Endovascular stenting of the superior sagittal sinus to alleviate venous compression caused by a parasagittal meningioma

Abstract

Idiopathic intracranial hypertension (IIH) is a challenging disease with unclear pathophysiology. Recognition of venous sinus stenting to improve intracranial pressure is increasing.

We present a 56-year-old man diagnosed with IIH. A parasagittal meningioma abutting the sagittal sinus causing venous compression was found. Venous sinus stenting via endovascular approach using a WALLSTENT was performed. Intravascular pressures recorded after stenting demonstrated resolution of the pressure gradient.

The patient had no complications from the procedure and reported substantial symptomatic improvement. Subsequent ophthalmologic exam demonstrated resolution of the bilateral papilledema noted prior to stenting. Endovascular treatment of venous sinus stenosis in the treatment of IIH is an emerging technique. Treatment of venous compromise due to a mass lesion with stenting is a rarely described concept. For our patient, endovascular stenting was the primary treatment modality, allowing the tumour to be followed with serial imaging.

Background

Idiopathic intracranial hypertension (IIH) is a challenging diagnosis with unclear pathophysiology. Recognition of venous stenosis as a component of this pathology in more than 90% of patients—particularly at the transverse-sigmoid junction—has led to promising new treatments.^{1 2} After first being reported in 2002, venous sinus stenting has been increasingly used in the management of IIH secondary to intracranial sinus stenosis.³ The consequence of venous sinus stenosis is poorly understood, as it is unclear whether venous congestion seen is the origin or result of IIH. Nevertheless, stenting of the transverse sinus has been gaining momentum as an alternative or even adjunct to surgery.^{1 2}

In this case report, we present a patient with an initial diagnosis of IIH. However, more thorough investigation revealed a parasagittal meningioma abutting the superior sagittal sinus (SSS) causing venous compression, with resultant increased intracranial pressure. We consider this to be a separate entity from IIH, but rather intracranial hypertension secondary to venous sinus compression. Stenting of the SSS resulted in resolution of the patient’s headaches and papilledema.

Case presentation

A 56-year-old man presented with IIH after his ophthalmologist noted papilledema on exam. Lumbar puncture revealed an opening pressure of 30 mm Hg, and despite acetazolamide therapy he continued to have worsening optic nerve oedema and headaches. Outpatient MRI demonstrated a 1.7 cm lesion in the right posterior parafalcine region, consistent with meningioma (figure 1A).

Figure 1.

(A) Sagittal T1+C MRI showing tumour location adjacent to the distal one-third of the superior sagittal sinus; (B) full skull and (C) zoomed in reconstructions using Brainlab software (Medtronic) showing a lesion (green) in the left occipital region compressing the superior sagittal sinus (purple).

Though initially referred for cerebrospinal fluid diversion, angiographic evaluation with CT confirmed venous compression of the posterior portion of the SSS (figure 1B, C). At our suggestion, he underwent venous sinus stenting via endovascular approach, though discussion was held that if unsuccessful in improving his papilledema he may need a ventriculoperitoneal shunt to relieve intracranial pressure.

Treatment

Prior to surgery, the patient was started on a full-dose (325 mg) daily aspirin for 7 days. Platelet function assay with epinephrine revealed a suitable response to antiplatelet therapy. The case was performed under conscious sedation. A standard 3 vessel arterial catheter angiogram was performed first to confirm stenosis of the SSS due to the tumour and to obtain preliminary measurements to aid in stent selection (figure 2A). Next, access to the venous system was obtained via a 6F 10 cm sheath in the left femoral vein. The patient was heparinised, with appropriate activated clotting time achieved. A 6F Envoy guide catheter (Codman Neurovascular) was advanced to the transverse-sigmoid sinus junction over a 0.35’ Glidewire (Terumo). A Prowler 0.027 catheter (Codman Neurovascular) was guided into the SSS proximal to the tumour over a Traxcess EX 0.014’ microwire (Microvention). A venous angiogram of the SSS was performed by injecting 8 mL of contrast through the microcatheter (figure 1B). A Compass pressure transducer (Centurion Medical) was connected to the microcatheter to record the pressure of the SSS proximal and distal to the tumour. The pressure in the SSS proximal to the tumour was 42 cm H₂O and 32 cm H₂O distal to the tumour, suggesting that the obstruction in the SSS was haemodynamically significant (figure 3A). The microwire was then advanced back into the proximal SSS and connected to its docking wire and the microcatheter was then removed. An 8×21 mm Carotid WALLSTENT (Boston Scientific) was then deployed across the stenotic segment of the SSS (figure 2B). A post-stent angioplasty was performed with a 7×20 mm Sterling Monorail Balloon Catheter (Boston Scientific). The Prowler 0.027 inch microcatheter was then advanced back through the stent over the microwire in order to perform a follow-up venous angiogram of the stent showing no significant residual stenosis. Intravascular pressures recorded after stenting demonstrated resolution of the pressure gradient across the previously stenotic segment with pressures both proximal and distal to the stent measuring 30 cm H₂O (figure 3B).

