| Title | Idiopathic Intracranial Venous Hypertension: Toward a Better Understanding of Venous Stenosis and the Role of Stenting in Idiopathic Intracranial Hypertension |
| Creator | Marc J. Dinkin; Athos Patsalides |
| Affiliation | Department of Ophthalmology and Neurology (MJD), Weill Cornell Medicine, New York Presbyterian Hospital, New York, NY; and Department of Neurosurgery (AP), North Shore University Hospital, Northwell Health, Great Neck, NY |
| Abstract | Background: Venous sinus stenosis, typically at the junction of the transverse and sigmoid sinus, is increasingly recognized as a contributor to the pathophysiology of idiopathic intracranial hypertension (IIH), whether it be the intrinsic type that does not reverse with normalization of intracranial pressure or the extrinsic type, which does. Efforts to treat the stenosis and reduce the associated transstenotic gradient through placement of a stent at the site of stenosis have been studied over the past 2 decades, primarily through retrospective studies, with variable emphasis on formal visual testing and direct assessment of poststent opening pressure. Most studies have presented evidence for utilization of stenting as an alternative to cerebrospinal fluid shunting or optic nerve sheath fenestration in patients with IIH who harbor the stenosis and are refractory to or intolerant of intracranial pressure-lowering medications, but an assessment of the current data is needed to better understand the role of stenting for this patient population. Evidence acquisition: A search in PubMed was made for "IIH," "papilledema," and "venous stenting." Data pre and post stenting, including symptoms attributable to IIH, intracranial pressure, papilledema, retinal nerve fiber layer thickening on optical coherence tomography, and visual field assessment (mean deviation), were collected. Need for retreatment and complications were assessed among all studies. Studies using stenting for special circumstances, such as cerebrospinal leaks or for stenosis along anomalous vessels, were reviewed. Results: In total, 49 studies (45 retrospective and 4 prospective) and 18 case reports (with 3 or less patients) were found and included in the analysis, for a total of 1,626 patients. In 250 patients in whom poststent intracranial pressure was measured, the mean value was 19.7 cm H 2 O, reduced from a mean of 33 cm H 2 O. Transient visual obscurations resolved in 79.6% of 201 patients who complained of it, pulsatile tinnitus resolved in 84.7% of 515, diplopia resolved in 93% of 86 patients, and nonspecific visual symptoms such as "blurry vision" improved in 76.2% of 537 patients. Headaches resolved in 36% and improved in a further 40.7% of 1,105 patients in whom they were documented before stenting. Of 1,116 with papilledema, 40.8% demonstrated resolution and 38.2% improvement. The mean retinal nerve fiber layer thickness improved from 170.2 µm to 89.2 µm among 402 eyes in which optical coherence tomography was used to measure it. Among 135 eyes in which formal visual fields were performed pre and post stenting, the prestent average mean deviation of -7.35 dB improved to -4.72 dB after stenting. Complications associated with stenting included in-stent stenosis or thrombosis, subdural hematoma, intracerebral hematoma, cerebral edema, stent migration, and death. A recurrence of symptoms requiring a follow-up surgical intervention occurred in 9%. Conclusions: A growing body of evidence supports the use of venous sinus stenting as a viable option for medically refractory IIH, especially when papilledema threatens visual function. Complication and failure rates seem to be similar to alternative surgical approaches, although serious neurological sequalae can rarely occur. Emerging studies evaluating stent type, including novel stents designed for use in the venous system, may help improve ease of the procedure and long-term success rates. Prospective head-to-head studies are needed to better understand the performance of stenting compared with other interventions. |
| Subject | Constriction, Pathologic / complications; Humans; Hypertension / complications; Intracranial Hypertension / complications; Papilledema / complications; Prospective Studies; Pseudotumor Cerebri / complications; Pseudotumor Cerebri / diagnosis; Pseudotumor Cerebri / surgery; Retrospective Studies; Stents; Treatment Outcome; Vision Disorders |
