Supracerebellar infratentorial resection of a torcular lesion causing fulminant intracranial hypertension: illustrative case

Jonathan Dallas Department of Neurological Surgery, Keck School of Medicine, University of Southern California, Los Angeles, California

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Jessica R Lane Department of Neurological Surgery, Virginia Commonwealth University School of Medicine, Richmond, Virginia

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Benjamin S Hopkins Department of Neurological Surgery, Keck School of Medicine, University of Southern California, Los Angeles, California

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Melinda Chang Division of Ophthalmology, Children’s Hospital Los Angeles, Los Angeles, California

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Mark Borchert Division of Ophthalmology, Children’s Hospital Los Angeles, Los Angeles, California

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Nestor R Gonzalez Department of Neurological Surgery, Cedars-Sinai Medical Center, Los Angeles, California; and

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Peter A Chiarelli Department of Neurological Surgery, Keck School of Medicine, University of Southern California, Los Angeles, California
Department of Surgery, Division of Neurological Surgery, Children’s Hospital Los Angeles, Los Angeles, California

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Jason K Chu Department of Neurological Surgery, Keck School of Medicine, University of Southern California, Los Angeles, California
Department of Surgery, Division of Neurological Surgery, Children’s Hospital Los Angeles, Los Angeles, California

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BACKGROUND

Venous sinus stenosis has been implicated in intracranial hypertension and can lead to papilledema and blindness. The authors report the unique case of a cerebellar transtentorial lesion resulting in venous sinus stenosis in the torcula and bilateral transverse sinuses that underwent resection.

OBSERVATIONS

A 5-year-old male presented with subacute vision loss and bilateral papilledema. Imaging demonstrated a lesion causing mass effect on the torcula/transverse sinuses and findings of increased intracranial pressure (ICP). A lumbar puncture confirmed elevated pressure, and the patient underwent bilateral optic nerve sheath fenestration. Cerebral angiography and venous manometry showed elevated venous sinus pressures suggestive of venous hypertension. The patient underwent a craniotomy and supracerebellar/infratentorial approach. A stalk emanating from the cerebellum through the tentorium was identified and divided. Postoperative magnetic resonance imaging showed decreased lesion size and improved sinus patency. Papilledema resolved and other findings of elevated ICP improved. Pathology was consistent with atrophic cerebellar cortex. Serial imaging over 6 months demonstrated progressive decrease in the lesion with concurrent improvements in sinus patency.

LESSONS

Although uncommon, symptoms of intracranial hypertension in patients with venous sinus lesions should prompt additional workup ranging from dedicated venous imaging to assessments of ICP and venous manometry.

ABBREVIATIONS

CSF = cerebrospinal fluid; EVD = external ventricular drain; ICP = intracranial pressure; IIH = idiopathic intracranial hypertension; MRI = magnetic resonance imaging; ONSF = optic nerve sheath fenestration

BACKGROUND

Venous sinus stenosis has been implicated in intracranial hypertension and can lead to papilledema and blindness. The authors report the unique case of a cerebellar transtentorial lesion resulting in venous sinus stenosis in the torcula and bilateral transverse sinuses that underwent resection.

OBSERVATIONS

A 5-year-old male presented with subacute vision loss and bilateral papilledema. Imaging demonstrated a lesion causing mass effect on the torcula/transverse sinuses and findings of increased intracranial pressure (ICP). A lumbar puncture confirmed elevated pressure, and the patient underwent bilateral optic nerve sheath fenestration. Cerebral angiography and venous manometry showed elevated venous sinus pressures suggestive of venous hypertension. The patient underwent a craniotomy and supracerebellar/infratentorial approach. A stalk emanating from the cerebellum through the tentorium was identified and divided. Postoperative magnetic resonance imaging showed decreased lesion size and improved sinus patency. Papilledema resolved and other findings of elevated ICP improved. Pathology was consistent with atrophic cerebellar cortex. Serial imaging over 6 months demonstrated progressive decrease in the lesion with concurrent improvements in sinus patency.

LESSONS

Although uncommon, symptoms of intracranial hypertension in patients with venous sinus lesions should prompt additional workup ranging from dedicated venous imaging to assessments of ICP and venous manometry.

