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Table of Contents
Year : 2021  |  Volume : 4  |  Issue : 3  |  Page : 44-51

Microsurgical techniques and tumor control in cavernous sinus meningiomas: A review

Department of Neurosurgery, Rutgers-Robert Wood Johnson Medical School and University Hospital, New Brunswick, New Jersey, USA

Date of Web Publication02-Nov-2021

Correspondence Address:
Dr. Anil Nanda
Department of Neurosurgery, Rutgers-Robert Wood Johnson Medical School, Rutgers-New Jersey Medical School, New Brunswick, New Jersey
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/IJNO.IJNO_407_21

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Meningiomas are the most common tumors of the cavernous sinus (CS) and are one of the most challenging/formidable tumors to operate on due to the complex anatomy and rich neurovascular contents of the space. Parkinson's initial approach to this surgical “no man's land” triggered the interest in the microsurgical removal of tumors within this region over the next three decades. However, this initial enthusiasm to attempt complete removal of meningiomas has been met with exceedingly high surgical morbidity, especially cranial nerve palsies, and considerable mortality, predominantly due to vascular complications. The later introduction of radiosurgery and its excellent tumor control rate and minimal complications has allowed surgeons to select less invasive approaches such as primary radiosurgery or partial resection followed by radiosurgery. The authors aim through this work to discuss the relevant microsurgical anatomy, evolution of approaches, and techniques of CS meningioma excision including the endoscopic endonasal approach. We discuss the available alternatives and adjuvant management options, proposing an up-to-date multimodality treatment algorithm to optimize outcomes.

Keywords: Cavernous sinus, clinoid, gamma knife radiosurgery, interdural approach, internal carotid artery, Meckel's cave, meningioma, oculomotor nerves

How to cite this article:
Raju B, Jumah F, Nagaraj A, Nanda A. Microsurgical techniques and tumor control in cavernous sinus meningiomas: A review. Int J Neurooncol 2021;4, Suppl S1:44-51

How to cite this URL:
Raju B, Jumah F, Nagaraj A, Nanda A. Microsurgical techniques and tumor control in cavernous sinus meningiomas: A review. Int J Neurooncol [serial online] 2021 [cited 2022 May 22];4, Suppl S1:44-51. Available from: https://www.Internationaljneurooncology.com/text.asp?2021/4/3/44/329802

  Introduction Top

Meningiomas involving the cavernous sinus (CS) are some of the most challenging tumors to manage due to the complex anatomy of the region, considerable surgical morbidity and mortality, and high rates of recurrence.[1] These tumors either primarily arise within the CS or by invasion from adjacent intracranial or extracranial regions. The primary cavernous tumors are presumed to originate from the arachnoidal cells of medial Meckel's cave or the oculomotor cistern.[2] Tumors arising from the medial sphenoid wing, clinoidal, sphenoidal, sellar, infratemporal fossa, and orbital regions may infiltrate the CS secondarily.

The treatment of CS meningiomas (CSM) has evolved over the past four decades. Initially, a more conservative approach was practiced due to the lack of anatomical knowledge and microsurgical techniques. However, the pioneering work of Parkinson and Dolenc was an important catalyst in the refinement of microsurgical techniques which in turn led to the adoption of more radical approaches to complete removal. However, this resulted in significant periprocedural morbidity and mortality owing to the complex neurovascular relationship around the tumor. Furthermore, despite complete tumor removal, there was a high chance of recurrence, which raised concerns over the efficacy of surgical management. Later, the introduction of radiosurgery which permitted safe and excellent tumor control allowed surgeons to fall back on a more conservative approach. Gamma Knife radiosurgery became the treatment of choice, especially in small, pure CSM or as an adjuvant to partial resection in large tumors encasing the internal carotid artery (ICA) and cranial nerves.

In this review, the authors discuss the surgical anatomy, microsurgical techniques, adjuvant therapies, and outcome of CSM.

