Spheno-orbital Meningioma

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Chapter 37 Spheno-Orbital Meningioma

The original description of sphenoid ridge meningiomas by Cushing and Eisenhardt in 1938 defines a global type, which grows outward into the sylvian fissure from its attachment, and an en-plaque type, which has a carpet-like growth pattern and evokes hyperostotic changes in the adjacent bone.1 Since the original description, myriad synonyms have been used in the literature to further describe hyperostosing meningiomas found along the sphenoid ridge, such as pterional tumors en plaque,2 intraosseous meningiomas,3 osteomeningiomas, hyperostosing lesions of the ala magna, hyperostosing meningiomas of the sphenoid wing,4,5 invading meningiomas of the sphenoid wing,6 and spheno-orbital meningiomas (SOMs).7

SOMs may be either globoid or en plaque; may invade the orbit, superior orbital fissure, or cavernous sinus; and may extend into the paranasal sinuses. Hyperostosis can occur regardless of lateralization on the sphenoid wing or invasion into the cavernous sinus.8 Typically, SOMs exhibit hyperostosis of the squamosal temporal bone, greater sphenoid wing, lateral orbital wall and orbital roof, lesser sphenoid wing, anterior clinoid, and middle fossa floor. Structures involved may include the basal foramina, superior orbital fissure, optic canal, and ethmoid and sphenoid sinuses. The hyperostotic bone has been shown to be secondary to tumor invasion in the vast majority of cases.9,10 The intradural component can be either globoid or carpet-like; can be attached to the convexity dura, basal sphenoid, and floor of the middle fossa dura; and can invade the cavernous sinus and superior orbital fissure. An intraorbital tumor can be extra- or intraperiorbital, can be extra- or intraconal, and can invade the orbital apex. Extracranial invasion of the temporalis muscle and the infratemporal fossa can occur.

Early management of these complex, hyperostosing meningiomas was conservative. In Castellano’s early report in 1952, he discloses a mortality rate of 13.3% in 15 patients undergoing surgery for hyperostosing sphenoid wing meningiomas.2 Based on this high perioperative mortality, the discomforts of severe proptosis and even unilateral vision loss were insufficient reasons to warrant surgical intervention.2,11 It was not until the work of Derome12 and others6,13,14 in the 1970s that more complete resections were safely achieved with use of a coronal incision, pericranial grafting, and reconstruction of the anterior skull base with iliac bone or split calvarial bone grafts. Today, with greater understanding of surgical anatomy and the development of advanced skull base techniques,1519 the perioperative mortality has dropped from 20%2,6,11,13 to 0% to 4%.3,7,8,2024 Even so, with efforts to preserve neurologic function,25 residual tumors involving the cavernous sinus, orbital apex, and superior orbital fissure remain problematic surgical limitations. These areas are major sites for residual tumors, recurrence, and continued neurologic deterioration.46,8,2224,26 Adjuvant radiotherapy for residual tumors or recurrence commonly forms part of modern management plans,27 but specific indications remain controversial.22,26,28

The most common presenting symptom of a SOM is by far unilateral eye bulging with the corresponding physical finding of proptosis.2 Hyperostosis of the lateral orbital wall, orbital roof, and intraorbital tumor invasion contribute to proptosis. Other common symptoms include decreased vision, double vision, headache, temporal swelling, facial numbness, and seizures. Correlative neurologic findings include optic atrophy, decreased acuity and deficits of visual field, cranial nerve (CN) paresis, and trigeminal hypesthesia. CN III, IV, and VI paresis is the result of cavernous sinus, superior orbital fissure, or both types of invasion. However, diplopia can also result from rectus muscle compression and restricted movement from orbital invasion by tumor. Facial hypesthesia in the V1 distribution typically indicates superior orbital fissure invasion. Tumor invasion in the cavernous sinus or hyperostotic stricture of the basilar foramina can cause facial hypesthesia in the V2 or V3 distributions. Presenting symptoms and neurologic findings are summarized in Tables 37-1 and 37-2.