ABBREVIATIONS

CSF = cerebrospinal fluid; EVD = external ventricular drain; ICP = intracranial pressure; IIH = idiopathic intracranial hypertension; MRI = magnetic resonance imaging; ONSF = optic nerve sheath fenestration

Obstruction of the torcula can cause elevated intracranial pressure (ICP) secondary to venous hypertension. Some patients develop symptoms of idiopathic intracranial hypertension (IIH) and can progress to papilledema and blindness.1–5 Arachnoid granulations and herniation of cerebral tissue into the venous sinuses have also been reported as rare and benign phenomena, with most patients being asymptomatic.6–13

We describe the case of a pediatric patient with symptomatic intracranial hypertension from the herniation of ectopic cerebellar tissue into the dural venous sinuses. This resulted in stenosis of the torcula and bilateral transverse sinuses. Resection led to improvement in ICP and patency of the venous sinuses.

Illustrative Case

A 5-year-old male presented with 3 weeks of progressive vision loss and intermittent headaches. He was evaluated by ophthalmology and noted to have bilateral papilledema with visual acuity of 20/400 in the right eye and no light perception in the left.

Magnetic resonance imaging (MRI) and magnetic resonance venography were notable for a nonenhancing, T1-hypointense, T2-hyperintense lesion causing mass effect on the torcula and bilateral transverse sinuses that was interpreted as a prominent arachnoid granulation (Fig. 1A–D). Other radiological findings suggestive of increased ICP were present, including papilledema, tortuous optic nerves, and pituitary flattening. The presumptive diagnosis was IIH/pseudotumor cerebri syndrome.

FIG. 1
FIG. 1

Preoperative MRI of the torcula/transverse sinus lesion shown on sagittal (A) and axial (B) T2-weighted and sagittal (C) and axial (D) postcontrast T1-weighted sequences. A transtentorial lesion from the cerebellum is identified (solid arrow) resulting in stenosis of the torcula and bilateral transverse sinuses (dotted arrows). Diagnostic angiographic images, anteroposterior (AP) venous phase (E) and lateral venous phase (F), demonstrating venous sinus stenosis at the torcula and bilateral transverse sinuses. Venous manometry confirmed a pressure gradient suggestive of venous hypertension.

Although the presumptive diagnosis was IIH, an infiltrative ophthalmological process was also considered. Furthermore, it was unclear whether the patient’s torcular lesion was incidental or related to his visual deficits. To diagnostically confirm elevated ICP, a lumbar puncture was performed and confirmed elevated pressure (41 cmH2O). During the same operative session, an emergent optic nerve sheath fenestration (ONSF) was also performed. The patient was started on acetazolamide postoperatively.

To determine if the torcular lesion was contributing to venous hypertension, the patient underwent cerebral angiography with venous manometry. This indicated a pressure gradient >20 mm Hg across the lesion (Table 1, Fig. 1E and F). Options for endovascular therapy and/or stenting were discussed but avoided given the patient’s age and need for antiplatelet agents. On detailed review of the imaging, a transtentorial connection from the lesion to the dorsal aspect of the cerebellar hemispheres was identified (Fig. 1A–D).

TABLE 1

Pressure gradients found on venous manometry during diagnostic angiography

LocationPressure Gradient
Rt—Rt Jugular (mm Hg)Lt—Lt Jugular (mm Hg)
Superior sagittal sinus—cephalic*21–630–8
Superior sagittal sinus—caudal*21–631–8
Torcula*26–631–8
Cephalic transverse sinus*26–630–8
Mid transverse sinus*26–621–9
Transverse-sigmoid junction7–66–9
Sigmoid sinus7–66–8

Above the lesion.

Below the lesion.