  Epidemiology Top

Meningioma is the most common intracranial primary neoplasm, accounting for 36.8% of all central nervous system tumors.[3] There is a growing trend in the incidence of intracranial meningiomas (6.0 per 100,000 person-years) with an overall annual increase of around 4.6%.[4],[5] Less than 1% of all intracranial tumors arise from the CS.[6] Meningiomas are one of the most common intracranial tumors and 25% of these arise within the skull base. CSM make up 14% of all skull-based meningiomas and <2% of all intracranial tumors. Meningiomas account for 41% of all CS tumors.[6],[7] Old age (>65 years), female sex, and Black race are risk factors for developing meningiomas.[3],[4]

  Historical Aspects of Cavernous Sinus Surgery Top

Claudius Galen described parasellar carotid retia (elaborate network of blood vessels and neurons) covered in venous blood based on his dissections of lower animals. Although many of Galen's findings were disproved by anatomists of the Renaissance era, this particular finding was never discussed or identified for the next sixteen centuries until Jacobus Benignus Winslow (1669–1770), a Swedish anatomist who coined the term “cavernous sinus” to describe these structures in his book An Anatomical Exposition of The Structure of The Human Body.[8],[9] He compared these structures to the corpora cavernosa of the penis and imagined this to be a single trabeculated venous space.[10] In the early 1960s, Parkinson's attempt to enter the CS to block a recurrent arteriovenous fistula paved the way for the modern concept of discontinuous venous channels in between the meningeal and periosteal layers of the temporal dura.[8],[11] This led modern neurosurgeons such as Dolenc, Rhoton, Hakuba, Kawase, and others to perform meticulous dissections of the CS region, describing various microsurgical approaches to this “no man's land.”[2],[12],[13],[14] Though clearly a misnomer, the name “CS” is still in vogue.

  Relevant Surgical Anatomy Top

Cavernous sinuses are the paramedian venous plexuses within the dural layers of the middle cranial fossa on either side of the sella, extending anteriorly from the level of posterior borders of the superior orbital fissure to the level lateral to the dorsum sella posteriorly.[13],[15] It contains the cavernous segment of the carotid artery and its branches, the sympathetic plexus, the third and fourth cranial nerves, and the first division of the trigeminal nerve along with multiple connecting venous channels and their tributaries.[13],[16] It has five walls: medial, lateral, anterior, posterior, and roof/superior. The dural layers/walls are formed by the splitting of the basal temporal dura into lateral dura propria or meningeal layer and a medial endosteal dura. The meningeal layer of dura forms the lateral wall, roof, and the upper part of the medial wall, whereas the endosteal layer divides into two separate layers to form the inner layer of the lateral wall and the lower part of the medial wall. The endosteal layer also continues anteriorly into the orbit through the superior orbital fissure to blend with the periorbita. This periorbital bridging dura is an important landmark during CS surgeries. Superficially incising this bridge will expose the interdural space which is necessary to peel the outer layer of the CS lateral wall to expose the transparent inner layer and the contents of the CS.[2] Lateral and medial walls merge anteriorly near the superior orbital fissure and the foramen rotundum. Thus, the maxillary division of the trigeminal nerve forms the most inferior limit of the CS. The inner endosteal layer forming the inner layer of the lateral wall invests multiple cranial nerves (3rd, 4th, 6th, and 5th) while ascending and ends in the roof. The outer endosteal layer continues medially over the sphenoidal bone and sella forming the lower medial cavernous wall. The anterior most part of the outer endosteal layer continues medially, covering the undersurface of the anterior clinoid, forming the “carotid-oculomotor membrane.” Medial to this point, it forms the lower/proximal carotid ring and then reflects above, covering the entire circumference of the carotid medial to the anterior clinoid, forming the “carotid collar,” and merges with the distal dural ring. The meningeal layer forming the outer lateral wall continues medially as the roof, distal dural ring, diaphragma, and then dips medially, forming the sellar (upper) part of the medial cavernous wall. The upper and lower parts of the medial wall, thus formed by the meningeal and endosteal dura, respectively, continue over the sellar floor with inferior intercavernous sinus between them. Appreciating the anatomy of the medial wall is crucial in transnasal transsphenoidal approaches to the CS.[13]

Cranial nerves 3, 4, and 6 occupy the lateral wall of the CS in that top-down order between the two layers of the lateral wall. The 6th cranial nerve is located inside the inner dural layer within the CS proper, inferolateral to the cavernous carotid artery. There will be a potential space around the 3rd and 4th cranial nerves and the dural ensheathing. However, the 5th and 6th cranial nerves are invested tightly within the inner dural layer separating the nerve into multiple fascicles. This explains the predilection for the potential infiltration of 5th and 6th nerves by even the small and benign tumors, with a high risk for recurrence and trigeminal neuralgia.[17],[18] Furthermore, the cavernous carotid artery lies freely within the CS without any protective meningeal covering, which can result in higher chances of adventitial infiltration by the pure CSMs.[18],[19] Arachnoid villi protrude into the venous systems along the mandibular branch of the trigeminal nerve near the posterolateral wall of the CS. This can be the origin for the CS wall meningiomas.[2] Thus, these tumors can be typically peeled off of the CS.

