Abstract BACKGROUND Surgical removal of cavernous sinus meningiomas is challenging and associated with high morbidities as a result of the anatomic location and the surrounding neurovascular structures that are often invaded or encased by the tumor. Advances in radiotherapy techniques have led to the adoption of more conservative approaches in the management of cavernous sinus meningioma. Internal carotid artery encasement and invasion has been documented in these cases; however, ischemic presentation secondary to internal carotid artery stenosis or occlusion by meningioma in the region of the cavernous sinus is rare, with only few cases reported in the literature. OBJECTIVE To report our surgical technique and experience with bypass grafting for cavernous sinus meningiomas that invade or narrow the internal carotid artery. METHODS We report 2 patients who presented with signs and symptoms attributed to cavernous carotid artery occlusion secondary to cavernous sinus meningioma in the last 5 yr. Both patients were treated with flow augmentation without surgical intervention for the cavernous sinus meningioma. RESULTS In both cases, the clinical and radiological signs of cerebrovascular insufficiency improved markedly, and the patients’ tumors are currently being monitored. CONCLUSION Although the cerebrovascular insufficiency in this subset of patients is attributed to the occlusion of the cavernous carotid artery caused by the tumor, we propose treating those patients with flow augmentation first with or without radiation therapy when there is a clear imaging feature suggestive of meningioma in the absence of significant cranial nerve deficit. Cavernous sinus, Cavernous sinus meningioma, Meningioma, Bypass, Internal carotid artery ABBREVIATIONS ABBREVIATIONS ACA anterior cerebral artery BTO balloon test occlusion CSMs cavernous sinus meningiomas CT computed tomography CTA computed tomography angiography ICA internal carotid artery MCA middle cerebral artery MR magnetic resonance MRI magnetic resonance imaging STA superficial temporal artery Cavernous sinus meningiomas (CSMs) are rare, representing approximately 1% of all meningiomas.1 However, meningioma is the most common tumor involving the cavernous sinus, accounting for around 41% of all tumors in this location.2 CSMs arise either as primary lesions within the cavernous sinus or secondarily from adjacent anatomic areas but involving and compressing the cavernous sinus.3 CSMs are divided into 3 categories based on the degree of internal carotid artery (ICA) invasion; Hirsch grade I tumors do not completely encircle the cavernous ICA (38% of lesions), whereas Hirsch grade II tumors encircle the artery but do not narrow it (30%) and Hirsch grade III tumors cause narrowing of the ICA (32%).4 Optimal management of patients with CSM remains an ongoing challenge, particularly when the ICA is involved and causing symptoms. Patients may rarely present with a constellation of vaso-occlusive symptoms, and the risk of impending or worsening stroke can be an immediate clinical concern. Optimal management of CSMs therefore must address both the tumor itself as well as the integrity of the vascular supply of the ICA. Surgery has historically been the mainstay of meningioma treatment; however, with the advancement of radiation therapy, CSMs are increasingly managed with a combination of surgical debulking and/or radiotherapy.5,6 This paradigm has been sustained by the morbidity profile of operating near the vital structures of the cavernous sinus and the observation that these tumors appear to have a distinct natural history than other meningiomas.1,7-9 Isolated vascular insufficiency, without cranial neuropathy, as a result of ICA narrowing or infiltration is only rarely encountered in CSMs In these patients, the method of sacrificing the involved ICA, aggressively resecting the CSM, and performing bypass grafting has been recommended.10-12 At our institution, we utilized a measured approach for patients with CSM and isolated vascular insufficiency without substantial cranial neuropathy. We treat the vascular involvement and tumor burden in such patients as separate problems. We have opted to treat these patients with low-flow extracranial–intracranial bypass surgery to restore distal blood flow in the middle cerebral artery (MCA). We have treated 2 such patients in the last 5 yr and have monitored them to assess outcomes from the perspective