and design of an intraoperative management algorithm. Neurosurg Rev. 2018;41(1):291301.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 20

    Masalha W, Heiland DH, Steiert C, et al. Progression-free survival, prognostic factors, and surgical outcome of spheno-orbital meningiomas. Front Oncol. 2021;11:672228.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 21

    Dalle Ore CL, Magill ST, Rodriguez Rubio R, et al. Hyperostosing sphenoid wing meningiomas: surgical outcomes and strategy for bone resection and multidisciplinary orbital reconstruction. J Neurosurg. 2020;134(3):711720.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 22

    Pritz MB, Burgett RA. Spheno-orbital reconstruction after meningioma resection. Skull Base. 2009;19(2):163170.

  • 23

    Artru F, Jourdan C, Convert J, et al. An effacement score for basal cisterns to predict ICP level and outcome after closed head injury. Intracranial Press VII. 1989;29(4):273279.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 24

    Honeybul S, Neil-Dwyer G, Lang DA, Evans BT, Ellison DW. Sphenoid wing meningioma en plaque: a clinical review. Acta Neurochir (Wien). 2001;143(8):749758.

  • 25

    Pace ST, Koreen IV, Wilson JA, Yeatts RP. Orbital reconstruction via deformable titanium mesh following spheno-orbital meningioma resection: ophthalmic presentation and outcomes. Ophthal Plast Reconstr Surg. 2020;36(1):8993.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 26

    Bassi M, Antonelli V, Tomassini A, et al. Synchronized “one-step” resection and cranio-orbital reconstruction for spheno-orbital lesions with custom made implant. J Craniofac Surg. 2021;32(5):18701873.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 27

    Chambless LB, Mawn LA, Forbes JA, Thompson RC. Porous polyethylene implant reconstruction of the orbit after resection of spheno-orbital meningiomas: a novel technique. J Craniomaxillofac Surg. 2012;40(1):e28e32.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 28

    Terrier LM, Bernard F, Fournier HD, et al. Spheno-orbital meningiomas surgery: multicenter management study for complex extensive tumors. World Neurosurg. 2018;112:e145e156.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 29

    Sandalcioglu IE, Gasser T, Mohr C, Stolke D, Wiedemayer H. Spheno-orbital meningiomas: interdisciplinary surgical approach, resectability and long-term results. J Craniomaxillofac Surg. 2005;33(4):260266.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 30

    Saeed P, van Furth WR, Tanck M, et al. Natural history of spheno-orbital meningiomas. Acta Neurochir (Wien). 2011;153(2):395402.

  • 31

    Stafford SL, Pollock BE, Foote RL, et al. Meningioma radiosurgery: tumor control, outcomes, and complications among 190 consecutive patients. Neurosurgery. 2001;49(5):10291038.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 32

    Peele KA, Kennerdell JS, Maroon JC, et al. The role of postoperative irradiation in the management of sphenoid wing meningiomas. A preliminary report. Ophthalmology. 1996;103(11):17611767.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 33

    Boari N, Gagliardi F, Spina A, Bailo M, Franzin A, Mortini P. Management of spheno-orbital en plaque meningiomas: clinical outcome in a consecutive series of 40 patients. Br J Neurosurg. 2013;27(1):8490.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 34

    Stafford SL, Pollock BE, Leavitt JA, et al. A study on the radiation tolerance of the optic nerves and chiasm after stereotactic radiosurgery. Int J Radiat Oncol Biol Phys. 2003;55(5):11771181.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 35

    Bachir S, Shah S, Shapiro S, et al. Neurofibromatosis type 2 (NF2) and the implications for vestibular schwannoma and meningioma pathogenesis. Int J Mol Sci. 2021;22(2):112.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 36

    Lee YS, Lee YS. Molecular characteristics of meningiomas. J Pathol Transl Med. 2020;54(1):4563.

  • 37

    Birzu C, Peyre M, Sahm F. Molecular alterations in meningioma: prognostic and therapeutic perspectives. Curr Opin Oncol. 2020;32(6):613622.

  • 38

    Lee S, Karas PJ, Hadley CC, et al. The role of Merlin/NF2 loss in meningioma biology. Cancers (Basel). 2019;11(11):1633.

  • 39

    Maas SLN, Stichel D, Hielscher T, et al. Integrated molecular-morphologic meningioma classification: a multicenter retrospective analysis, retrospectively and prospectively validated. J Clin Oncol. 2021;39(34):38393852.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 40

    Venur VA, Santagata S, Galanis E, Brastianos PK. New molecular targets in meningiomas: the present and the future. Curr Opin Neurol. 2018;31(6):740746.

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