The roof is formed posteriorly by the oculomotor triangle and anteriorly is covered by the anterior clinoids and the dura covering it. The oculomotor triangle is formed by the posterior petroclinoidal fold (PPF) posteriorly, anterior petroclinoidal fold (APF) laterally, and the interclinoidal fold medially. The trochlear nerve enters the roof at the junction of the PPF and APF and continues in the lateral wall below the oculomotor nerve and above the V1 branch of the fifth cranial nerve. The oculomotor nerve enters the roof in the oculomotor triangle anteromedial to the trochlear nerve. After entering the dural roof, the nerve enters a meningeal pocket in the lateral wall where the superficial dural layer is not attached to the nerve. As the nerve approaches the level of anterior clinoids, the layers fuse to invest the nerve snugly.[13] The anterior clinoidal process forming the anterior roof of the CS is a triangular bony projection with three roots attached to the sphenoid bone. The anterolateral root attaches to the lesser wing of sphenoid, the anteromedial root forms the roof of the optic canal, and the posteromedial root forms the optic strut. The anterior bend of the carotid artery lies medial to the clinoids. Understanding the anatomy of the anterior clinoids and their dural reflections described earlier are critical in the surgeries involving the CS.

The posterior wall of the CS extends above the upper margin of the petroclival fissure with petrosphenoid ligament forming the inferior limit, the lower lateral edge of dorsum sella forming the medial limit, trigeminal porus forming the lateral limit, and posterior petroclinoid fold forming the superior limit. Sixth cranial nerve enters through the Dorello's canal below the petrosphenoid ligament.[13] Surgeries of petroclival meningioma with CS involvement or CSM with posterior fossa extension need a thorough understanding of the anatomy of this area.

More than ten triangles are described in relation to the CS. However, two each in the roof and the lateral wall are critical in surgical approaches to CSMs. The triangles in the lateral wall are supratrochlear and infratrochlear (Parkinson's) triangles. Because of the typical attachment points of the cranial nerves, tumors arising from within the CS can be typically approached through the infratrochlear triangle.[13]

Intracavernous carotid starts at the level lateral to posterior clinoid and traverses upward and forward along the carotid sulcus and then turns upward medial to the anterior clinoid and posterior to the optic strut to become intradural. Intracavernous carotid is divided into five segments based on morphology. It gives two major branches within the CS. The first is the meningohypophyseal trunk at the posterior bend, and the second, inferolateral trunk from the horizontal segment of the artery. This portion of the carotid artery is extrameningeal, and hence purely intracavernous tumors can invade the adventitia and can cause arterial injury during the surgical decompression.[2],[13],[19] Branches of the inferolateral trunk supply the oculomotor nerves, the proximal trochlear nerve in 80% of cases, distal trochlear nerves in all cases, distal two-thirds of abducent nerves, ophthalmic, and proximal maxillary nerves. Branches of the meningohypophyseal trunk supply the proximal trochlear nerve in 20% of cases and the proximal abducent nerve.[20] Damage to these arteries or smaller arterioles during the CS tumor surgeries can explain many cases of postoperative cranial nerve palsies.

  Clinical Presentation and Natural History Of Cavernous Sinus Meningiomas Top

As mentioned previously, meningiomas can arise from within the CS or extend into it from surrounding structures. CSM can be purely intracavernous or arise from the lateral dural wall with extracavernous extension. Depending on the location and extension of the tumor, they present with diverse neurovascular symptoms. Most commonly, these tumors present with a varied combination of oculomotor and trigeminal signs and symptoms such as ptosis, diplopia, anisocoria, headache, facial pain, and numbness (CN III: 10%–62%, CN IV: 7.7%–14%, CN VI, and CN V: 10%–50%).[21],[22],[23] Tumors involving the anterior CS or sphenocavernous meningiomas may cause visual deficits (43%) by extension into the optic canal compressing the optic nerve [Figure 1].[21] Complete CS syndrome with ophthalmoplegia occurs rarely.[24] CSMs can also invade, encircle, or compress the intracavernous carotid artery, causing ischemic symptoms or stroke.[25] Rarely, CSMs invading the medial wall can compress the pituitary stalk and cause pituitary dysfunction.[25],[26]
Figure 1: Magnetic resonance imaging brain (a) T1 W postcontrast axial and (b) coronal images showing small right intracavernous meningioma with extension anteriorly into the optic canal. Internal carotid artery appears to be narrowed

