Cavernous Sinus Meningioma
Meningiomas involving the cavernous sinus can originate from within the sinus or more typically invade the venous sinus secondarily from other points of origin. These secondary tumors commonly originate from the petrous temporal bone, clivus, clinoid processes, or the lesser wing of the sphenoid.
Meningiomas of the cavernous sinus make up a very small percentage of all cranial meningiomas, but their location within the cavernous sinus makes their surgical resection most challenging. Controversy exists regarding whether surgical intervention for these lesions should even be attempted. This is partially because there is some degree of unfamiliarity with intracavernous surgery and its possibilities.
Historically, the cavernous sinus has been considered a surgical “no man's land” because dissection within its confines often resulted in neurologic morbidity from injury to multiple cranial nerves (CNs), the cavernous internal carotid artery (ICA) or its branches, or this artery's accompanying sympathetic plexus.
However, as microneurosurgical techniques and knowledge of the cavernous sinus anatomy improved, morbidity from surgical resection of these lesions has significantly decreased. This improvement is also a result of more refined indications for surgical intervention.
The presenting symptoms of patients with cavernous sinus meningiomas emanate from the mass effect exerted by the tumor on the neurovascular structures housed within the sinus.
Patients with these tumors typically present with headaches, proptosis due to obstruction of venous outflow, facial pain or numbness, and visual disturbances such as diplopia, anisocoria, ptosis, or scotoma.
Less frequently, they may present with symptoms of carotid stenosis due to mass effect on the ICA. These syndromes include transient ischemic attacks (TIAs), amaurosis fugax, or cerebrovascular accidents (CVAs). Another less frequent presentation includes pituitary dysfunction secondary to mass effect from the meningioma on the pituitary gland or stalk.
The surgeon's evaluation begins with a thorough history, including specific questions about previous surgery or radiation therapy to the area. It is also important to question about involvement of any inflammatory (i.e., sarcoid) and metastatic systemic disease processes with dural involvement that could mimic meningioma on imaging. Nontumorous lesions can readily mimic meningiomas in the cavernous sinus, and their consideration in the differential diagnoses list can have a significant impact on the preoperative workup and ultimately the surgical decision-making process.
Physical and neurologic exams are performed with particular attention to CNs II-VI. This evaluation should also include formal visual field testing to rule out isolated scotomas. A pituitary endocrine evaluation is necessary, including a complete laboratory investigation as is indicated by clinical or radiographic findings, such as mass effect on the hypothalamus or infundibulum.
A MR imaging study analyzes the complex anatomy of the cavernous sinus region. I approximate the origin of the tumor, its degree of cavernous sinus involvement, and abutment of the optic nerve and canal.
MR and CT angiography allow evaluation of the ICA caliber. Any stenosis of the artery implies that the wall of the artery is infiltrated by the tumor and subtotal resection is indicated; the artery should not be manipulated during surgery. Any history of radiation to the cavernous sinus also significantly increases the risk of arterial injury during surgery.
Some of my colleagues advocate for conventional angiography with a balloon test occlusion for patients who have a history of cavernous sinus surgery or radiation or for whom there is significant concern of intraoperative cavernous ICA injury. If poor collateral circulation is demonstrated, they recommend preparation for a high-flow bypass as part of the surgical plan. For more information on this procedure, see the High-Flow Revascularization chapter.
My personal philosophy differs with this recommendation. I do not recommend the use of revascularization to facilitate resection of the infiltrated ICA with the goal of gross total tumor resection. Radiosurgery provides a reliable method for control of small and medium-size residual intracavernous tumors.
Treatment options for meningiomas include observation, surgical resection, and stereotactic radiosurgery. Most asymptomatic or minimally symptomatic cavernous sinus meningiomas are observed with serial imaging or undergo radiosurgical treatment. A review of current studies supports the finding that more than 60% of patients treated for these tumors harbor quiescent tumors. The recommended follow-up interval for imaging the conservatively managed lesions is at least once a year.
Tumors causing any degree of vision loss due to optic apparatus compression are surgical lesions because vision often improves once the mass effect on CN II is relieved. Documented tumor growth or progressive neurologic deficits are indications for surgical intervention.
Surgical intervention also permits histopathologic diagnosis and grading, which guides future management.
When pursuing surgical intervention, the surgeon must be mindful that the goal is (primarily) safe and (secondarily) near gross total resection during the first operation. Reoperation for these lesions is associated with a high risk of neural and vascular injury.