of their tumor and the viability of their graft. In this account, we report our surgical technique and experience with bypass grafting for CSMs that invade/narrow the ICA. ILLUSTRATIVE CASES These cases are presented with a waiver of informed consent as per the Institutional Review Board. Case 1 A 42-yr-old woman presented to an outside hospital after an acute transient episode of aphasia, right facial droop, and right-hand numbness. A computed tomography (CT) scan of the brain showed no hemorrhage or stroke but demonstrated a lesion involving the left cavernous sinus. Computed tomography angiography (CTA) showed complete occlusion of the cavernous carotid artery. The patient's symptoms and signs resolved markedly except for mild word-finding difficulties, and she was started on aspirin and levetiracetam. The patient was transferred to our institution for further management. A magnetic resonance imaging (MRI) scan of the brain revealed a left anterior clinoid meningioma extending into the cavernous sinus and orbital apex, causing complete occlusion of the cavernous carotid artery (Hirsch grade III). Diffusion-weighted sequence showed areas of restricted diffusion between the left anterior cerebral artery (ACA) and MCA distributions consistent with watershed infarctions. Cerebral angiography showed complete occlusion of the left ICA just distal to the origin of the ophthalmic artery (Figure 1). CT perfusion studies demonstrated normal cerebral blood flow and cerebral blood volume but increased mean transient time and time to peak consistent with hypoperfusion with no core infarct (Figure 2). Her presentation and clinical findings were attributed to cerebrovascular insufficiency, and in the absence of significant ophthalmalgia and visual loss, we recommended a flow-augmentation procedure for the left ICA territories and postoperative radiation therapy/stereotactic radiosurgery to the CSM. FIGURE 1. View largeDownload slide Case 1. A, Axial CT scan of the brain demonstrates hyperdense lesion in the region of the left cavernous sinus with no evidence of hemorrhage or stroke. Axial B and coronal C CTA demonstrate hyperdense lesion in the left cavernous sinus associated with hyperostosis of the left anterior clinoid process and causing complete occlusion of the left cavernous carotid artery. Axial D and coronal E T1-weighted MRI with gadolinium contrast demonstrate enhancing lesion in the left cavernous sinus. F and G, Diffusion-weighted imaging demonstrates restricted diffusion areas in watershed zone between MCA–ACA and MCA–posterior cerebral artery territories. H, Anteroposterior cerebral angiogram projection of the right ICA injection demonstrates cross filling of the left MCA from the anterior communicating artery. Anteroposterior I and lateral J cerebral angiogram projection of the left internal carotid injection demonstrate tumor blush with complete occlusion of the ICA above the origin of the ophthalmic artery. FIGURE 1. View largeDownload slide Case 1. A, Axial CT scan of the brain demonstrates hyperdense lesion in the region of the left cavernous sinus with no evidence of hemorrhage or stroke. Axial B and coronal C CTA demonstrate hyperdense lesion in the left cavernous sinus associated with hyperostosis of the left anterior clinoid process and causing complete occlusion of the left cavernous carotid artery. Axial D and coronal E T1-weighted MRI with gadolinium contrast demonstrate enhancing lesion in the left cavernous sinus. F and G, Diffusion-weighted imaging demonstrates restricted diffusion areas in watershed zone between MCA–ACA and MCA–posterior cerebral artery territories. H, Anteroposterior cerebral angiogram projection of the right ICA injection demonstrates cross filling of the left MCA from the anterior communicating artery. Anteroposterior I and lateral J cerebral angiogram projection of the left internal carotid injection demonstrate tumor blush with complete occlusion of the ICA above the origin of the ophthalmic artery. FIGURE 2. View largeDownload slide Case 1. Mean transient time (MTT, top row) and time to peak (TTP, bottom row) CT perfusion of the brain preoperatively A, at 3 mo postoperative B, and at 6 mo postoperative C demonstrate gradual improvement of the brain perfusion in the left side. FIGURE 2. View largeDownload slide Case 1. Mean transient time (MTT, top row) and time to peak (TTP, bottom row) CT perfusion of the brain preoperatively A, at 