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The natural history of the CS meningioma is poorly studied. Amelot et al., described a consecutive series of 53 patients of CSM managed conservatively to show that these tumors are clinically and radiologically indolent. Approximately 53% of their patients had major neurovascular symptoms, and the remaining 47% were detected incidentally or presented with minor symptoms. They reported resolution of more than two-thirds of major symptoms and 80% of minor symptoms after a short course of steroids. After resolution, the majority of these patients remained asymptomatic and did not show further radiological growth. Less than 10% of tumors showed some growth or clinical deterioration requiring additional radiation, but they did so in a slow, unpredictable fashion, thereby raising questions over the need for any intervention in CSM.[7]

  Radiological Evaluation Top

Computed tomography (CT) and magnetic resonance imaging (MRI) of brain are the primary modalities of evaluation of CSM. Frequently, CSMs are detected incidentally on imaging. T2-weighted MRI will show marked enlargement of the CS with the thickened lateral wall of the sinus. The presence of meningeal dural tail on contrast, sometimes with extension to ipsilateral tentorium, is characteristic [Figure 2].[26],[27],[28] Three-dimensional time time-of-flight magnetic resonance angiography can help visualize encasement and narrowing of the ICA. Occasionally, CSMs can invade the medial wall compressing the normal pituitary gland. T2 weighted imaging (WI) and dynamic contrast imaging (DCI) are particularly helpful in differentiating the pituitary adenoma from the meningioma in these cases. CSM is slightly hyperintense compared to the isointense normal pituitary gland on T2 WI, and DCI MRI shows differential enhancement.[28],[29],[30] Thin-section CT head with bone windows may show areas of calcifications and sometimes hyperostosis of the surrounding bony structures such as anterior clinoid, sphenoid sinus wall, and medial sphenoid wing.[30],[31] MRI will also reveal the extent of tumor invasion anteriorly into the optic canal, posteriorly into the prepontine cistern, laterally into Meckel's cave, medially into the sella, and inferiorly into the sphenoid sinus.[31] Digital subtraction angiography typically shows the tumor blush persisting into the late venous phase without neovascularity or the early draining veins. This finding is probably the most consistent feature to substantiate the diagnosis of CSM.[27] However, a biopsy of the tumor with histopathological examination remains the only confirmatory test.[21]
Figure 2: Magnetic resonance imaging brain T1 W postcontrast images showing left medium-sized cavernous sinus meningioma.(a) Left cavernous sinus homogenously enhancing mass lesion with the complete encasement of internal carotid artery and its narrowing. (b and c) Coronal images and sagittal images showing the meningioma. (c) Enhancing dural tail seen along the tentorium (White Arrow). Carotids are not visualized in these images. (d-f) Showing postoperative images with adequate decompression. Probably a small residual seen medial to the intracavernous internal carotid artery

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  Treatment Strategies Top

Optimal management of the CSM is still debatable. These tumors can be either observed or managed by microsurgery, stereotactic radiosurgery, or a combination of the two. Although controversies exist in selecting the modalities, they should be individualized depending on the patient's symptoms, neurological deficits, and radiological extension. Generally, larger tumors with significant extracavernous extension presenting with cranial neuropathies, visual pathway compromise, brainstem compression, and any symptoms affecting the activities of daily living may benefit from surgical decompression with or without radiosurgery.[7],[21],[24] Asymptomatic or minimally symptomatic, smaller tumors confined to the CS are usually considered for stereotactic radiosurgery alone [Figure 3].[21] Our experience indicates that many of the asymptomatic incidentally detected CSMs could be observed.[21]
Figure 3: (a and b) Magnetic resonance imaging Brain T1 W post contrast images in another patient showing left cavernous sinus meningioma. Left intracavernous internal carotid artery appears to be pushed medially and narrowed by the tumor (Red Arrow). There is no obvious tumor seen medial to carotid. However, narrowing of internal carotid artery suggest partial encasement in this case

