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MGH / MEEI Cranial Base Center Sphenoid Meningioma

Medial Sphenoid Wing Meningioma by Robert G. Ojemann, M.D.
Stephen B. Tatter,M.D., Ph.D. , HTML editor

medial sphenoid wing meningioma line drawing
Figure 1: Medial Sphenoid Wing Meningioma

In the last issue of this Newsletter, I discussed tuberculum sellae meningiomas which arise in the midline of the skull base from the region of the tuberculum sellae and planum sphenoidale In this issue we move laterally to discuss medial sphenoid wing meningiomas.

These meningiomas involve the region of the anterior clinoid, adjacent medial sphenoid wing, superior orbital fissure, and cavernous sinus (Fig 1). They may grow into the orbit. As the tumor becomes larger, it may encase the internal carotid and proximal middle and anterior cerebral arteries. The optic nerve may be compressed or be surrounded by tumor. Large tumors put pressure on the frontal and temporal lobes and provoke edema in the adjacent brain tissue resulting in neurologic deficits or seizures.

Magnetic resonance imaging (MRI) outlines the extent of the tumor and shows the relationship to the arterial structures (Fig 2). It is often hard to define the optic nerves and chiasm. Angiography may be needed to determine the extent of encasement of the internal carotid artery and its branches and determines the blood supply to the tumor. Embollization of external carotid artery branches is occasionally indicated prior to operation.

The treatment decisions are often difficult because symptoms may be mild, the natural history is variable with some tumors having a very indolent course, the long-term results of microsurgical radical resections that have been proposed and the newer radiation therapy modalities (single dose radiosurgery or fractionated radiotherapy programs) are unknown.

MRI images
Figure 2: MRI Medial Sphenoid Wing Meningioma
This 57 year old man presented with worsening vision in the right eye and increasing dificulty with recent memory and judgement. On the T1 coronal image (left) with gadolinium enhancement the internal carotid and proxinial middle and anterior cerebral arteries are encased. The T2 axial image (right) shows marked edema in the surrounding brain. An extensive subtotal removal of the tumor was done and he made a good recovery except for residual visual loss in tha right eye.

However, some general guidelines for the treatmeni of these tumors can be outlined. For those with mild or non-progressive symptoms, it may be appropriate to follow the patient with periodic MRI and examination to determine if the lesion is growing and to see whether the symptoms are significantly interfering with the pafient's life. The indications for surgery in younger patients are worsening symptoms and/or growth seen on follow-up scans, and in older patients a large tumor with worsening symptoms. Radiotherapy is used in older patients with small and medium size tumors with worsening symptoms and for regrowth after subtotal or radical subtotal removal.

For most patients, a lateral subfrontal and anterior temporal exposure is used. Internal decompression of the tumor is done staying away from the region of the internal carotid and middle cerebral arteries. Some soft tumors can be more easily removed than very firm, hard tumors. The distal branches of the middle cerebral artery are identified and followed to the tumor capsule to determine if it is feasible to dissect them. In some situations arachnoid planes help in separating the tumor from and around the encased arteries. At some point, the relationship of the optic nerve and chiasm to the tumor is determined.

In my series of 16 patients treated over a 15 year period, there were 12 females and four males ranging in age from 28-79 years with two over 70 years of age. In no patient could I be absolutely sure of a total removal of the tumor because of involvement of important arteries and/or cranial nerves or the extension of the tumor into the cavernous sinus or orbit. However, 15 patients have had a good result. One patient had a postoperative intracerebral hemorrhage two weeks after surgery and has a permanent dysphasia and hemiparesis.

In 10 patients no radiation therapy has been given and on follow-up scan there is no change in their tumor over a period of 2 to 14 years (mean 7.2 yr) after operation. Six patients were given radianon therapy, two immediately after operation and four when there was evidence of recurrence. Two of the patients with recurrence had reoperation and then radiation therapy to the small residual tumor Following radiation therapy, five patients are stable and one has shown slight growth over a follow-up of 2-13 years (mean, 5-6 yr).

REFERENCES
  • Ojemann RG. Management of cranial and spinal meningiomas. Clin Neurosurg 1993; 40: 321-383.
  • Ojemann RG. Surgical management of olfactory groove, suprasellar and medial sphenoid wing meningiomas. In: Schmidek HH, ed. Meningiomas and Their Surgical Management, Philadelphia: WB Saunders Co 1991:242-259.
  • Ojemann RG. Meningiomas: Clinical features and surgical management. In: Wilkins RH, Rengachary SS, eds. Neurosurgery, New York: McGraw-Hill 1985:635-654.
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