3 mo postoperative B, and at 6 mo postoperative C demonstrate gradual improvement of the brain perfusion in the left side. The bypass graft procedure was uncomplicated, and her immediate postoperative course was uneventful except for a self-reported episode of word-finding difficulty. Although the patient was offered consultation with radiation oncology, she opted for watchful observation given the dramatic improvement in her symptoms. Follow-up imaging at 3 mo showed a stable meningioma with no growth and patent superficial temporal artery (STA)–MCA anastomosis. CT perfusion studies demonstrated delayed perfusion compared with the contralateral side; however, the cerebral perfusion was significantly improved between the 2-mo and 6-mo follow-up intervals (Figure 2). At her last follow-up appointment 7 mo after surgery, her speech difficulties had resolved completely, and her most recent MRI and CT angiogram showed patent bypass and stable CSM (Figure 3). FIGURE 3. View largeDownload slide Case 1. A, CT angiogram three-dimensional reconstruction showing patent STA–MCA bypass graft 1 yr after surgery. Axial B and coronal C follow-up T1-weighted MRIs with gadolinium contrast demonstrate stable CSM 6 mo after surgery. FIGURE 3. View largeDownload slide Case 1. A, CT angiogram three-dimensional reconstruction showing patent STA–MCA bypass graft 1 yr after surgery. Axial B and coronal C follow-up T1-weighted MRIs with gadolinium contrast demonstrate stable CSM 6 mo after surgery. Case 2 A 73-yr-old woman presented to an outside hospital after experiencing intermittent episodes of expressive aphasia and visual changes in her left eye over the course of several weeks. CTA, MRI, and magnetic resonance (MR) angiography of the brain revealed a left CSM that had completely occluded the left ICA (Hirsch grade III; Figure 4). CT perfusion of the brain with acetazolamide challenge test was performed, demonstrating maximal dilation of the vessel and hypoperfusion of the left MCA territories suggestive of decreased cerebrovascular reserve (Figure 5). The patient was started with aspirin prior to undergoing STA-to-MCA bypass without resection or biopsy of the cavernous sinus lesion. FIGURE 4. View largeDownload slide Case 2. Axial A and coronal B CTA demonstrate a lesion in the left cavernous sinus with complete occlusion of the cavernous carotid artery. Axial C and coronal D T1-weighted MRI with gadolinium demonstrate enhancing lesion in the left cavernous sinus. E, MR arteriography demonstrates complete occlusion of the left cavernous carotid artery with weak cross filling of the left MCA branches. FIGURE 4. View largeDownload slide Case 2. Axial A and coronal B CTA demonstrate a lesion in the left cavernous sinus with complete occlusion of the cavernous carotid artery. Axial C and coronal D T1-weighted MRI with gadolinium demonstrate enhancing lesion in the left cavernous sinus. E, MR arteriography demonstrates complete occlusion of the left cavernous carotid artery with weak cross filling of the left MCA branches. FIGURE 5. View largeDownload slide Case 2. Mean transient time (MTT, top row) and time to peak (TTP, bottom row) CT perfusion scans of the brain showing improved perfusion of the left cerebral hemisphere 1 mo postoperatively when compared with the preoperative CT perfusion studies. FIGURE 5. View largeDownload slide Case 2. Mean transient time (MTT, top row) and time to peak (TTP, bottom row) CT perfusion scans of the brain showing improved perfusion of the left cerebral hemisphere 1 mo postoperatively when compared with the preoperative CT perfusion studies. The operation and hospital course were uncomplicated except for another episode of transient aphasia that resolved without intervention. Postoperative ophthalmologic examination demonstrated subtle left-sided cranial nerve VI and afferent pupillary defects. The patient has been monitored for 5 yr since the operation and does not complain of any difficulty with speech or vision. Her management has comprised only medical optimization of her cerebrovascular risk factors and no radiotherapy or surgical resection of the CSM itself. Interval imaging during this time has demonstrated stable size of the cavernous sinus lesion with no evidence of interval growth. Her most recent MRI and CTA demonstrate patent STA–MCA bypass graft 5 yr following the surgery and stable CSM (Figure 6). FIGURE 6. View largeDownload slide Case 2. A Sagittal