Sphenoid Wing Meningioma Clinical Presentation

Updated: Apr 07, 2023
  • Author: William T Couldwell, MD, PhD; Chief Editor: Hampton Roy, Sr, MD  more...
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The classic triad of sphenoid (spheno-orbital) wing meningioma is proptosis,(86%) which may be painless; visual impairment (78%); and ocular paresis (20%). [62, 63] Headache also is a common manifestation [63]  and sometimes ptosis. Patients may present with retro-orbital pain or a sensation of pressure. Proptosis is often the first presentation. It is gradual and easily detectable on a review of previous photographs.

Slowly growing scalp masses have been reported.

Transient ischemic attack–like presentation has been reported. [66]

Variants of the clinical syndrome include the following:

  • Eye swelling and hearing loss secondary to compression of the eustachian tube [67]
  • Blindness and optic atrophy in 1 eye, sometimes with papilledema of the other eye (Foster Kennedy syndrome) [68]
  • Mental changes
  • Increased intracranial pressure and intracranial hemorrhage secondary to bony hyperostosis and stretching of underlying venous structures [69]


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. [70] Swelling of the sphenoid bone and exophthalmos are common examination findings.

Spheno-orbital meningiomas that present with proptosis will have a “woody proptosis.” On retropulsion, the globe and orbital tissues will be firm, compared with the softer proptosis seen with orbital tumors like hemangiomas, dermoids, etc. The slow, progressive orbital pressure also often presents with chemosis and conjunctivochalasis, often with associated lagophthalmos and symptoms of corneal exposure.



An increased incidence of meningiomas has been reported in patients with neurofibromatosis type II and in those with abnormalities of chromosome 22, as follows [32, 35, 36] :

  • 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 an 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 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. [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. [32, 38, 40]

The beta-receptor beta subtype of PDGF was identified in 100% of meningiomas in 1 study. [36]

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. [36]

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. [36]

Epidermal growth factor has been described in a large percentage of meningiomas in tissue culture. [71]

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. [72]

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.