As previously described, cavernous sinus meningiomas carry a high risk of ICA and intracavernous cranial nerve injury secondary to tumor infiltration of the ICA adventitia and CN perineurium. To prevent injury to these structures, some tumor should be left behind.
Removal of the cavernous sinus meningiomas should focus on safe removal of the extracavernous tumor on the lateral wall of the sinus. I do not attempt aggressive intracavernous tumor resection, particularly in cases where the cavernous ICA is encased (Hirsch grades 2 and 3) and preoperative CN deficits are not present.
The residual tumor can be observed (my preference) or treated with stereotactic radiosurgery (SRS). Increasingly, the combination of planned subtotal resection with SRS is being established as an acceptable paradigm. However, there are limited reports of SRS potentially causing a more aggressive course in patients with late recurrence.
Other studies have shown a recurrence rate of 20% at 20 years following extracavernous resection and conservative intracavernous paradigm. These results suggest the potential efficacy of observation for the residual tumor. Although no consensus exists regarding the best course of action for cavernous sinus meningiomas, I advocate a more conservative surgical strategy with serial imaging to follow residual tumors and radiosurgery in the event of regrowth and recurrence.
The microsurgical anatomy of the cavernous sinus is complex and requires an in-depth study in the laboratory. Intimate anatomic knowledge should be translated from this Atlas to three-dimensional concepts in the cadaver laboratory before its application in the operating room.
Click here to view the interactive module and related content for this image.
The ICA, with its adherent sympathetic plexus, passes through the cavernous sinus and feeds the meningohypophyseal trunk, inferolateral trunk, and occasionally McConnell's capsular artery or a persistent trigeminal artery.
The Hirsch grading of cavernous sinus meningiomas classifies these lesions according to their degree of radiographic involvement of the cavernous segment of the ICA. Hirsch grade 1 lesions come in contact with or partially encase the cavernous ICA. Grades 2 and 3 lesions completely encase the ICA, with grade 2 lesions causing no radiographic narrowing of the ICA lumen and grade 3 lesions causing radiographic narrowing of the artery.
The Hirsch grade serves as an important indicator of the resectability of the tumor. Grade 1 lesions carry the most favorable and grade 3 tumors the least favorable prognosis, due to the requirement for a more aggressive attempt at resection and the correlated higher risk of ICA injury.
This risk can be attributed to the pathologically verified invasion of the adventitia of the cavernous ICA, lacking an intervening arachnoid membrane. Other pathologic studies have shown that meningiomas become continuous with the perineurium of CNs, particularly CN III, accounting for the high risk of injury during aggressive attempts at surgical resection.
RESECTION OF CAVERNOUS SINUS MENINGIOMA
Most cavernous sinus meningiomas are best approached via an orbitozygomatic craniotomy(OZ) and extradural clinoidectomy. This approach is flexible and provides multiple working angles to the entire venous sinus, as well as proximal and distal control over the ICA.
As discussed above, the goal of the craniotomy is removal of all extracavernous components of the tumor and conservative excision of the tumor within the lateral-most aspect of the cavernous sinus. If preoperative CN deficits are present, an attempt at these nerves' decompression is justified.
The surgeon should maximize the operative working window by means of liberally removing bone during the approach (i.e., subtemporal craniectomy). I prefer to install a lumbar drain for cerebrospinal fluid drainage to relax the dural sac and facilitate extradural dissection. Cranial nerves III, IV, and VI are monitored during the operation.
For meningiomas within the posterior cavernous sinus, the zygomatic craniotomy or middle fossa/subtemporal craniotomy offers favorable exposure of the posterior cavernous sinus and petrous apex, but suboptimal control over the distal ICA. I do not believe the osteotomy of the zygomatic arch offers significant expanded working angles, and therefore it is superfluous.
The orbitozygomatic osteotomy can be optimally performed with the patient in the supine position and head tilted 30 degrees toward the contralateral side. The patient's neck should be prepared to facilitate proximal carotid artery control.
After the bone flap is elevated, the orbital contents are exposed and electromyographic electrodes are directly placed into the superior oblique, superior rectus, and lateral rectus muscles to monitor CNs III, IV, and VI.
Throughout the procedure, I also attempt removal, or at least cauterization, of any infiltrated dura in order to minimize the foci of potential recurrence.