The patient underwent suboccipital craniotomy and a supracerebellar infratentorial approach to the lesion. An external ventricular drain (EVD) was placed with an opening pressure of >40 cmH2O. The EVD was placed for both posterior fossa dural protection/cerebrospinal fluid (CSF) leakage prevention and to obtain objective ICP measurements postoperatively. After dural opening, a stalk was seen emanating from the dorsal cerebellum and ascending through a midline tentorial defect; this stalk appeared to consist largely of cerebellar tissue with small overlying vessels. This tissue was soft but large enough that it could not be compressed entirely with Weck clips or suture ligation. After placement of the Weck clips, the stalk was fully cauterized and divided. A portion was also sent for pathological evaluation. The tentorial defect was occluded with Gelfoam and Tisseel. The dura was closed with a watertight expansile duraplasty. The bone was replaced, and the incision was closed (Fig. 2A and B, Video 1). Permanent pathological analysis revealed atrophic cerebellar cortex.

FIG. 2
FIG. 2

Intraoperative photographs from a supracerebellar infratentorial approach to the lesion. A stalk was seen emerging from the dorsal aspect of the cerebellum (arrow) and entering a tentorial defect into the torcula (A). The lesion was isolated and divided and the tentorial occluded with Gelfoam and Tisseel (B).

VIDEO 1. Clip showing the suboccipital craniotomy and supracerebellar/infratentorial approach for resection of the patient’s torcular lesion. HPI = history of present illness. Click here to view.

Of note, the procedure was considered a moderate- to high-risk procedure, primarily given the proximity of the lesion to the venous sinuses. Although most of the risks were similar to those of a standard suboccipital craniotomy/posterior fossa approach, specific risks were believed to include 1) venous hemorrhage given the lesion’s involvement with the torcula/venous sinuses, 2) venous infarction given a possible risk of venous sinus injury, and 3) postoperative CSF leakage and wound healing complications given the patient’s known history of elevated ICP.

Postoperative MRI showed a decrease in the size of the lesion and the amount of mass effect on the torcula/transverse sinuses (Fig. 3A and B). Other radiological findings associated with intracranial hypertension also improved. The patient’s EVD was initially left open to drain at 10 cmH2O for approximately 5 days for a combination of ICP control and wound healing. The EVD was then iteratively weaned beginning on postoperative day 6 and was clamped on postoperative day 8. The drain was left clamped for 48 hours to ensure that the patient’s ICP had normalized, and it was ultimately removed on postoperative day 10 (Fig. 4). The patient had improvement of papilledema on serial ophthalmological examinations, although his vision remained poor.

FIG. 3
FIG. 3

Sagittal postcontrast T1-weighted MRI from preoperatively (A) to postoperative day 1 (B), postoperative day 149 (C), and approximately 1 year postoperatively (D). Postoperatively, the patient’s lesion demonstrated a progressive decrease in size with associated improvement in venous sinus patency through the torcula and transverse sinuses.

FIG. 4
FIG. 4

Average ICP and standard deviation values averaged over 24 hours. There was normalization of ICP immediately postoperatively, and it remained within the normal range throughout the patient’s immediate postoperative course. POD = postoperative day.

After discharge, the patient was followed up by ophthalmology and neurosurgery, with serial imaging demonstrating a progressive decrease in the size of the lesion over 1 year (Fig. 3A–D). He remained legally blind at his approximately 1-year ophthalmological examination with visual acuity of 20/200 in the right eye and light perception in the left eye. His papilledema had resolved, but he had significant optic atrophy and gliosis due to prior optic disc edema. He was referred for low vision services including Braille education.

Patient Informed Consent

The necessary patient informed consent was obtained in this study.

Discussion

Observations

Dural venous sinus stenosis and venous hypertension are well-documented causes of intracranial hypertension. The resolution of intracranial hypertension involves addressing the primary lesion. Common causes include tumors or sinus thrombosis. Cases of large arachnoid granulations into the dural venous sinuses have also been reported; however, this is uncommon and rarely symptomatic.14 One report has described a large vermiform arachnoid granulation 6 cm in length, although this was an incidental finding.9 A second report described a patient with symptoms of IIH who had an arachnoid granulation causing a large sinus pressure gradient (16 cmH2O). Venous stenting of this lesion led to symptomatic improvement.13 The herniation of brain tissue into an arachnoid granulation has also been reported but is believed to be both rare and typically asymptomatic.8,10,15