CT angiogram showing patent STA–MCA bypass graft 5 yr after surgery. Axial B and coronal C follow-up T1-weighted MRIs with gadolinium contrast demonstrate stable CSM 4 yr after surgery. FIGURE 6. View largeDownload slide Case 2. A Sagittal CT angiogram showing patent STA–MCA bypass graft 5 yr after surgery. Axial B and coronal C follow-up T1-weighted MRIs with gadolinium contrast demonstrate stable CSM 4 yr after surgery. SURGICAL TECHNIQUE The patient is started on 325 mg of aspirin daily prior to surgery. The patient is positioned supine, a large shoulder booster is placed underneath the ipsilateral side, and the head is affixed in the 3-point fixation head clamp. Doppler ultrasound is used to map the course of the parietal or frontal branch (whichever is the largest) of the STA, and the incision is planned directly over the artery. The patient is prepped and draped in the standard fashion with placement of neurophysiology monitoring for motor evoked potentials, somatosensory evoked potentials, and electroencephalography. An incision is made at the superior end of the STA, extending down towards the root of the zygoma. Dissection with scissors and forceps is carried down through the subcutaneous tissue until the artery is freed in its entirety. A cuff of connective tissue measuring 0.5 cm on either side of the graft is kept with the artery. The artery is left in situ, and the underlying temporalis fascia and muscle are incised in a linear fashion using monopolar cautery to expose the underlying bone. Self-retaining retractors are placed under the musculocutaneous flap and reflected anteriorly and posteriorly. Using image guidance stereotactic CTA, a small craniotomy is centered over the distal sylvian fissure, which is usually located 6 cm superior to the external auditory meatus. Once the bone flap is elevated, the dura is incised in a cruciate fashion. Using microsurgical technique, the sylvian fissure is opened, and the target recipient M4 or M3 branch is identified. The recipient vessel is dissected, the small tributary vessels are cauterized to mobilize the artery, and a rubber dam is placed under the recipient vessel. A temporary aneurysm clip is placed at the proximal end of the STA, which is suture-ligated distally. The artery is cut free and irrigated with diluted heparin. If the artery is in vasospasm, a papaverine-soaked cottonoid is wrapped around the artery for a few minutes before proceeding. At this point, burst suppression is initiated under neurophysiological monitoring, and an intravenous heparin bolus of approximately 40 units per kilogram is administered to decrease the thrombosis risk. The distal 1 cm of the STA is dissected from the subcutaneous tissue by using microforceps and microscissors. A side cut is made in one side of the donor artery (fish-mouth incision) to increase the surface area for the anastomosis. Temporary aneurysm clips are placed proximally and distally to the anastomosis site on the recipient MCA vessel. An arteriotomy is made in the recipient vessel and extended with microscissors. Methylene blue is applied to clear the incision edges for anastomosis, and both donor and recipient vessels are flushed with heparinized saline. A 9-0 Prolene suture is used to anchor the heel and toe of the anastomosis followed by interrupted stitches along the interface. The temporary clips on the MCA and STA are released. Flow through both recipient and donor vessels is confirmed with Doppler ultrasound and indocyanine green administration. Any leaking areas of the anastomosis are identified and reinforced with further 9-0 Prolene interrupted stitches. Careful hemostasis is achieved with hemostatic agents, and the dura is reapproximated and tacked in place with stitches. The temporalis muscle fascia is reflected to the lower end of the brain surface, creating a dural muscular synangiosis. The lower part of the bone flap is removed to create a conduit for the STA and fixed with small plates to the superior end of the cranium, creating a hinge flap to ensure there are no bony obstructions to blood flow. Skin and subcutaneous tissues are closed, taking special care to avoid injury of the STA. Postoperatively, the patients are kept on 325 mg of aspirin for life. DISCUSSION Isolated vascular insufficiency secondary to stenosis or occlusion of the ICA without substantial cranial neuropathy is uncommon with CSMs. Only a handful of such cases have been reported