| OCR Text | Show State-of-the-Art Review Section Editors: Fiona Costello, MD, FRCP(C) Sashank Prasad, MD Idiopathic Intracranial Venous Hypertension: Toward a Better Understanding of Venous Stenosis and the Role of Stenting in Idiopathic Intracranial Hypertension Marc J. Dinkin, MD, Athos Patsalides, MD, MPH Background: Venous sinus stenosis, typically at the junction of the transverse and sigmoid sinus, is increasingly recognized as a contributor to the pathophysiology of idiopathic intracranial hypertension (IIH), whether it be the intrinsic type that does not reverse with normalization of intracranial pressure or the extrinsic type, which does. Efforts to treat the stenosis and reduce the associated transstenotic gradient through placement of a stent at the site of stenosis have been studied over the past 2 decades, primarily through retrospective studies, with variable emphasis on formal visual testing and direct assessment of poststent opening pressure. Most studies have presented evidence for utilization of stenting as an alternative to cerebrospinal fluid shunting or optic nerve sheath fenestration in patients with IIH who harbor the stenosis and are refractory to or intolerant of intracranial pressure– lowering medications, but an assessment of the current data is needed to better understand the role of stenting for this patient population. Evidence Acquisition: A search in PubMed was made for “IIH,” “papilledema,” and “venous stenting.” Data pre and post stenting, including symptoms attributable to IIH, intracranial pressure, papilledema, retinal nerve fiber layer thickening on optical coherence tomography, and visual field assessment (mean deviation), were collected. Need for retreatment and complications were assessed among all studies. Studies using stenting for special circumstances, such as cerebrospinal leaks or for stenosis along anomalous vessels, were reviewed. Results: In total, 49 studies (45 retrospective and 4 prospective) and 18 case reports (with 3 or less patients) were found and included in the analysis, for a total of 1,626 patients. In 250 patients in whom poststent intracranial pressure was measured, the mean value was 19.7 cm H2O, reduced from a mean of 33 cm H2O. Transient visual obscurations resolved in 79.6% of 201 patients who complained of it, pulsatile tinnitus resolved in 84.7% of 515, diplopia resolved in 93% of 86 patients, and nonspecific visual symptoms such as “blurry vision” improved in 76.2% of 537 patients. Headaches resolved in 36% and improved in a further 40.7% of 1,105 patients in whom they were documented before stenting. Of 1,116 with papilledema, 40.8% demonstrated resolution and 38.2% improvement. The mean retinal Department of Ophthalmology and Neurology (MJD), Weill Cornell Medicine, New York Presbyterian Hospital, New York, NY; and Department of Neurosurgery (AP), North Shore University Hospital, Northwell Health, Great Neck, NY. The authors report no conflicts of interest. Address correspondence to Marc Dinkin, MD, Weill Cornell Medicine, New York Presbyterian Hospital, 1305 York Avenue, 11th Floor, New York, NY 10021; E-mail: mjd2004@med.cornell.edu Dinkin and Patsalides: J Neuro-Ophthalmol 2023; 43: 451-463 nerve fiber layer thickness improved from 170.2 mm to 89.2 mm among 402 eyes in which optical coherence tomography was used to measure it. Among 135 eyes in which formal visual fields were performed pre and post stenting, the prestent average mean deviation of 27.35 dB improved to 24.72 dB after stenting. Complications associated with stenting included in-stent stenosis or thrombosis, subdural hematoma, intracerebral hematoma, cerebral edema, stent migration, and death. A recurrence of symptoms requiring a follow-up surgical intervention occurred in 9%. Conclusions: A growing body of evidence supports the use of venous sinus stenting as a viable option for medically refractory IIH, especially when papilledema threatens visual function. Complication and failure rates seem to be similar to alternative surgical approaches, although serious neurological sequalae can rarely occur. Emerging studies evaluating stent type, including novel stents designed for use in the venous system, may