Venous manometry provided objective evidence of venous hypertension secondary to dural venous sinus stenosis from the lesion. There is growing evidence of a relationship between venous sinus stenosis and IIH/pseudotumor cerebri syndrome. One study found a bilateral transverse sinus stenosis rate of 94% among patients with IIH; this rate was only 3% in the control population.16 Furthermore, manometry performed in a group of patients with IIH found elevated sinus pressure in each patient with an average pressure gradient of 13.3 mm Hg.17 A recent review found that venous sinus stenting for IIH showed headache improvement in 81% of cases, papilledema improvement in 90% of cases, and a sinus pressure gradient decrease from 18.5 to 3.2 mm Hg.18

Venous stenting is an uncommon procedure for pediatric patients. One study assessed 8 pediatric patients with IIH undergoing stenting; 7/8 patients had symptomatic improvement, and 4/4 had resolution of papilledema.15 In a second study of 14 pediatric patients with IIH, 4/5 had resolution of papilledema.19 In our patient, venous sinus stenting was believed to be an unfavorable treatment option given the size of the lesion and extension from the torcula through the bilateral transverse sinuses. Furthermore, there are severe potential long-term complications of stent placement in pediatric and younger aged patients. Not only are long-term stents at risk for thrombosis or stent fracture, but it is theoretically possible for a child to outgrow the stent in place.20,21 Furthermore, the risks of long-term antiplatelet medication in children have not been studied thoroughly.

The exact nature of our patient’s lesion remains somewhat debatable, although it is believed most likely to reflect a cerebellar meningoencephalocele with extension into the torcula. On MRI, a midline stalk can be seen connecting the posterior fossa to the lesion. The fluid signal inside the lesion matches the CSF signal on MRI, thus suggesting a meningocele. Furthermore, the pathological findings of atrophic cerebellar cortex and intraoperative visualization of the lesion would suggest that a portion of atrophic tissue from the cerebellar cortex had extended through the midline stalk, resulting in a meningoencephalocele. Interestingly, although the lesion itself is extrinsic to the actual sinus and there did not appear to be direct violation of the wall, the radiographic pattern of stenosis does appear to be more consistent with intraluminal stenosis as opposed to purely extrinsic compression. The diagnosis of a meningoencephalocele is further supported by the decrease in the size of the lesion over time after division. Although it is not entirely clear, we hypothesize that division of the stalk resulted in isolation of the meningoencephalocele and that the CSF in this space was ultimately reabsorbed over time. Tissue ischemia of the meningoencephalocele after division may also play a role in progressive resolution.

Unfortunately, our patient’s vision remains poor. Although his papilledema has improved, the resolution of papilledema does not always result in improved vision, especially when the edema is severe or long-standing.22 It has been suggested that the degree of visual deficit at presentation is the largest predictor of posttreatment vision; this patient was largely blind at presentation.23 Furthermore, in cases of fulminant IIH, treatment is ideally provided on the order of hours to days.24 Thus, in a patient with 3 weeks of visual deficit, visual prognosis remains unfavorable.

Lessons

We describe a unique pediatric patient with a cerebellar herniation intruding the torcula presenting with vision loss, papilledema, and elevated ICP. Venous hypertension was resultant from stenosis of the torcula and bilateral transverse sinuses, and a large pressure gradient was found across the lesion on venous manometry. Medical therapy and ONSF stabilized but failed to improve the patient’s vision, and he underwent lesion resection with the normalization of ICP, venous sinus patency, and improvement in papilledema. Based on imaging, pathological findings, and intraoperative visualization, the lesion was believed to best be characterized as a cerebellar meningoencephalocele.

There are multiple takeaways from this case. First, whereas most lesions of the venous sinuses/torcula appear to be asymptomatic (both in the literature and in our experience), there is a subset of lesions that causes hemodynamically significant stenosis and resultant symptoms. Thus, when there is clinical suspicion for elevated ICP or associated symptoms, a complete workup is indicated. Ideally, this would include both 1) an objective measurement of elevated ICP (i.e., via EVD or lumbar puncture) and 2) venous manometry to assess the hemodynamic significance of the stenotic lesion. Finally, this case highlights the urgent nature of fulminant IIH/elevated ICP with regard to visual outcome. Although this patient’s visual prognosis is likely poor secondary to the duration of symptoms prior to presentation, urgent workup and intervention should still be provided to maximize visual outcomes.