in the literature.13-19 In a series of 1617 patients with skull base meningiomas reviewed by Komotar et al,19 the estimated incidence of ischemic presentation secondary to ICA stenosis or occlusion was only 0.19% (3 patients). Various authors have recommended aggressive surgical resection of the CSM to decompress the neurovascular structures.10-12 Moreover, some authors believe that ICA sacrifice is essential when addressing these lesions to achieve a gross total resection of the lesion and decrease the recurrence rate.10-12 However, these aggressive surgeries carry a substantial morbidity and mortality risk to the patients. DeMonte et al,20 O’Sullivan et al,21 and Nanda et al22 reported the postoperative incidence of new permanent cranial neuropathy was 18%, 12%, and 22%, respectively, among their patients. Moreover, De Jesús et al11 and Heth and Al-Mefty23 reported that 5% and 4% of their patients, respectively, developed postoperative cerebral infarction. DeMonte et al20 reported a mortality rate of 7% whereas Sindou et al7 had a 5% mortality rate in their series. Recent studies have allowed us to better understand CSMs and their behavior. Multiple studies have shown that meningiomas of the skull base tend to be low grade at higher rates than those distributed elsewhere throughout the meninges,1,24 possibly because of a distinct embryologic origin. The growth rate of incidentally discovered meningiomas ranges from 0.19 to 0.796 cm/year in the literature.25-28 It has been reported that the growth rate for skull base meningiomas is slower than the growth rate of meningiomas encountered in other locations.29,30 Interestingly, several studies have reported that CSMs tumor cells are deposited in the surrounding neurovascular structures.12,31,32 Thus, even if a gross total resection of the tumor was achieved, microscopic deposits would still be present on those structures, increasing the risk of recurrence. We agree with this hypothesis, which is supported by various studies that have reported a high recurrence rate of CSMs that underwent surgical resection. O’Sullivan et al21 reported a recurrence or progression rate of 13% at 2 yr, while DeMonte et al20 reported an 11% recurrence at a mean follow-up of 45 mo. De Jesús and colleagues11 reported 19% recurrence rate at 5-yr follow-up. The role of bypass surgery in skull base tumors is well established and recognized; however, with the recent advancements in medical management including chemotherapy and radiation therapy, the degree to which it is employed has substantially decreased. In contrast to other skull base tumors, skull base meningiomas have a tendency to invade the adjacent vasculature, necessitating vessel sacrifice to achieve a total surgical removal of the tumor.33 Therefore, many surgeons recommend leaving residual tumor on the invaded vessel, which can be addressed later by radiation therapy. Others, however, recommended vessel sacrifice and bypass in such cases to enable complete removal of the tumor and avoid the need for radiation therapy.12 In their experience with 44 skull base meningiomas in which cerebral revascularization was utilized, Sekhar et al34 achieved gross total removal in 31 patients, subtotal resection in 12 patients, and partial resection for 1 patient. In their series, only 1 patient experienced a recurrence in the total resection group while 3 patients had recurrence in the subtotal resection group. Additionally, Sekhar and Kalavakonda35 reported their experience with cerebral revascularization among 50 patients with aneurysms and 83 patients with skull base tumors. The authors reported an overall patency rate of 95.6%, with late graft patency of 94% from a graft occlusion 5 yr postoperatively. Their cerebral infarction rate was 17.3%, and a Glasgow Outcome Scale score of ≥4 was noted in 75.9% of patients. Various reports and studies have followed documenting the usefulness of cerebral revascularization in patients with skull base tumors.36 Considering the high operative risk, relatively benign natural history, and low malignant potential of CSMs, we have adopted a distinct approach to treating these tumors. We have previously reported our experience with symptomatic CSMs.5,37 We believe that these tumors should be addressed with debulking surgery followed by radiation therapy. We achieved satisfactory outcomes using this treatment modality in our patients with 95% tumor control rate at a mean