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Initial enthusiasm for the radical excision of CS meningioma with a rescue bypass (cavernous sinusectomy) has fallen apart due to the high morbidity and mortality associated with it.[7],[21],[32],[33] Although benign, meningiomas can invade the cranial nerves and carotid artery within the CS for anatomical reasons peculiar to this region.[17],[19],[34],[35],[36] Hence, even gross total resection sparing the cranial nerves and the carotid artery has no long-term benefits due to possible recurrence from the microscopic residual within the nerve fascicles and the adventitia of the vessel wall.[2],[34] Hence, the evidence supports the consensus of resecting the extracavernous component of the tumor followed by adjuvant radiosurgery for the residual, especially if the tumor is invasive, firm, or calcified. Complete excision can be attempted if the tumor is soft and arising from the lateral dural wall without cranial nerve invasion.[21],[35]

  Surgical Approaches Top

Routinely used surgical approaches for lesions of the CS are frontotemporal orbito-zygomatic (FTOZ) approach, frontotemporal (FT) craniotomy with an orbital osteotomy (FTO), conventional FT approach, and middle fossa (MF) approach.[21] Our experience in treating small to midsized CSM has shown adequate exposure and reasonable decompression using conventional FT craniotomy with the extra and intradural approach.[14],[32],[36],[37] FTOZ approaches are particularly effective in larger tumors with significant superior extension and/or in tumors involving the floor of the MF. As demonstrated in previous studies, this approach permits more surgical maneuverability and larger superior projection angle, allowing for a better visibility of superior extension with minimal brain retraction.[21],[38],[39],[40] Extradural approaches allow for the identification of external carotid artery/ICA vascular supply/anastomosis and early devascularization of the tumor.[21] Among numerous other approaches described in the literature, the transmaxillary approach, lateral orbitotomy approach, and endoscopic transnasal transsphenoidal approaches are noteworthy.[41],[42],[43],[44] With the advances in neuroendoscopy and anatomical knowledge, the transnasal transsphenoidal approach has become the first choice in some experienced hands. However, due to the steep learning curve and complex anatomy of the region, this approach should be used cautiously. A brief overview of the commonly used FT surgical approach described in our previous publication is given below.[21]

After craniotomy, the dura from the frontal and temporal base is elevated to expose the sphenoid ridge and the anterior clinoid. From the temporal side, the foramen spinosum with the stem of the middle meningeal artery is identified, coagulated, and divided extradurally. On further elevation of the temporal dura in anterolateral-to-posteromedial direction, the greater superficial petrosal nerve (GSPN) and petrous apex are identified. GSPN should be sacrificed in all cases to avoid traction injury to the facial nerve, and the petrous apex can be drilled if there is a posterior extension of the tumor. Anteriorly, the dura around the maxillary nerve (foramen rotundum) is sharply dissected and released. Then, the orbitomeningeal band passing through the superior orbital fissure is identified and divided superficially. This leads to the interdural space between the dura propria and the endosteal layer. The outer temporal basal dura is peeled off the CS lateral wall exposing the underlying transparent inner dural layer with cranial nerves. Venous bleeding at this point can be controlled with Surgicel or fibrin glue. The superior wall of the optic canal is drilled to free the optic canal and thus avoid damage to the optic nerve during the procedural manipulation. Using the high-speed drill, the anterior clinoid process is thinned and removed by piecemeal resection. This exposes the anterior-most part of the roof of the CS, oculomotor membrane, and the clinoidal portion of the carotid artery and its dural rings.

Meningiomas within the CS can be removed either through the lateral wall or the roof, depending on the location and prominence of the tumor. Predominantly extracavernous tumors involving the lateral wall can be peeled off with the outer layer of the lateral wall. In contrast, the purely intracavernous tumors can be better exposed through the intradural lateral wall approach. Typically, the majority of CSMs can be debulked through Parkinson's triangle by incising the dural wall in a posterosuperior-to-anteroinferior direction parallel to the oculomotor nerve. Tumors involving the superior or medial compartments of the CS can be accessed easily via the roof. The dural rings and the collar around the clinoidal ICA are cut and extended posteriorly up to the level of posterior clinoids, and the two leaves are rolled apart to expose the tumor.