Vascular Control of the ICA
I secure control of the ICA along its full extent (petrous, cavernous, and clinoidal segments) to approximate the location of the ICA engulfed by the artery, avoid inadvertent vascular injury, and minimize the risk of massive blood loss.
To achieve this goal, once elevation of the dura from the middle fossa is complete, the petrous segment of the ICA can be exposed through the Glasscock's triangle. This maneuver is indicated only if aggressive tumor resection is contemplated. The middle meningeal artery is also coagulated and divided during elevation of the middle fossa dura.
Exposure of the ICA is accomplished by first identifying the greater superficial petrosal nerve (GSPN), dividing it, then drilling through the bone with a diamond bit while using copious irrigation. The bone is often dehiscent in this area. Traction on the GSPN is avoided to prevent injury to the geniculate ganglion; such injury can lead to facial palsy.
The apices of the Glasscock triangle are the facial hiatus, the anterior aspect of the foramen ovale, and the intersection of the GSPN and the lateral aspect of the V3. This triangle overlies the carotid artery, and drilling within this triangle using a diamond bit and constant irrigation uncovers the carotid artery.
Proximal control is secured by placement of a temporary clip on the petrous ICA. Alternatively, and more often, a Fogarty catheter is inserted into the carotid canal. When proximal control is necessary, the catheter balloon can be inflated to occlude the carotid artery in the carotid canal.
Distal control is possible by exposing the segment of the ICA between the dural rings. This exposure is achieved by opening the superior orbital fissure.
Entry into the Cavernous Sinus
If an intracavernous dissection is planned, the sinus can be entered via a superior or a lateral approach, or a combination of the two. Most often, the tumor reaches the surface of the lateral wall of the sinus and guides the surgeon regarding the point of entry.
Moreover, each tumor displaces the intra- and paracavernous sinus structures in a unique way. The operator should use the space created by tumor debulking as the operative route.
This is an approach for masses near the anterior, superior, and/or medial to the cavernous ICA.
The dura over the optic nerve is incised over the length of the optic canal to untether the optic nerve. Next, the distal carotid ring is divided. The dura is then incised toward the oculomotor nerve, providing initial entry into the cavernous sinus. Exposure can be expanded by additional incisions along and around the carotid artery.
Further exposure can become available via a posterior clinoidectomy and resection of the dorsum sellae. Entry into the posterior fossa is possible. The planum sphenoidale may also be drilled away. Any connection to the nasal sinuses should be sealed off.
The lateral approach is favorable for lesions lateral and/or inferior to the ICA and those that are posteriorly located within the cavernous sinus.
Extradural entry begins by incising the dura propria encasing V3. The dura propria is peeled away until the ganglion is in view. The bone around the foramina rotundum and ovale is removed to allow exposure of the infratemporal fossa.
The Parkinson's (infratrochlear) triangle is a reasonable corridor to reach the intradural/intracavernous portion of the tumor. CNs III and IVare found at the edge of the tentorium, and the dural incision is just beneath the route of CN IV. A dural flap is created by extending the dural incision inferiorly and reflecting the flap over the trigeminal ganglion. Tumor mobilization should protect CNVI which often consists of two to five fascicles.
Finally, in the case of tumors with large intradural and suprasellar extension, I incise the convexity frontotemporal dura in standard curvilinear pattern and dissect the extracavernous portion of the meningioma from the brain. The tumor is peeled away from the optic apparatus and pituitary stalk. The parts of the tumor filling the opticocarotid and oculomotor-carotid triangles are also resected.
The surgeon should attempt to remove as much of the infiltrated or hyperostotic bone as safely as possible throughout the resection, decreasing the foci for recurrence.
Within the cavernous sinus, CN VI is identified and protected; stimulation mapping may be used for its localization. Venous bleeding is easily controlled with gentle thrombin-soaked gelfoam packing. Importantly, any traction injury in the nerves is avoided via the use of microdissectors and sharp dissection. Some of these steps are summarized below.
The spheno-cavernous sinus meningiomas often harbor a dissection plane in proximity to the lateral cavernous wall, thereby allowing more aggressive dissection of the tumor from the neural structures.
If the tumor is infiltrating the Meckel's cave, the dura over the trigeminal ganglion is incised and the tumor is followed posteriorly for its removal. As in the case of other cavernous sinus meningiomas, the tumor creates the most viable, practical, and safe route for its access and removal.
Thick fibrous tumors and those with calcified texture are not safely resectable away from the neurovascular structures.