help improve ease of the procedure and long-term success rates. Prospective head-to-head studies are needed to better understand the performance of stenting compared with other interventions. Journal of Neuro-Ophthalmology 2023;43:451–463 doi: 10.1097/WNO.0000000000001898 © 2023 by North American Neuro-Ophthalmology Society S ome diseases are just hard to name. Initially described as a “meningitis serosa” by Quinke1 and later renamed as “pseudotumor cerebri” and “benign intracranial hypertension” by Nonne2 and Foley,3 respectively, the condition of elevated intracranial pressure (ICP) without tumor, meningitis, or thrombosis was ultimately renamed “idiopathic intracranial hypertension,”4 (IIH) an honest admission that we, as a scientific community, really do not fully understand its etiology. Yet, there have been clues: its predilection for woman of childbearing age with elevated body mass index (BMI) or recent weight gain and its high prevalence in woman with polycystic ovarian syndrome5 have suggested an association with metabolic and endocrine dysfunction, which has been supported by recent evidence.6,7 But of all the bread crumb trails left for us to follow, the observation that 27 of 29 (93%) patients with IIH harbored bilateral stenosis at the junction of the transverse and sigmoid sinus8 has been of particular importance. Because a good portion of cerebrospinal fluid (CSF) drainage occurs by way of arachnoid granulations into the large venous sinuses, and because diseases that compromise sinus drainage, including tumoral compression and venous sinus 451 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. State-of-the-Art Review thrombosis, may mimic IIH,9,10 it is logical to assume that this venous sinus stenosis (VSS) could play an important role in the pathophysiology of IIH. Evidence that VSS resulted in a hemodynamically significant transstenotic pressure gradient (TSG) was provided by King et al11 in 1995, who demonstrated superior sagittal sinus (SSS)–internal jugular (IJ) gradients of 10–20 mm Hg in 9 patients with IIH, whereas 3 patients without elevated ICP and 2 with intracranial hypertension induced by minocycline had gradients of 2–7 mm Hg. King concluded that his findings “raised some therapeutic possibilities for the future of patients with IIH” but probably did not foresee the burgeoning field of venous stenting that would soon emerge. Higher rates of accessory drainage pathways, such as an occipital emissary vein connecting the torcula to the occipital veins in IIH patients vs controls,12 support a role of venous pressure in the pathophysiology of the disease. THEORETICAL UNDERPINNINGS Multiple studies soon demonstrated a reversal of stenosis13 and venous hypertension14 after reduction in CSF pressure, suggesting that they were simply a downstream effect due to extrinsic intracranial hypertension. Other studies demonstrated persistent VSS despite normalization of opening pressure (OP) with treatment,15 suggestive of an intrinsic stenosis not responsive to changes in ICP. Such intrinsic stenoses need not be congenital and may result from organized thrombus, septal bands, and most notably swollen arachnoid granulations (AG). AG are invaginations of the arachnoid into the dural sinus, providing a major source of CSF drainage. Lenck et al16 have proposed that paravascular AG found near larger cortical veins are continuations of the perivenous channels that contain CSF and interstitial fluid from what has been termed the “glymphatic” (glial lymphatics) system.17 They further postulate that reduced permeability through the AG in patients with IIH may lead to enlargement of the AG. Although the resultant increase in exchange surface between the CSF and venous sinus may initially compensate for the glymphatic dysfunction, eventually, the AG grows to the point of sinus stenosis and exacerbation of the disease. This framework could explain why intrinsic stenosis occurs most frequently at the transverse sinus because the sizable Vein of Labbe is a tributary with which vascular AGs are associated.18 In light of studies demonstrating the efficacy of venous stenting for both the extrinsic and intrinsic type of stenosis,19,20 it has been postulated that once an inciting event (i.e., weight gain) has led to intracranial hypertension