Sphenoid Wing Meningioma

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Background

In 1614, Felix Plater first described meningiomas at an autopsy. In 1938, Harvey Cushing introduced them as a separate category of extraparenchymal tumors.[1] Meningiomas are believed to arise from arachnoid cap cells, and they usually are attached to the dura. These tumors may arise from any location where meninges exist (eg, nasal cavity, paranasal sinuses, middle ear, mediastinum). See the image below.


View Image

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

Meningiomas of the anterior skull base constitute 40% of all intracranial meningiomas. Of these, about one half occur in the sphenoid wing, and one half occur in the tuberculum sella or the olfactory groove. Anterior clinoid (medial sphenoid wing) meningiomas are a subcategory of the sphenoid wing meningiomas; they fall into 1 of 3 categories, according to the presence of an interfacing arachnoidal membrane between the tumor and the cerebral vessels. Meningiomas of the tuberculum sella arise from the tuberculum sella, chiasmatic sulcus, limbus sphenoidale, and diaphragma sella; they may extend into both optic canals. Olfactory groove meningiomas arise more anteriorly than the tuberculum sella meningiomas, and they may be symmetrical around the midline or extend to the side. Of these, about 15% grow into the ethmoid sinuses.

The relative incidence of meningiomas of the sphenoid ridge is 17%. This tumor usually arises from the lesser wing of the sphenoid bone. Sphenoid wing meningiomas, or ridge meningiomas, are the most common of the basal meningiomas. These meningiomas may be associated with hyperostosis of the sphenoid ridge and may be very invasive, spreading to the dura of the frontal, temporal, orbital, and sphenoidal regions. Medially, this tumor may expand into the wall of the cavernous sinus, anteriorly into the orbit, and laterally into the temporal bone.

Pathophysiology

Meningiomas account for approximately 13-19% of all brain tumors. A common etiology for meningiomas is radiation exposure in the range of 132-315 roentgens, which is equivalent to rad dose of 1-3 Gy. Characteristics of radiation-induced meningiomas include an average latent period of 36-38 years for patients who were exposed to low-dose radiation to the head, whereas patients who develop meningiomas after exposure to high-dose radiation may show signs as early as 5 years postradiation.

In general, radiation-induced meningiomas occur more frequently over the convexities; in about 80% of cases, they have a more frequent recurrence rate and exhibit malignant behavior, as indicated histologically by hypercellularity and pleomorphism.

Head trauma used to be considered a possible risk factor, but recent large studies do not support this association. Other factors that have been studied include hereditary predisposition. Loss of DNA on chromosome 22 has been shown in 40% of meningiomas, and, in cytogenetic studies, genetic abnormalities at the level of chromosome 22 are seen frequently in meningiomas with loss of a copy of chromosome 22 as the most commonly reported abnormality. Monosomy of chromosome 22 has been reported to occur in 70-80% of meningiomas. Abnormalities of chromosome 22 have been associated with type II neurofibromatosis.

Hormonal factors (eg, estrogen, progesterone) have been studied extensively as risk factors for meningiomas because of the striking predominance of meningiomas in women. Other evidence to substantiate the implication of gender-specific hormones comes from data showing increased growth of meningiomas during pregnancy and size changes with menses. Initially, interest was focused on estrogen because it had been found in one series that 30% of meningiomas have estrogen receptors. However, no further studies were conducted, and interest became focused on other hormones (ie, progesterone).

The progesterone receptor is the best candidate as an etiology for meningiomas. Progesterone receptors have been shown to be expressed in 81% of women and in 40% of men with meningiomas. Other studies indicate that progesterone binds to meningiomas in 50-100% of tested specimens; however, most reports show binding in the higher end of this range. No relation has been found between progesterone receptor status and age, sex, location of tumor, or menopausal state. 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.

Androgen receptors have been found in 40-100% of meningiomas studied, but their receptor expression is variable, making them less likely candidates in the pathophysiology of meningiomas. Meningiomas vary in expression of receptors for other hormones (eg, epidermal growth factor [EGF], platelet derived growth factor [PDGF], fibroblast growth factor), which makes 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. Infectious agents that have been associated with meningiomas include simian vacuolating virus 40 (SV-40) and adenovirus.

Epidemiology

Frequency

United States

Meningiomas account for approximately 13-19% of all brain tumors.

International

Same as in the United States.

Mortality/Morbidity

In one series, the overall survival rate for all patients at 5 was 87% and 58% at 10 years. For atypical meningiomas, the 5-year survival rate was 87% and the 10-year survival rate was 58%; for malignant meningiomas, the survival rate was 60% at 5 years and 60% at 10 years. All patients in this series had received surgery and high-dose radiation. No difference in survival of patients as a function of dural or cortical invasion was apparent. Long-term survival is possible for patients with atypical and malignant meningiomas treated with surgery and postoperative radiation.

Race

Variability has been shown in the prevalence of meningiomas among Caucasians, Africans, African Americans, and Asians. A greater incidence exists among Africans than among Caucasians.

Sex

Age

Average age of onset is 50 years. Incidence of meningiomas increases steadily thereafter.

History

Physical

Sphenoid wing meningiomas can be associated with various cranial nerve dysfunction resulting from foraminal encroachment of cranial nerves located at the skull base.[3] Rarely, a bruit can be heard over a highly vascular tumor.

Causes

Laboratory Studies

Imaging Studies

Other Tests

Histologic Findings

Historically, classification of meningiomas has been based upon cell shapes, cell patterns, and cell products. The macroscopic appearance of meningiomas may be hemispheric, bun shaped, or globular, and they may vary in gross appearance as epithelial or mesenchymal. They usually are attached to the dura and invaginate into adjacent neural structures. Enveloped in a thin capsule derived from the adjacent meninges, they remain extraaxial and are separated easily from the brain or spinal cord.

According to the World Health Organization (WHO) in 1993, 3 types of meningiomas exist based on malignant behavior, as follows:

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 increased incidence of late distant metastasis. The papillary type is considered malignant by definition and is encountered more frequently in children.

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.

Meningiomas are generally slow growing. Their annual growth rate can be anywhere from 1-21%. True metastases are extremely uncommon, and dissemination usually is believed to occur hematogenously, with the lungs as the most common site. Bony invasion is not evidence of malignancy in meningiomas, and invasion of mesenchymal components (eg, bone, muscle, dura) can occur with benign meningiomas.

Growth type classification of meningiomas according to cell type is as follows:

Surgical Care

Medication Summary

Anecdotal reports exist in the literature regarding the usage of antihormonal agents in the treatment of meningiomas. Medical treatment is reserved for the following: atypical and malignant meningiomas as an adjunct to surgery, partially resected benign meningiomas, and recurrence of meningiomas after a surgical resection.

Tamoxifen, an antiestrogen hormone, has been reported in a handful of patients with refractory or unresectable meningiomas; in one study, usage of this agent resulted in stabilization of 6 out of 9 cases.

Tamoxifen (Nolvadex)

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 (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.

Complications

Prognosis

Author

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: none None None

Coauthor(s)

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

Disclosure: Nothing to disclose.

Specialty Editors

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

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri

Disclosure: Nothing to disclose.

Chief Editor

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

Disclosure: Nothing to disclose.

Additional Contributors

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.

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

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.