24 Clinoidal Meningiomas
Introduction
Clinoidal meningiomas are best described as meningiomas arising in the vicinity of the anterior clinoid process. The typical clinoidal meningioma seen on magnetic resonance imaging (MRI) looks as if it were mushrooming out from the anterior clinoid process ( Fig. 24.1 ). Some, however, may grow into the region of the mesial sphenoid wing and be confused with medial sphenoid wing meningiomas ( Fig. 24.2 ). When clinoidal meningiomas grow to a very large size they can involve the parasellar region in its anteroposterior and mediolateral extensions. In this case the tumor may extend laterally into the cavernous sinus or posteriorly into the region of the posterior clinoid and the petroclival region ( Fig. 24.3 ).
Anatomical Considerations
The anterior clinoid process is a complex anatomical entity that has several neurovascular structures passing in its immediate vicinity.1 The oculomotor nerve course is along the superolateral aspect of the anterior clinoid process. The internal carotid artery crosses the inferior aspect of the anterior clinoid process, and the optic nerve passes along its superomedial aspect ( Fig. 24.4 ). Based on surgical findings and observations regarding the site of origin ( Fig. 24.5 ) and the adhesiveness of the tumor to the internal carotid artery and its branches, Al-Mefty suggested that clinoidal meningiomas be classified into three different types.2 Type I clinoidal meningiomas are thought to arise from the subclinoidal dura at the most proximal point of intradural entry of the internal carotid artery, just before the carotid enters into the arachnoidal cisternal space. As a result, Al-Mefty suggested that these tumors are extraarachnoidal and because of this tend to become more adherent to the internal carotid artery and much more difficult to remove surgically. These are the tumors that have a higher rate of subtotal resection and recurrence.
Type II clinoidal meningiomas are thought to originate from the superolateral aspect of the anterior clinoid process. When these tumors grow, they are invested by the arachnoid layers around the carotid cistern. As a result, the tumor is separated from the internal carotid wall by arachnoidal layers that prevent the significant adherence of the tumor to the adventitia of the internal carotid artery wall. This makes the tumors easier to dissect off the wall of the internal carotid artery; as a result, a more complete resection is achievable. Al-Mefty also makes the observation that the growth of type I and II clinoidal meningiomas starts at a distance from the optic nerve; as a result, the arachnoid membranes of the chiasmatic cistern invest the optic nerve and help protect it from immediate invasion by the tumor.
Type III clinoidal meningiomas originate from the region of the optic foramen and extend into the optic canal. Because of the pattern of their growth within the region of the optic canal, these tumors become symptomatic at an early stage and are diagnosed earlier before they achieve a large size, unlike types I and II.
Clinical Presentation
The most common clinical presentation of clinoidal meningiomas consists of visual disturbances and headaches.2–14 Other clinical symptoms usually correlate with the size of the tumor and its extension. Tumors that achieve a large size with more lateral extension result in symptoms due to compression of the parasellar structures. Extension of the tumor into the cavernous sinus region may result in associated cranial neuropathies.15–20 Occasionally some of the tumors extend to the middle temporal fossa and may enlarge posteriorly to compress the temporal lobe, resulting in seizures, or may even compress the brain stem, resulting in hemiparesis. Some patients with associated significant hyperostosis of the sphenoid wing may present with proptosis and orbital pain.
As with all meningiomas, clinoidal meningiomas are more common in females. However, the ratio of females to males is larger in clinoidal meningiomas compared with other meningiomas.
Radiological Evaluation
Traditionally, a computed tomographic (CT) scan of the head with evidence of hyperostosis involving the anterior clinoid process was strongly suggestive of a clinoidal meningioma ( Fig. 24.6 ). Nowadays clinoidal meningiomas are best evaluated with an MRI scan of the brain ( Fig. 24.7 ). Thin-cut MRI with fat suppression through the optic canal can help identify the presence of tumor extension into the orbit. Four-vessel cerebral angiography was also typically part of the workup of patients with clinoidal meningiomas ( Fig. 24.8 ). Today, magnetic resonance angiography (MRA), or in some cases CT angiography, is as informative and provides the needed information about the relationship of the tumor to the supraclinoid internal carotid artery and its branches. However, in recurrent cases or in patients who have had previous radiation, four-vessel cerebral angiography with balloon test occlusion may be necessary to have a plan in place in case of injury to the carotid artery.
Treatment
Surgery remains the most effective treatment modality for clinoidal meningiomas. This is true even for small lesions that may be considered for radiosurgery in other locations, because of their proximity to the optic apparatus and the higher possibility of radiation injury.
Surgery on clinoidal meninigomas demands a full understanding of the bony as well as the neurovascular anatomy of the sellar and parasellar region. A full understanding of the three-dimensional aspect of the anterior clinoid process and the adjacent neurovascular structures is of utmost importance. In addition, the knowledge of the vascular anatomy and potential normal anatomical variations is essential for a safe resection of these tumors.