follow-up of 27.6 mo.5 In accordance with our observation, Abdel-Aziz et al38 reported a significant reduction in ocular nerve dysfunction in patients with large sphenoid wing meningioma and secondary cavernous sinus involvement; the rate of ocular nerve dysfunction among their patients decreased from 55% to 16% despite using limited resection of only the lateral portion of the intracavernous tumor. Maruyama and colleagues39 reported a tumor control rate of 94.1% at 5 yr after combined nonradical surgery and radiosurgery. More recently, we have encountered a subgroup of patients with CSMs who demonstrate isolated vascular insufficiency without any substantial concurrent cranial neuropathy. Given the stability of the tumor in long-term follow-up for our patients, we attributed the presentation of vaso-occlusive symptoms to decreased cerebrovascular reserve as the patients aged, and perhaps slowly progressive carotid narrowing without appreciable overall tumor dimension change. This is supported by negative work-up for embolic cause or seizures and disappearance of symptoms after the bypass procedure in both patients. In such patients, we believe that addressing the vascular insufficiency with bypass grafting is optimal given the indolent behavior of the tumor and the high morbidity and mortality rate of surgery. The cases reported here further reinforce the viability of treating Hirsch grade III CSMs with isolated vascular insufficiency with bypass grafting. Whereas revascularization for difficult skull base tumors including CSMs is usually accompanied by partial or total resection of the lesion,5,7,11,20,21,23,36,37,39 in our 2 patients with CSM, bypass grafting alone dramatically improved their symptoms to complete or near resolution without perioperative morbidity. Furthermore, neither of these patients has had symptomatic disease progression in the follow-up interval (even without resection or radiotherapy), nor have their grafts failed. Symptoms associated with cortical deficits in particular were markedly improved. This experience suggests that vascular insufficiency can be an important contributing cause of neurological symptoms in these patients and that treatment focused on that, rather than the lesion itself, can be safe and effective. This approach of focusing treatment on the vascular supply should be balanced with the natural history of the tumor. Most CSMs are low grade and tend to be radiosensitive, but approximately 10% of skull base meningiomas are WHO grade II or III at initial diagnosis.1 These tumors are considerably less radiosensitive, and these patients may benefit from more aggressive treatment.40 Furthermore, even WHO grade I tumors can harbor subsequent mutations that could change their behavior significantly.11,41 Therefore, frequent radiological surveillance is essential among such patients to document stability of the lesion and patency of the graft. To the best of our knowledge, there are no reports on the management of Hirsch grade III CSMs with only bypass grafting without surgical resection. Our indications for bypass grafting are stable tumor and objective evidence of vascular insufficiency, without cranial neuropathy, in CSM patients who are suitable for revascularization. With a presentation of cranial neuropathy, a more aggressive approach is chosen with subtotal resection of the meningioma and decompression of the cavernous sinus to improve cranial nerve function5,37 Recent results indicate about one third of patients with oculomotor dysfunction from III or VI nerve paresis will improve with this technique (manuscript in preparation). Radiation therapy (stereotactic radiosurgery or radiotherapy) is performed if there is documented growth of residual tumor. In the uncommon instances in which there is recurrence after radiation therapy for a low-grade meningioma, aggressive surgical exenteration of the cavernous sinus is undertaken with high-flow interpositional bypass grafting.42 However, in the very unusual presentation of these patients in the present report, the flow augmentation procedure represents a lower risk option for symptom resolution given the lack of cranial nerve deficits at presentation. In general, our strategy for revascularization depends on patient age, the pathology, and the preoperative imaging findings. Flow-augmentation procedures are considered in patients presenting with signs and symptoms of decreased cerebrovascular