Author Contributions

Conception and design: Dallas, Borchert, Gonzalez, Chiarelli, Chu. Acquisition of data: Dallas, Lane, Chang, Borchert, Gonzalez, Chu. Analysis and interpretation of data: Dallas, Lane, Chang, Gonzalez, Chiarelli, Chu. Drafting the article: Dallas, Lane, Gonzalez. Critically revising the article: Dallas, Lane, Chang, Borchert, Gonzalez, Chiarelli, Chu. Reviewed submitted version of manuscript: Dallas, Hopkins, Chang, Borchert, Gonzalez, Chiarelli, Chu. Approved the final version of the manuscript on behalf of all authors: Dallas. Administrative/technical/material support: Hopkins Study supervision: Borchert, Chu.

Supplemental Information

Videos

Video 1. https://vimeo.com/884420770.

References

  • 1

    Ball AK, Clarke CE. Idiopathic intracranial hypertension. Lancet Neurol. 2006;5(5):433442.

  • 2

    Kesler A, Fattal-Valevski A. Idiopathic intracranial hypertension in the pediatric population. J Child Neurol. 2002;17(10):745748.

  • 3

    Agarwal MR, Yoo JH. Optic nerve sheath fenestration for vision preservation in idiopathic intracranial hypertension. Neurosurg Focus. 2007;23(5):E7.

  • 4

    Shaia JK, Elzie C. Acute presentation of idiopathic intracranial hypertension with severe vision deficits. SAGE Open Medical Case Rep. 2020;8:2050313X2094557.

  • 5

    Gurney S, Ramalingam S, Thomas A, Sinclair A, Mollan S. Exploring the current management idiopathic intracranial hypertension, and understanding the role of dural venous sinus stenting. Eye Brain. 2020;12:113.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 6

    Arjona A, Delgado F, Fernandez-Romero E. Intracranial hypertension secondary to giant arachnoid granulations. J Neurol Neurosurg Psychiatry. 2003;74(4):418.

  • 7

    Choi HJ, Cho CW, Kim YS, Cha JH. Giant arachnoid granulation misdiagnosed as transverse sinus thrombosis. J Korean Neurosurg Soc. 2008;43(1):4850.

  • 8

    Karatag O, Cosar M, Kizildag B, Sen HM. Dural sinus filling defect: intrasigmoid encephalocele. BMJ Case Rep. 2013;bcr2013201616-bcr2013201616.

  • 9

    Mamaliga T, Hadi M. An unusual vermiform giant arachnoid granulation. Radiol Case Rep. 2019;14(12):15251528.

  • 10

    Malekzadehlashkariani S, Wanke I, Rüfenacht DA, San Millán D. Brain herniations into arachnoid granulations: about 68 cases in 38 patients and review of the literature. Neuroradiology. 2016;58(5):443457.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 11

    Park H, Lim GY, Eom TH. Giant arachnoid granulation in a child with benign intracranial hypertension: an unusual case. Childs Nerv Syst. 2018;34(12):25252527.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 12

    Roche J, Warner D. Arachnoid granulations in the transverse and sigmoid sinuses: CT, MR, and MR angiographic appearance of a normal anatomic variation. AJNR Am J Neuroradiol. 1996;17(4):677683.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 13

    Zheng H, Zhou M, Zhao B, Zhou D, He L. Pseudotumor cerebri syndrome and giant arachnoid granulation: treatment with venous sinus stenting. J Vasc Interv Radiol. 2010;21(6):927929.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 14

    Battal B, Hamcan S, Akgun V, et al. Brain herniations into the dural venous sinus or calvarium: MRI findings, possible causes and clinical significance. Eur Radiol. 2016;26(6):17231731.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 15

    Liebo GB, Lane JJI, Van Gompel JJ, Eckel LJ, Schwartz KM, Lehman VT. Brain herniation into arachnoid granulations: clinical and neuroimaging features. J Neuroimaging. 2016;26(6):592598.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 16

    Morris PP, Black DF, Port J, Campeau N. Transverse sinus stenosis is the most sensitive MR imaging correlate of idiopathic intracranial hypertension. AJNR Am J Neuroradiol. 2017;38(3):471477.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 17

    King JO, Mitchell PJ, Thomson KR, Tress BM. Cerebral venography and manometry in idiopathic intracranial hypertension. Neurology. 1995;45(12):22242228.