Surgical Steps
Removal of clinoidal meningioma is best achieved with a wide frontoorbital craniotomy. Other names used for this craniotomy are extended pterional approach or extended pretemporal approach. In addition the craniotomy should include a very low threshold to include the orbital roof in the craniotomy flap (cranioorbitozygomatic approach) to be able to access the suprasellar extension of these tumors without the need of excessive frontal lobe retraction. In the overall majority of our cases, we are able to avoid or minimize the use of self-retaining retractors.
Once the craniotomy is established, we proceed with the extradural work that leads to the removal of the anterior clinoid process. The steps include dissection of the pretemporal and subfrontal dura away from the sphenoid wing, which will be removed with the posterior roof of the orbit. Then the dural fold at the level of the meningioorbital artery is cut to allow disconnection of the dura propria of the temporal lobe from its attachment to the frontal dura across the sphenoid wing over anterior clinoid process. This will bring the anterior clinoid process to a more superficial point. This process of exposing the anterior clinoid process in and of itself leads to significant devascularization of the tumor, which gets its blood supply from anterior dural branches of the middle meningeal artery as well as the meningioorbital artery. It also gets blood supply from posterior ethmoidal branches, which normally provide blood supply to the clinoidal and frontal fossa dura. In addition to tumor devascularization, this extradural work will help expose the clinoidal internal carotid artery segment. The exposure of the clinoidal internal carotid artery and later exposure of the sylvian fissure arterial branches will provide the two normal ends of the vascular tree, which can then be dissected proximally and distally as the tumor is being resected. This provides a good road map for the course of the internal carotid artery as it merges with the middle cerebral artery and anterior cerebral artery at the level of the carotid bifurcation.
Once the extradural work is done, the intradural exposure is performed by opening the dura and visualizing the suprasellar and posterior borders of the tumor. The sylvian fissure is routinely opened from the level of the limen insulae toward its proximal point to help visualize the whole course of the middle cerebral artery. Once this is achieved, debulking of the tumor is started with intermittent dissection of the tumor away from the adjacent brain and blood vessels. Once adequate debulking is achieved and the course of the different arterial branches is visualized, final tumor removal is performed. The dura at the base of the skull and over the clinoid region is totally removed. The underlying bone, which has partially been removed during the extradural removal of the anterior clinoid process, is further drilled and resected with a high-speed diamond drill and copious irrigation aiming at as complete a resection as possible and at the same time achieving bone hemostasis.
As part of the process of removing the anterior clinoid, the optic canal is decompressed by removing the optic strut and the optic roof. The dural layer over the optic canal is opened along the optic nerve. This allows access to tumor extending into the optic canal. Even though this is more common in type III tumors, we perform this step in all tumor types. The tumor is followed along its extension into the orbit. Extra caution is taken while dissecting the optic nerve to preserve the very small blood vessels providing blood supply to the optic canal from the superior hypophyseal branches. It is also important to pay attention to the fact that occasionally direct arterial supply from the ophthalmic artery close to its origin may inadvertently be injured. This can best be avoided by careful dissection with magnification and with the anatomical knowledge of those vessels.
In tumors that extend further laterally, the dissection of the temporal dura away from the lateral wall of the cavernous sinus may be extended to a more posterior point to remove tumor extending into the region of the cavernous sinus. In tumors with extensions toward the suprasellar and subchiasmatic regions, it is important that the dural ring around the internal carotid artery be dissected to widen the space between the internal carotid artery and the optic nerve to gain access to the tumor segments extending into the subchiasmatic and possibly retrochiasmatic region. Occasionally these tumors extend more posteriorly along the tentorial edge and compress the third nerve inferiorly. The third nerve can be identified extradurally at the level of the superior orbital fissure and followed from its extradural to its intradural segments under full visualization to mobilize and avoid its injury during tumor resection.
Gross total resection should always be the goal of surgery ( Fig. 24.9 ). However, in type I tumors where there is no arachnoid layer to separate the tumor from the wall of the internal carotid and its branches, good judgment is exercised to decide the extent of tumor resection to avoid injury to adherent vessels and to avoid additional morbidity ( Fig. 24.10 ).
Once the appropriate degree of resection is achieved, the reconstruction of the skull base is carefully attended to. The dural defect is reconstructed with dural replacement materials. In our experience, the best tissue to be used is either fascia lata or pericranium. This is reinforced with subcutaneous fat harvested from an abdominal incision to be used for obliteration of the clinoidal space, especially if there is communication with the sphenoid sinus. The closure is reinforced with fibrin glue. We avoid the use of lumbar drains because adequate closure rarely leads to a spinal fluid leakage.