reserve such as transient ischemic attacks. In these patients, we perform CTA and a CT perfusion study to define the area of decreased cerebrovascular reserve and the donor artery (STA) status. The usual donor vessels for these cases are either the STA (parietal branch, frontal branch, or both) or the occipital artery. Flow-replacement procedures, on the other hand, are considered for patients when surgical treatment entails a major blood vessel sacrifice, such as in giant aneurysms that cannot be otherwise treated or in some complex skull base tumors or infections.43 For these patients, we routinely perform clinical balloon test occlusion (BTO) combined with electroencephalography and CT perfusion with acetazolamide challenge study. Patient selection for the flow-replacement procedure is more complex. For malignant lesions, we replace the flow only when the patient fails the BTO; however, for benign lesions in patients with long life expectancy, we plan flow replacement regardless of the BTO results. For flow-replacement procedures, we use high-flow or intermediate-flow conduits, especially when the sacrificed artery is the ICA, or proximal MCA, or ACA. Intraoperatively, after completion of the anastomosis, the patency of the bypass is confirmed using indocyanine green videoangiography and Doppler ultrasonography for both flow-augmentation and flow-replacement procedures. Although flow-assisted revascularization techniques have been proven to be a useful intraoperative surgical adjunct more recently,44 it is probably more relevant to flow-replacement procedures than to flow-augmentation procedures. The senior author and others45 have used similar anatomic approaches rather than a flow-assisted approach for bypass procedures based on the caliber of the recipient artery and the extent of the vascular territory to be revascularized. Favorable outcomes have been reported compared with flow-assisted approaches.46,47 Finally, despite the advancements in endovascular techniques and their increased use in clinical practice, their utility in skull base tumor management remains limited to delineation of tumor vascularization, outlining the tumor's relationship to surrounding vasculature, and preoperative embolization of hypervascular lesions. Moreover, endovascular techniques are frequently employed in cases of iatrogenic vascular injury from skull base tumor surgery.48 Interestingly, recent reports on preoperative stenting for patients with paragangliomas and bilateral carotid body tumors have demonstrated great outcomes with minimal morbidity rates.49-51 Only 1 case of successful endovascular stenting of a high-grade cavernous ICA stenosis due to a medial sphenoid wing meningioma has been reported in the literature.52 Therefore, the role of endovascular techniques for flow augmentation in cases of vascular encasement and stenosis by skull base tumors (especially skull base meningiomas) remains unclear and should be investigated. CONCLUSION STA–MCA bypass grafting for CSMs infiltrating the cavernous ICA without substantial cranial neuropathy improved the neurological functions without risking the morbidity and mortality of cavernous sinus surgery. In our 2 cases, surgery was performed without perioperative complications and the vascular anastomoses have remained patent for the duration of follow-up. Symptomatic disease progression was not encountered in either patient, even without treatment of the tumor itself. We believe that once vascular insufficiency has been demonstrated in Hirsch grade III CSMs, patients may dramatically benefit from bypass grafting. CSMs present a unique clinical scenario where the high morbidity of resection and low risk of progression makes bypass grafting without tumor resection a potential surgical option. Disclosure The authors have no personal, financial, or institutional, interest in any of the drugs, materials, or devices described in this article. REFERENCES 1. Kane AJ , Sughrue ME , Rutkowski MJ et al. Anatomic location is a risk factor for atypical and malignant meningiomas . Cancer . 2011 ; 117 ( 6 ): 1272 – 1278 . Google Scholar CrossRef Search ADS PubMed 2. 