A 54-year-old woman presented with progressive facial numbness.
Before the bone flap is replaced, the surgical cavity is inspected so that any source of cerebrospinal fluid leakage can be obliterated using pieces of autologous muscle or fat. The area of the clinoidectomy is filled with a small pledget of muscle harvested from the temporalis muscle.
Patients are typically observed in the Intensive Care Unit for 24 to 48 hours after surgery. The steroid dosage is tapered off within 1 week, depending on the extent of cerebral edema and the patient's neurologic status. Seizure prophylaxis is continued for 7 days postoperatively; if the patient presented with a seizure, seizure prophylaxis is continued for 6 months to a year. Follow-up MRI is obtained within 48 hours of surgery, and once discharged from the hospital, the patient undergoes follow-up 3-month postoperative imaging followed by yearly surveillance imaging for early detection of recurrence.
Cerebrovascular accidents represent a major complication to keep in mind following surgery in the cavernous sinus, but this complication has a relatively infrequent incidence.
The requirement of adjuvant radiation therapy is becoming an important topic of discussion for management of cavernous sinus meningiomas. Use of adjuvant radiation therapy permits a more conservative resection and decreases the rates of postoperative morbidity.
I focus on the use of radiotherapy for treating aggressive local disease, which commonly demands a subtotal resection due to the involvement of critical cavernous sinus anatomy. One important caveat regarding this adaptive approach is the need to sufficiently clear the tumor mass away from the optic nerves/chiasm to allow for the application of higher dose adjuvant radiotherapy/radiosurgery without concern for radiation-related optic neuropathy.
Pearls and Pitfalls
- Extracavernous tumor resection and conservative lateral intracavernous resection are reasonable strategies for handling meningiomas of the region.
- Preoperative palsy caused by tumor compression on CNs III, IV, and VI can improve after effective tumor decompression. The extent of tumor resection is not necessarily related to the chance of recovery of CN function. Therefore, the principles of conservative tumor removal and CN decompression are wise strategies for patients with compromised preoperative CN function.
Contributors: Andrew R. Conger, MD, MS, and Benjamin K. Hendricks, MD
Couldwell WT, Cole CD, Al-Mefty O. Patterns of skull base meningioma progression after failed radiosurgery. J Neurosurg. 2007;106:30-35.
Demonte F, Al-Mefty O. Cavernous sinus meningioma management with carotid preservation, in: Eisenberg MB, Al-Mefty O (eds): The Cavernous Sinus: A Comprehensive Text. Philadelphia: Lippincott Williams and Wilkins, 2000, 251-261.
Dunn I, Al-Mefty O. Cavernous sinus meningiomas, in: Demonte F, McDermott M, and Al-Mefty O (eds): Al-Mefty's Meningiomas. 2nd ed. New York: Thieme, 2011, 235-247.
Hirsch WL, Sekhar LN, Lanzino G, Pomonis S, Sen CN. Meningiomas involving the cavernous sinus: Value of imaging for predicting surgical complications. AJR Am J Roentgenol. 1993;160:1083-1088.
Johnson MD, Powell SZ, Boyer PJ, Weil RJ, Moots PL. Dural lesions mimicking meningiomas. Human Pathol. 2002;33:1211-1226.
Kawase, T, Van Loveren, H, Keller, J, and Tew, J. Meningeal architecture of the cavernous sinus: Clinical and surgical implications. Neurosurgery. 1996;39:527-534.
Larson J, Van Loveren HR, Balko G, and Tew JM Jr. Evidence of meningioma infiltration into cranial nerves: clinical implications for cavernous sinus menigiomas. J Neurosurg. 1995;83:596-599.
O'Sullivan MG, van Loveren HR, Tew JM Jr. The surgical respectability of meningiomas of the cavernous sinus. Neurosurgery. 1997;40:238-244, discussion 245-247.
Rhoton A. The cavernous sinus, the cavernous venous plexus, and the carotid collar. Neurosurgery. 2002;51:S1-375-410.
Sindou M, Wydh E, Jouanneau E, Nebbal M, Lieutaud T. Long-term follow-up of meningiomas of the cavernous sinus after surgical treatment alone. J Neurosurg. 2007;107:937-944.
Tagle P, Villanueva P, Torrealba G, Huete I. Intracranial metastasis or meningioma? An uncommon clinical diagnostic dilemma. Surg Neurol. 2002;58:241-245.
Please login to post a comment.