Despite the fact that spheno-orbital meningiomas (SOM) with hyperostosis represent only 2‑9% of meningiomas, they still form a challenge to the neurosurgeon to achieve total resection [4,5,6]. Although the soft tissue component of the tumor is usually small, the hyperostotic bone with extension into the orbit, potential cavernous sinus invasion, and extension into infra-temporal region all pose a challenge to total resection [7, 8].
The challenge mainly lies in the fact that the aim of surgery is not only the total resection of the intracranial tumor soft tissue but also the resection of hyperostotic bone that has meningioma cells in its Haversian canals, which are an important site for recurrence. Another important aim is to improve the proptosis and/or visual symptoms that the patients present with. In some cases, resection of the meningioma is not sufficient to achieve this, as the hyperostotic bone is often the cause of the visual involvement. Typically, this occurs in cases with hyperostosis of the anterior clinoid and narrowing of the optic foramen and/or optic canal. In those cases, with hyperostosis of the lateral orbital wall with or without tumor soft tissue extension into the orbit, proptosis is the main clinical manifestation [7, 8].
There are several surgical approaches described for resection of SOM [11,12,13,14]. After using the mini OZ approach (modified OZ) in two cases, we did not see any added benefit from the osteotomy in the orbital rim. Although it does increase the vertical angle, in cases with spheno-orbital meningioma, this is not deemed necessary as the soft tissue component was superficial and small and the excision of the intraorbital part can be achieved without an osteotomy of the orbital rim. Also, drilling of the orbital roof and lateral orbital wall just behind the orbital rim achieves adequate decompression of the periorbita and gives access to the intraorbital soft tissue located lateral and superior to the globe and could be done without removing the orbital rim.
In all patients with visual symptoms and in selected cases where the tumor was extensive and where near-total resection was achieved; optic nerve decompression was done. This was achieved through drilling the roof and lateral walls of the optic canal.
The extent of resection of spheno-orbital meningiomas is variable. In the series of Mirone and Schick and colleagues, the gross total resection was as high as 60‑82%. In other series such as those described by Jaaskelainen and colleagues; gross total resection was achieved in only 50% of cases with hyperostosis, and in 15% of patients with extension into the orbit [5, 23, 24].
In some series, the goal of surgery was the relief of symptoms rather than the gross total resection of the tumor. This was true with Ringel and colleagues, where total resection was achieved in 24% of their patients, with 60% of the sub-totally resected tumors remaining stationary [25].
In our series, described above, we were able to achieve total resection in 47.4% of cases, subtotal resection in 21.1% of cases, and partial resection in 26.3% of cases. The main factor limiting gross total resection was the soft tissue extension into the cavernous sinus, adherence of tumor tissue to the orbital musculature, and infratemporal extension of the hyperostotic bone into the pterygoid plates.
There is still no consensus within the neurosurgical community regarding the reconstruction of the drilled superior and lateral orbital walls after surgical resection of the tumor. Some authors believe it is necessary to perform reconstruction to decrease the occurrence of pulsatile exophthalmos. On the other hand, there is a belief that as long as the orbital floor and orbital margins are not drilled off, there is no need for such reconstruction [23, 26]. As far as our series go, we opted not to perform any reconstruction to the orbital roof or lateral wall. Our bone reconstruction was limited to the fronto-temporal region. Bone reconstruction of the drilled off hyperostotic diseased bone was done in 8 cases (36.36%). None of our patients developed postoperative enophthalmos.
Postoperative complications following resection of SOMs are numerous, including worsening of vision, hemiplegia, ophthalmoplegia, facial numbness, hematomas, and injury to the trigeminal [27, 28]. Two of our patients developed a postoperative CSF leak, one of which was managed conservatively while the other patient developed late postoperative hydrocephalus that required management with a ventriculo-peritoneal shunt. Three patients in our series suffered an injury to the trigeminal nerve manifesting as hypoesthesia of V1 distribution. All of the cases were, however, temporary and had fully recovered by 3 months postoperatively. One patient had temporary ophthalmoplegia that recovered over 2 months.
The reported mortality after resection of SOMs was around 6% with Jaaskelainen and colleagues [24]. The main cause of mortality reported in the literature results from a vascular insult. We had 2 mortalities (9%), with one patient suffering an ICA injury intraoperatively leading to their death 2 weeks postoperatively, the other patient died of a pulmonary embolism in the postoperative period.
The role of irradiation for skull base lesions, especially those with associated hyperostosis, is debatable [19,20,21]. At our center, patients are only referred for radiosurgery treatment when there is tumor left in the cavernous sinus. In general patients with WHO grades II or III meningiomas are also possible candidates for radiosurgery. In all cases where total resection was achieved, including the hyperostotic bone, follow up was done every 3 months for 1 year then yearly afterward. In those patients with residual hyperostotic bone, we chose to follow them up rather than offering them adjuvant radiotherapy.