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COMMENTS Specialists treating so-called cavernous sinus (CS) meningiomas are not so exceptionally confronted with the tumor invading and/or stenosing the internal carotid artery (ICA), although this rarely manifests by clinically patent symptoms of cerebrovascular insufficiency. The report by the authors of their experience of revascularization in 2 cases (that did not required surgical resection), can be useful to the neurosurgical community, not only when facing “quiescent“ tumors not necessitating surgical or radiotherapeutic treatment but also when dealing with surgical remnants encasing the ICA. At present there is a rather generally admitted consensus that CS meningiomas strictly enclosed within the limits of the (osteoperiosteal - dural) parasellar lodge be simply followed, and treated with stereotactic radiosurgery (SRS) or fractionated radiotherapy (FRt) if they grow. Regarding CS meningiomas with extension(s) outside the walls of the lodge, recommendations are to limit the resection to the extracavernous extension(s) only and leave in place the intracavernous portion. For remnant, there are 2 different policies: either immediate postoperative radiotherapy (RT) or simple survey and only RT if remnant grows on imaging. The later is our preference, as –according to our KM study at 15 years of follow-up –only 13% of the tumors with only extracavernous resection had remnant growing.1 For evaluating ICA stenosis and consequences on cerebral blood flow, like the authors, we do think that the pre-decisional work-up should include selective DSA to have optimal information, not only on the tumor vascularization but also on the intracranial arterial circulation (namely the supply by the anterior and posterior communicating arteries, and also by the external carotid anastomoses especially the one through the ophtalmic artery).2,3 As regards to the mode of revascularization, from our experience we think that the STA-cortical MCA anastomosis is sufficient to assure proper additional blood supply. Marc Sindou Lyon, France 1. 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 . CrossRef Search ADS PubMed 2. Nebbal M, Sindou M. Imaging for the management of cavernous sinus meningiomas . Neurochirurgie . 2008 ; 54 : 739 – 749 . CrossRef Search ADS PubMed 3. Sindou M, Nebbal M, Guclu B. Cavernous sinus meningiomas: imaging and surgical strategy . Adv Tech Stand Neurosurg . 2015 ; 42 : 103 – 121 . CrossRef Search ADS PubMed The authors describe a well-defined and cogent approach to this rare subset of patients with non-progressive meningiomas of the cavernous sinus and vascular insufficiency. Like the authors, I have found this to be quite a rare phenomenon. The improvement in flow and the resolution of symptoms attest to the success of this approach. Franco DeMonte Houston, Texas The authors report 2 cases of patients with Hirsch grade III cavernous sinus meningiomas presenting with vaso-occlusive symptoms but without cranial neuropathy. Given that the etiology of symptoms was decreased perfusion to the ipsilateral hemisphere, the authors performed low-flow extracranial-intracranial bypass to increase perfusion to the distal MCA. The 2 patients described had resolution of their clinical symptoms and follow-up imaging demonstrated bypass patency and stable tumor size throughout the duration of follow-up. Based on their experience, the authors propose considering symptoms due to vascular insufficiency separately from the oncologic problem of tumor burden. The options to manage cavernous sinus meningiomas include observation, radiation, or surgical resection with its associated morbidity. In the absence of cranial neuropathies or visual loss attributable to the lesion, most clinicians would not advocate for surgical resection. It stands to reason that patients presenting solely with symptoms attributable to vessel occlusion from these lesions would be likely to benefit from flow-augmentation with little to no additional benefit from surgical resection of the tumor. The documented success of this approach in treating this small number of patients may provide a guide for surgeons confronted with similar patients. These 2 patients had complete ICA occlusion, studies evaluating the utility of this approach in patients with decreased caliber of the ICA and concomitant decreased flow, but with maintained patency may be a useful next step. Angela M. Richardson Ricardo J. Komotar Miami, Florida Copyright © 2018 by the Congress of Neurological Surgeons This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices)
Operative Neurosurgery – Oxford University Press
Published: May 30, 2018
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