Figure 2.

(A) Arterial phase angiogram confirming stenosis of the superior sagittal sinus by the lesion (dotted white circle); (B) deployment of Carotid WALLSTENT (Boston Scientific; black outline) along stenotic portion, prior to angioplasty; (C) CT angiography 3 months after stenting demonstrating patency of the stent.

Figure 3.

(A) Venous angiogram showing stenosis of the superior sagittal sinus due to mass effect of the tumour (white arrow); (B) venous angiogram after stenting demonstrating improvement in the degree of stenosis.

Outcome and follow-up

The patient had no complications from the procedure. He continued taking a full-dose aspirin for 6 months, after which he was continued on 81 mg of aspirin daily. He reported substantial improvement of his headaches and blurry vision by his 1 month follow-up appointment. A subsequent ophthalmologic exam 2 months poststenting demonstrated resolution of the previously noted bilateral papilledema. CT angiography 3 months after the procedure showed a widely patent stent (figure 2C).

Discussion

The endovascular treatment of venous sinus stenosis in the treatment of IIH is an emerging technique. Our patient suffered from intracranial hypertension secondary to venous sinus stenosis caused by a meningioma. Dural venous sinus distortion has shown to increase intracranial pressures in dynamic models.⁴ In patients with a demonstrated venous sinus stenosis and physiologic pressure gradient, stenting can lead to symptomatic relief.⁵ In this scenario, we were faced with a patient with visible angiographic compression causing a similar clinical scenario, with headaches, papilledema and visual loss in the absence of other neurological compromise.

Though treatment of venous compromise with stenting is not a novel concept in neoplasm treatment,⁶ similar treatment of increased intracranial pressures and papilledema resulting from a lesion compressing an intracranial venous sinus has been rarely described. In the previous report, a similarly sized (1.7 cm) parasagittal meningioma—also located along the posterior third of the SSS—was treated by stenting of the stenotic portion. The patient’s headaches and visual symptoms subsequently resolved.

Similarly, another report notes a meningioma that was resected multiple times and treated with radiotherapy. Ultimately, the patient developed extensive venous outflow obstruction secondary to cerebral oedema due to radiation-induced cell necrosis. Endovascular stenting of the transverse sinus was able to relieve the patient’s symptomatology.⁷

In our case, endovascular stenting was used as the primary treatment in order to symptomatically manage an otherwise benign lesion, allowing the tumour to be followed with serial imaging. Furthermore, resection alone may not resolve the sinus stenosis. If the surgery is required in the future, the stent may act as a landmark and scaffold for identification and reconstruction of the SSS.

The option of treating venous congestion secondary to an intracranial lesion in this manner provides an option to providers who are met with lesions near vital structures or derived from the venous sinus dural leaflets.⁸ In addition, given the increasing use of radiotherapy to treat meningiomas near the venous sinuses and the consequent risk for oedema secondary to cell necrosis,⁷ stenting may become an increasingly useful option.

Thorough work-up of any visual deficit should be completed before attributing symptoms to IIH. In this case, venous compression due to a parasagittal meningioma was found to be the cause of elevated intracranial pressure and was successfully treated via endovascular stenting of the SSS.

One particular limitation to note is that this treatment did not address the meningioma itself. It is uncommon for small meningiomas to compress the venous sinus system, or cause a pressure gradient such as this. Our patient’s lesion did not grow in size, but if it had there would be the additional task of performing open cranial surgery for tumour resection on a patient who required aspirin therapy for the stent. Pursing this treatment path requires ample discussion with the patient regarding the risks, especially if the lesion should grow, prior to stenting of the compressed sinus.

Learning points.

• Patients with idiopathic intracranial hypertension (IIH) should have a full work-up to rule out mass effect as a cause for increased intracranial pressure.

• Stenting of venous sinus stenosis can be a useful adjunct in the management of IIH.

• Venous compromise caused by mass effect resulting in increased intracranial pressure can be effectively managed with sinus stenting.