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Sections Sphenoid Wing Meningioma
Overview
Presentation
- History
- Physical
- Causes
- Complications
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DDx
Workup
Treatment
Medication
Media Gallery
References

Workup

Laboratory Studies

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

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]}

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.

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MRI

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]

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.

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Angiography

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:

Preoperative evaluation of patients with anterior basal meningiomas, including formal visual field and acuity testing.
Metastatic work-up, such as CT scanning of the chest, abdomen, and pelvis; skeletal survey; radionucleotide scanning; and PET scanning
Intraoperative radiodetection of somatostatin receptors is feasible, especially in bone-invasive meningiomas using gamma probe. ^[74]

Histologic Findings

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

Grade I (benign), with a recurrence rate of 7%-25%, does not meet atypical or malignant meningioma criteria. Despite involvement of the adjacent bony structures, grade I meningiomas do not invade the brain parenchyma. Grade I meningiomas include 9 histological subtypes: meningothelial, fibrous, transitional, psammomatous, angiomatous, macrocystic, secretory, lymphoplasmacyte-rich, and metaplastic.
Grade II (atypical), with a recurrence rate of 29%-52%, includes atypical, clear cell, and chordoid histological subtype or increased mitotic activity (4-19 mitoses per 10 high-powered fields) or brain invasion, or three or more of the following features: increased cellularity, small cells with a high nuclear:cytoplasmic ratio, prominent nucleoli, uninterrupted patternless or sheetlike growth, or foci of spontaneous or geographic necrosis.
Grade III (malignant), with a recurrence rate of 50%-94%, includes anaplastic, papillary, and rhabdoid histological subtypes. Anaplastic meningiomas have 20 or more mitoses per 10 high-powered fields or malignant characteristics resembling carcinoma, sarcoma, or melanoma.

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]

Treatment & Management

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Media Gallery

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.

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Author

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

William T Couldwell, MD, PhD is a member of the following medical societies: American Academy of Neurological Surgery, American Association for the Advancement of Science, American Association of Neurological Surgeons, American College of Surgeons, American Neurological Association, California Association of Neurological Surgeons, California Medical Association, Congress of Neurological Surgeons, International Meningioma Society, Los Angeles Academy of Medicine, Los Angeles County Medical Association, Neurosurgical Society of America, New York Academy of Sciences, New York State Neurosurgical Society, North American Skull Base Society, North Dakota Medical Association, Pituitary Society, Society for Neuro-Oncology, Society of Neurological Surgeons, Utah State Neurosurgical Society, World Academy of Neurological Surgery

Disclosure: Nothing to disclose.

Coauthor(s)

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

Gmaan Ali M Alzhrani , MBBS, MA is a member of the following medical societies: American Academy of Neurological Surgery, Congress of Neurological Surgeons, Saudi Association of Neurological Surgery

Disclosure: Nothing to disclose.

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

Bhupendra C K Patel, MD, FRCS is a member of the following medical societies: American Academy of Ophthalmology, American Society of Ophthalmic Plastic and Reconstructive Surgery, Royal College of Surgeons of England, Royal Society of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

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

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

Chief Editor

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

Hampton Roy, Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Additional Contributors

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

Andrew W Lawton, MD is a member of the following medical societies: American Academy of Ophthalmology, Arkansas Medical Society, Southern Medical Association

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

Sally B Zachariah, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Society of Neuroimaging

Disclosure: Partner received none from none for none.

Acknowledgements

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.