The extent of tumor removal depends on the characteristics of the tumor such as consistency, invasiveness, and size. Gross total tumor decompression can be achieved in 61%–76% of patients.[24],[45] In cases with partial resection, adjuvant radiosurgery for the residual tumor can be considered. Postoperative new cranial nerve deficits are reported in 18%–54% of the patients.[21],[24],[46] Preexisting cranial nerve deficits recovered in 14%–23% of patients. During follow-up, trigeminal nerve dysfunction resolves in most patients, while the least recovery is observed in trochlear nerve function.[21] Recurrence after the microsurgery is seen in 5%–13% patients, depending on the extent of resection and duration of follow-up.[24],[32],[47] Our practice is to follow-up every patient 6 months for the first 2 years after surgery, then annually for the next 3 years, and every alternate year after that to monitor neurological improvement and recurrence.[21]

  Role of Radiosurgery Top

The superb safety and efficacy of radiosurgery in treating intracranial tumors have it as the primary modality of treatment in many intracranial pathologies, especially in challenging tumors such as CSMs. They offer excellent local control with the least complications compared to the microsurgery. From a radiobiological standpoint, meningiomas, being a late responding tissue, are better controlled with a higher dose or less fractionation than conventional radiation practices.[48] Although this modality is considered as primary or adjuvant therapy in patients with CSM with an excellent control rate, the validation of those results is restricted by the paucity of randomized controlled studies.[49] One of the major limitations is the associated radiation injury to cranial nerves, a complication likely due to damage of small vessels and protective Schwann cells.[48] The other limitations related to this modality of treatment are the size of the lesion and the risk of radiation toxicity to the surrounding radiosensitive structures such as the carotid artery and the brainstem.

Most radiosurgical case series report progression-free survival rates at 5 and 10 years of 80%–100% and 73%–98%, respectively, and a radiographic response in 29%–69%.[50],[51],[52],[53],[54],[55],[56],[57],[58],[59],[60],[61],[62],[63],[64],[65],[66],[67],[68],[69] The peripheral dose of 12–14 Gy is accepted in most cases for CSM radiosurgery.[3],[4],[5],[6],[7],[8],[9],[10],[11],[12],[13],[14],[15],[16],[17],[18],[19],[20] The overall dose maybe a little less than usual considering the proximity of these tumors to the optic pathways. The risk of visual impairment is related to the amount of the optic apparatus receiving high doses. A distance of 5 mm between the meningioma and the optic nerve is considered to be safe in a single fraction radiosurgery.[61],[67]

Within most of the series where RS is employed as the first-line treatment, a rate of 3%–15% of new cranial nerve deficits is reported. A recent meta-analysis of the patients undergoing either RS or surgery followed by radiotherapy or RS showed a significantly higher rate of neurological morbidity in the latter group than the former group undergoing RS alone (59.6% vs. 25.7%).[70] This discrepancy could be explained by the negative impact of the microsurgical manipulation on microvasculature of the cranial nerves along with the consequent additional insult imparted by the radiosurgery itself.[58],[71]

In larger meningiomas, single-fraction radiosurgery can be detrimental to the surrounding normal tissues and possibly reduce the rate of local control due to the low marginal doses usually used. Furthermore, a radiosurgical complication rate of around 21% was reported in patients with large CSMs compared to a much lower rate observed in patients with small lesions (<10 cm3).[66] Although the reported 5-year local control in radiosurgical series reached 85%, microsurgical debulking followed by radiosurgery will be an optimal management strategy in patients with larger tumors.[62],[72]

  Conclusions Top

Management of the CSMs necessitates a multidisciplinary collaboration. Due to the lack of adequate knowledge of the natural history of CSMs, high surgical morbidity and mortality, and limitations of radiosurgery, an optimal management algorithm cannot be established. The therapeutic goal should be to achieve adequate tumor control while minimizing any treatment-related morbidity and mortality. With the available evidence, we propose observation in small, asymptomatic, and incidental intracavernous meningiomas, and radical resection in larger meningiomas involving only the lateral wall of the CS. We recommend primary radiosurgery for small, purely intracavernous meningiomas, and excision of the extracavernous portion with adjuvant radiosurgery of the larger/invasive meningiomas. Finally, performing selective, partial resection, decompressing the critical structures with or without the adjuvant radiosurgery seems to be the most appropriate solution in patients with extensive spheno-petro-cavernous meningiomas.

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