  • 18

    Teleb MS, Cziep ME, Lazzaro MA, et al. Idiopathic intracranial hypertension. A systematic analysis of transverse sinus stenting. Intervent Neurol. 2013;2(3):132143.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 19

    Lee KE, Zehri A, Soldozy S, et al. Dural venous sinus stenting for treatment of pediatric idiopathic intracranial hypertension. J Neurointerv Surg. 2021;13(5):465470.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 20

    Alexy RD, Levi DS. Materials and manufacturing technologies available for production of a pediatric bioabsorbable stent. Biomed Res Int. 2013;2013:137985.

  • 21

    Nia NV, Fishbein GA, Levi DS. Can a self-expanding pediatric stent expand with an artery? Relationship of stent design to vascular biology. Catheter Cardiovasc Interv. 2021;98(1):139147.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 22

    Chagot C, Blonski M, Machu JL, Bracard S, Lacour JC, Richard S. Idiopathic intracranial hypertension: prognostic factors and multidisciplinary management. J Obes. 2017;2017:5348928.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 23

    Takkar A, Goyal MK, Bansal R, Lal V. Clinical and neuro-ophthalmologic predictors of visual outcome in idiopathic intracranial hypertension. Neuroophthalmology. 2018;42(4):201208.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 24

    Mollan SP, Davies B, Silver NC, et al. Idiopathic intracranial hypertension: consensus guidelines on management. J Neurol Neurosurg Psychiatry. 2018;89(10):10881100.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • Collapse
  • Expand
  • FIG. 1

    Preoperative MRI of the torcula/transverse sinus lesion shown on sagittal (A) and axial (B) T2-weighted and sagittal (C) and axial (D) postcontrast T1-weighted sequences. A transtentorial lesion from the cerebellum is identified (solid arrow) resulting in stenosis of the torcula and bilateral transverse sinuses (dotted arrows). Diagnostic angiographic images, anteroposterior (AP) venous phase (E) and lateral venous phase (F), demonstrating venous sinus stenosis at the torcula and bilateral transverse sinuses. Venous manometry confirmed a pressure gradient suggestive of venous hypertension.

  • FIG. 2

    Intraoperative photographs from a supracerebellar infratentorial approach to the lesion. A stalk was seen emerging from the dorsal aspect of the cerebellum (arrow) and entering a tentorial defect into the torcula (A). The lesion was isolated and divided and the tentorial occluded with Gelfoam and Tisseel (B).

  • FIG. 3

    Sagittal postcontrast T1-weighted MRI from preoperatively (A) to postoperative day 1 (B), postoperative day 149 (C), and approximately 1 year postoperatively (D). Postoperatively, the patient’s lesion demonstrated a progressive decrease in size with associated improvement in venous sinus patency through the torcula and transverse sinuses.

  • FIG. 4

    Average ICP and standard deviation values averaged over 24 hours. There was normalization of ICP immediately postoperatively, and it remained within the normal range throughout the patient’s immediate postoperative course. POD = postoperative day.

  • 1

    Ball AK, Clarke CE. Idiopathic intracranial hypertension. Lancet Neurol. 2006;5(5):433442.

  • 2

    Kesler A, Fattal-Valevski A. Idiopathic intracranial hypertension in the pediatric population. J Child Neurol. 2002;17(10):745748.

  • 3

    Agarwal MR, Yoo JH. Optic nerve sheath fenestration for vision preservation in idiopathic intracranial hypertension. Neurosurg Focus. 2007;23(5):E7.

  • 4

    Shaia JK, Elzie C. Acute presentation of idiopathic intracranial hypertension with severe vision deficits. SAGE Open Medical Case Rep. 2020;8:2050313X2094557.