and secondary extrinsic stenosis, the stenosis then leads to an even further elevation in ICP, compounding the stenosis, resulting in a positive feedback loop that only stabilizes once the transvenous wall pressure can no longer overcome dural compressibility.21 It is also conceivable that in patients with intrinsic stenosis, intracranial hypertension is secondary to venous hypertension caused by impaired venous outflow. Venous sinus stenting may help patients with intrinsic stenosis by removing the primary etiology for intracranial 452 hypertension, whereas it can help patients with extrinsic stenosis by breaking the vicious cycle of elevated ICP and collapse of the venous sinuses. Although the degree of VSS does not appear to predict CSF pressure or clinical course,22 the risk of having a pathological TSG, defined as $8 mm Hg, increases with higher OP (odds ratio [OR] 1.14).23 META-ANALYSIS OF OUTCOMES DATA FOR VENOUS STENTING FOR IDIOPATHIC INTRACRANIAL HYPERTENSION The first report of stenting as a potential treatment for IIH was by Higgins,24 who reported a striking improvement in symptoms in one patient, but this was soon followed by larger reports. In an attempt to evaluate our collective experience with venous stenting for IIH, the literature was reviewed for all cases and studies reporting on outcomes of stenting for VSS. A PubMed search was performed for “idiopathic intracranial hypertension,” “pseudotumor cerebri,” “stenting,” and “endovascular.” Weighted averages were used to calculate patient data for the entire cohort. When 2 studies appeared to consist of mostly overlapping patient sets, only the larger study was used whenever possible. In total, 49 studies with 4 or more stented patients (4 prospective19,25–27 and 45 retrospective20,21,28-70) and 18 reports with 1–3 patients71–88 were found, yielding a total of 1,626 IIH patients treated with venous stenting. Figure 1 details a demonstrative case in which a worsening of visual fields despite medical treatment led to the decision to advance to venous stenting. Demographics and Prior Surgeries Of the 1,626 patients, 1,351 (83%) were female, the mean age was 36 years, and the mean BMI was 32.6. A total of 110 patients had undergone prior surgical treatment for IIH, including 40 (2.5%) treated with optic nerve sheath fenestration, 51 (3.1%) with CSF shunts, and 19 (1.2%) with cranial vaults expansion. Effect on CSF Pressure Of 949 patients in which prestent OP was checked, values were available for 719, among whom, the mean OP was 33 cm H2O. Of 318 patients in whom poststent OP was checked, values were available for 250, among whom, the mean OP was 19.7 cm H2O. The average drop in OP following stenting was 13.3 cm H2O. Most studies performed poststent LP at least 1 month after stenting because patients are typically on dual antiplatelet therapy until then; it is therefore difficult to ascertain the speed at which stenting reduces ICP. However, Matloob et al44 studied patients with real-time ICP monitoring and found an immediate reduction in ICP right after stenting that was maintained for 24 hours. Figure 2 provides a summary of OP evaluation pre and post stenting. Dinkin and Patsalides: J Neuro-Ophthalmol 2023; 43: 451-463 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. State-of-the-Art Review FIG. 1. A 45-year-old healthy woman noted headaches, intermittent blackouts of vision for a few seconds, and horizontal diplopia for 6 months, all of which had worsened in the past 2 months. She also noted left pulsatile tinnitus. She went to an optometrist for glasses and was found to have bilateral optic disc swelling and was sent to the emergency room where ophthalmological examination revealed papilledema. MRI revealed tortuosity and enlargement of the bilateral optic nerve sheaths and anterior bowing of the posterior globes consistent with papilledema. Parenchymal herniation of the right posterolateral temporal lobe into the right transverse sinus was noted, with associated focal narrowing (A, arrow) and more proximal moderate segment severe stenosis of the right transverse sinus, also observed on MRV (B). A lumbar puncture revealed normal contents and an elevated opening pressure of 36 cm H2O, and she was started on acetazolamide 500 mg twice a day. Baseline