eMedicine Specialties > Ophthalmology > Neurologic Disorders

Meningioma, Sphenoid Wing

Author: Sally B Zachariah, MD, Associate Professor, Department of Neurology, University of South Florida; Director, Department of Neurology, Division of Strokes, Veteran Affairs Medical Center of Bay Pines
Coauthor(s): Suzan Khoromi, MD, Fellow, Pain and Neurosensory Mechanisms Branch, National Institute of Dental and Cranial Research, National Institutes of Health
Contributor Information and Disclosures

Updated: Jan 27, 2010

Introduction

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).


Coronal T1-weighted MRI with gadolinium enhanceme...

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

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Coronal T1-weighted MRI with gadolinium enhanceme...

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.

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

  • Among Caucasians, 75% of meningiomas occur in women, and 25% occur in men.
  • Africans show an equal gender ratio.
  • In one series of 517 patients with meningiomas at Brigham and Women's Hospital, the female-to-male ratio was 24:1.

Age

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

Clinical

History

  • Common symptoms include slowly developing unilateral exophthalmos and slight bulging of the bone in the temporal region.
  • Diffuse tumor infiltration of the orbital area may result in painless proptosis.
  • Transient ischemic attack-like presentation has been reported.
  • Variants of the clinical syndrome include the following:
    • Anosmia
    • Oculomotor palsy
    • Painful ophthalmoplegia (Tolosa-Hunt syndrome)
    • Blindness and optic atrophy in 1 eye, sometimes with papilledema of the other eye (Foster Kennedy syndrome)
    • Mental changes
    • Increased intracranial pressure

Physical

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

Causes

  • 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.
  • An increased incidence of meningiomas has been reported in patients with neurofibromatosis type II, and increased incidence of meningiomas has been reported in patients with abnormalities of chromosome 22.
    • Deletions on chromosome 22 have been demonstrated in 40% of meningiomas. These deletions seem to be associated mainly with the terminal portions of the long arm of chromosome 22.
    • Loss of heterozygosity has been reported in at least 1 locus of chromosome 22 in 60-65% of patients with benign meningiomas. The incidence of abnormality on chromosome 22 increases in atypical and malignant meningiomas. The possible culprit may be a 664-kb gene on this locus coding for an N -acetylglucosaminyltransferase gene. This gene codes for an amino acid glycosyl transferase enzyme, and absence of this enzyme may lead to abnormal glycosylation of proteins and lipids, resulting in tumor formation.
    • Other chromosomal abnormalities have been reported in association with the following: chromosome arms 1p, 7p, 14p, 18q, and 6q, and chromosome 10.
  • Various viruses that have been described in association with primary brain tumors, including SV-40, adenovirus, and papovavirus, have been identified in meningiomas.
  • 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.
  • The beta-receptor beta subtype of PDGF has been identified in 100% of meningiomas in one study.
  • 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.
  • 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.
  • Epidermal growth factor has been described in nearly 100% of meningiomas in tissue culture.

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References
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Keywords

sphenoid wing meningioma, brain tumor, intracranial meningioma, meningeal neoplasm, nerve tissue neoplasm, vascular tissue neoplasm

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Contributor Information and Disclosures

Author

Sally B Zachariah, MD, Associate Professor, Department of Neurology, University of South Florida; 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, and American Society of Neuroimaging
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
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.

Medical Editor

Andrew W Lawton, MD, Medical Director of Neuro-Ophthalmology Service, Section of Ophthalmology, Baptist Eye Center, Baptist Health Medical Center
Andrew W Lawton, MD is a member of the following medical societies: American Academy of Ophthalmology, Arkansas Medical Society, and Southern Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

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.

CME Editor

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
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

 
 
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