  • 5

    Gurney S, Ramalingam S, Thomas A, Sinclair A, Mollan S. Exploring the current management idiopathic intracranial hypertension, and understanding the role of dural venous sinus stenting. Eye Brain. 2020;12:113.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 6

    Arjona A, Delgado F, Fernandez-Romero E. Intracranial hypertension secondary to giant arachnoid granulations. J Neurol Neurosurg Psychiatry. 2003;74(4):418.

  • 7

    Choi HJ, Cho CW, Kim YS, Cha JH. Giant arachnoid granulation misdiagnosed as transverse sinus thrombosis. J Korean Neurosurg Soc. 2008;43(1):4850.

  • 8

    Karatag O, Cosar M, Kizildag B, Sen HM. Dural sinus filling defect: intrasigmoid encephalocele. BMJ Case Rep. 2013;bcr2013201616-bcr2013201616.

  • 9

    Mamaliga T, Hadi M. An unusual vermiform giant arachnoid granulation. Radiol Case Rep. 2019;14(12):15251528.

  • 10

    Malekzadehlashkariani S, Wanke I, Rüfenacht DA, San Millán D. Brain herniations into arachnoid granulations: about 68 cases in 38 patients and review of the literature. Neuroradiology. 2016;58(5):443457.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 11

    Park H, Lim GY, Eom TH. Giant arachnoid granulation in a child with benign intracranial hypertension: an unusual case. Childs Nerv Syst. 2018;34(12):25252527.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 12

    Roche J, Warner D. Arachnoid granulations in the transverse and sigmoid sinuses: CT, MR, and MR angiographic appearance of a normal anatomic variation. AJNR Am J Neuroradiol. 1996;17(4):677683.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 13

    Zheng H, Zhou M, Zhao B, Zhou D, He L. Pseudotumor cerebri syndrome and giant arachnoid granulation: treatment with venous sinus stenting. J Vasc Interv Radiol. 2010;21(6):927929.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 14

    Battal B, Hamcan S, Akgun V, et al. Brain herniations into the dural venous sinus or calvarium: MRI findings, possible causes and clinical significance. Eur Radiol. 2016;26(6):17231731.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 15

    Liebo GB, Lane JJI, Van Gompel JJ, Eckel LJ, Schwartz KM, Lehman VT. Brain herniation into arachnoid granulations: clinical and neuroimaging features. J Neuroimaging. 2016;26(6):592598.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 16

    Morris PP, Black DF, Port J, Campeau N. Transverse sinus stenosis is the most sensitive MR imaging correlate of idiopathic intracranial hypertension. AJNR Am J Neuroradiol. 2017;38(3):471477.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 17

    King JO, Mitchell PJ, Thomson KR, Tress BM. Cerebral venography and manometry in idiopathic intracranial hypertension. Neurology. 1995;45(12):22242228.

  • 18

    Teleb MS, Cziep ME, Lazzaro MA, et al. Idiopathic intracranial hypertension. A systematic analysis of transverse sinus stenting. Intervent Neurol. 2013;2(3):132143.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 19

    Lee KE, Zehri A, Soldozy S, et al. Dural venous sinus stenting for treatment of pediatric idiopathic intracranial hypertension. J Neurointerv Surg. 2021;13(5):465470.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 20

    Alexy RD, Levi DS. Materials and manufacturing technologies available for production of a pediatric bioabsorbable stent. Biomed Res Int. 2013;2013:137985.

  • 21

    Nia NV, Fishbein GA, Levi DS. Can a self-expanding pediatric stent expand with an artery? Relationship of stent design to vascular biology. Catheter Cardiovasc Interv. 2021;98(1):139147.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 22

    Chagot C, Blonski M, Machu JL, Bracard S, Lacour JC, Richard S. Idiopathic intracranial hypertension: prognostic factors and multidisciplinary management. J Obes. 2017;2017:5348928.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 23

    Takkar A, Goyal MK, Bansal R, Lal V. Clinical and neuro-ophthalmologic predictors of visual outcome in idiopathic intracranial hypertension. Neuroophthalmology. 2018;42(4):201208.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 24

    Mollan SP, Davies B, Silver NC, et al. Idiopathic intracranial hypertension: consensus guidelines on management. J Neurol Neurosurg Psychiatry. 2018;89(10):10881100.

    • PubMed
    • Search Google Scholar
    • Export Citation

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