Table 37-1 Symptoms in Patients with Hyperostosing SOMs

Symptom Percentage of Patients (mean)
Eye bulging 36-100 (78)2,5,8,10,21,24
Decreased vision 16-60 (32)2,5,8,10,24
Double vision 5-21 (14)5,10,21,24
Headache 8-41 (25)2,5,8,10,24
Mass or swelling 7-61 (27)2,5,21,24
Facial numbness or pain 2-5 (3)5,8,24
Seizures 1-16 (8)2,5,8,21,24

Table 37-2 Findings in Patients with Hyperostosing SOMs

Neurologic Finding Percentage of Patients (mean)
Proptosis 36-100 (79)2,5,8,21,24
Optic atrophy 16-29 (23)2,5
Decreased acuity 24-58 (43)2,5,24
Visual field deficit 10-32 (18)2,5,24
CN paresis 21-33 (26)2,5,24
Temporal swelling 7-61 (27)2,5,21
Trigeminal hypesthesia 3-8 (5)2,5,24

Data from the Central Brain Tumor Registry of the United States reveals that the most frequently reported primary brain tumors are meningiomas, at 33.4%. They are the most common type of tumor from age 35 on and occur more often in females than males, with a 2.2:1 (cbtrus.org). In Castellano’s 1952 report of 608 cases of verified meningiomas,2 18.4% (n = 111) were located along the sphenoid ridge and 2.5% (n = 15) were associated with hyperostosis. Other series report a range of 4% to 9% for hyperostosis associated with sphenoid wing meningiomas.5,29

Presurgical Management

Neurologic Imaging

Neurologic imaging should begin with high-resolution thin section computed tomography (CT) scan of the head and skull base. Assessment of the bony windows identifies the affected hyperostotic bone. Structures commonly involved include the orbital roof and lateral wall, greater and lesser sphenoid wing, anterior clinoid, temporal squamosal bone, body of the sphenoid bone, and lateral wall of the sphenoid and ethmoid sinuses. Brain magnetic resonance imaging (MRI) with gadolinium enhancement gives greater detail of intradural and dural involvement. Fat-suppressed T1 sequences are essential when evaluating intraorbital invasion. Preoperative angiography is typically not necessary. Figure 37-1 demonstrates the variable radiologic presentations found with SOMs.

Operative Techniques

The surgical approach for SOMs is typically frontotemporal with possible modifications to include transzygomatic, orbitozygomatic, and orbital frontal approaches. The initial approach is extradural, which consistently enables access to the orbit and middle fossa for removal of hyperostotic bone and decompression of the optic canal. This also allows coagulation and control of extradural arterial blood supply and minimizes brain retraction during intradural tumor removal.8,19 Accessing of the superior orbital fissure, cavernous sinus, and intraorbital compartment is facilitated by this approach as well. A coronal incision allows harvest of a vascularized pericranial graft for reconstruction purposes. The patient is typically positioned in the supine position. The head is rotated 30 degrees to the contralateral side and fixed. The patient’s surgical position is then registered to the preoperative imaging data sets to allow intraoperative navigation. Preoperative high-resolution CT and MRI with gadolinium and fat suppression are coregistered. CT is utilized to assess intraoperative bone removal, and MRI with gadolinium and fat suppression is utilized to guide intradural and intraorbital tumor removal. An area of the abdomen is prepped for an autologous fat graft. The coronal incision is made, and the anterior branch of the superficial temporalis artery is preserved. Sharp dissection is utilized to elevate the scalp in the immediate subgaleal plane. The scalp is reflected anteriorly, leaving the periosteum and overlaying loose connective tissue layer attached to the calvarium. The posterior edge of the scalp is undermined 2 to 3 cm.

The temporalis fascia is incised 2 cm above the “keyhole” region and continued to the root of the zygoma (Fig. 37-2A

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