neuro-ophthalmological assessment 2 days later revealed grade III papilledema OD and grade IV OS (C). OCT revealed a positive Bruch membrane angle OD and RNFL thicknesses of 442 mm and 428 mm OS (D) and automated visual fields showed enlarged blind spots OU and an inferonasal depression OS. E. Despite increasing doses of acetazolamide, papilledema persisted (F) 1 month later with only a mild reduction in RNFL on OCT (G). Concerningly, the visual fields worsened, revealing a worsening nasal defect and inferotemporal defect OD and dense inferior arcuate and superior arcuate defects OS. H. The patient was therefore referred for conventional venogram, which revealed a transstenotic gradient of 26 mm Hg. Two overlapping Precise Pro stents were deployed across the stenosis, with resolution of the stenosis (I, arrow) and reduction of the gradient to 2 mm Hg. Upon awakening, pulsatile tinnitus immediately resolved, and headaches resolved within a few days, although she experienced a new mild headache ipsilateral to the stent. Over the next month, papilledema improved to grade I OD and grade II OS with improvement in visual fields and by 1 month later, there was a watermark OU but almost no observable papilledema (J), near resolution of RNFL thickening on OCT (K) and except for an enlarged blind spot OD and a small nasal defect OS, all visual field loss resolved (L). MRV indicates magnetic resonance venogram; OCT, optical coherence tomography; OD, right eye; OS, left eye; OU, both eyes; RNFL, retinal nerve fiber layer. Effect on Symptoms Not all studies reported on all symptoms, so the prevalence of associated symptoms are likely underestimated. Transient visual obscurations (TVO) were reported in 201 (12.4%) and resolved in 160 (79.6%). Pulsatile tinnitus (PT) was present in 515 patients (31.7%) in whom poststent data were also reported and resolved in 436 (84.7%). In our experience, PT has resolved in nearly every patient who underwent technically successful stenting and has done so immediately, reflective of its direct relationship to transverse sinus stenosis. We used the tinnitus handicap inventory (THI) scale to measure subjective PT and found a complete resolution in 28 of 29 patients (mean drop of 2.7) with a median time of resolution of 0 days, although it recurred in 3 patients who developed recurrent stent-adjacent stenosis at a mean followup of 12 months.89 Diplopia, typically from abducens palsies, was reported in 86 (5.3%), among whom, it resolved in 83 (93%). Nonspecific visual symptoms, such as “blurry vision,” were found in 537 (33%) and were said to improve in 409 Dinkin and Patsalides: J Neuro-Ophthalmol 2023; 43: 451-463 (76.2%) and worsen in 9 (1.7%) after stenting. Finally, headaches were reported in 1,105 patients (68%) and resolved after stenting in 405 (36.7%) and improved in a further 450 (40.7%). As in other studies of IIH, headache was the least likely to resolve with treatment, reflective of multiple contributors including migraines and tension headaches.90 In most studies, the prevalence of concurrent migraine was not reported, but some authors, such as Shields,52 attributed residual poststent headaches to migraines and other headache syndromes. Figure 3 provides a summary of symptom outcomes. Effect on Papilledema Of the 1,626 patients, 1,116 (68.6%) were described as having papilledema before stenting, although this may be an underestimation because several studies did not include detailed ophthalmic assessment. Of these patients, 881 (78.9%) either demonstrated resolution (455, 40.8%) or improvement (426, 38.2%). The timing in which the follow-up examination was performed was variable but was 453 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. State-of-the-Art Review FIG. 2. Opening pressure (OP) pre and post stenting. The average OP pre and post stenting is reported for 19 studies or case reports in which lumbar puncture was performed serially. The n for each study refers to the number of patients in each study. Overall mean OP was calculated using weighted averages accounting for size of each study. typically within 1–4 months. A worsening was reported in 3 (0.3%), and importantly, optic atrophy was observed in only 40 (3.6%). The rate of optic atrophy may be underestimated because most studies did not specifically comment on the presence or absence of disc pallor. Furthermore, although its rarity suggests that the effect of stenting on papilledema was fast enough to avoid permanent damage, any conclusions must be tempered by the fact that many of the studies did not include detailed ophthalmic examinations. Furthermore, even in cases where ophthalmologists did not note atrophy, occult damage with vision loss can still be present (Figure 4). fields improved not only in 7 of these cases but also in 2 patients in whom the RNFL was stable. One study looked at ganglion cell layer (GCL) thicknesses in 57 patients and showed no change (76.56–76.44 mm).69 Worsening in 2 patients may have been artifactual related to choroidal folds and occurred in the setting of improved visual fields. Because the GCL looks only at atrophy and is not affected by improvement in papilledema, these findings suggest that stenting helped preserve optic nerve structure. Figure 5 provides a summary of studies using OCT in the assessment pre and post stenting. Optical Coherence Tomography Assessment Visual Function Visual assessment of papilledema severity is inherently subjective and qualitative and can be complemented by the use of optical coherence tomography (OCT). Quantitative assessment of the peripapillary retinal nerve fiber layer (pRNFL) with OCT was performed in several studies, adding to our understanding of the structural outcomes following stenting of VSS. We combined the results of individual patients from 11 studies26,27,43,54,57,61,67–69,85,91 with a total of 402 eyes and found a mean prestent pRNFL of 170.2 mm. The mean poststent pRNFL was 89.2 mm (mean reduction 281 mm, 247.6%). In our prospective study using OCT, pRNFL thinning did not develop in any eye in which it was not present before stenting.26 A 12th study did not report individual patient thicknesses and could not be incorporated in the metanalysis.40 However, the authors reported a decrease in RNFL in 8 of 11 patients, including 2 who were not noted to have papilledema on fundus examination before stenting. Visual The primary disability that may result from poorly controlled IIH is vision loss, manifesting predominantly as peripheral visual field loss except in rare cases of severe or prolonged disc edema, in which case central visual acuity can be affected. As such, the most important means of assessing any proposed IIH treatment, including stenting, is the formal visual field. Of 386 eyes reported to have formal visual field testing, 239 were said to improve, 125 had no change, and 17 worsened. We found 10 studies that presented quantitative data on pre- and poststent mean deviation (MD),25,26,38,40,43,67,69,70,81 including a total of 135 patients (270 eyes). Nine of the studies used automated visual fields (HVF), among which 2 used a 24-2 program, 2 used a 30-2 program, and 4 did not specify. One study also used kinetic perimetry for a few patients with severe loss,69 whereas another study did not describe the type of visual field analyzer used. Although 7 studies listed the MDs pre- and poststenting for each patient, 3 studies only included 454 Dinkin and Patsalides: J Neuro-Ophthalmol 2023; 43: 451-463 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. State-of-the-Art Review FIG. 3. Symptoms pre and post stenting. the average MD scores for the entire cohort. To estimate the overall scores, a weighted average was calculated based on the number of eyes in each study. The prestent average MD of 27.35 dB improved to 24.72 dB after stenting. Although there was a trend toward improvement, in some studies where the initial VF loss was not that severe,69 the change was not significant. Figure 6 summarizes visual field results. Failure and Need for Retreatment Of 1,626 patients, 145 (9%) demonstrated ongoing or recurrent symptoms and signs requiring a secondary surgical procedure, such as repeat angioplasty or stent in 92 (5.7%), CSF shunting in 50 (3.1%), or bariatric surgery in 3 (0.2%). This is likely a significant underestimate because some studies in this metanalysis did not include follow-up beyond 3–6 months. In our own series of 79 patients followed for a minimum of 18 months, we found stent failure in 13.9%, and a latency of up to 2 years.92 Among 81 patients followed for a mean of 10 months, Garner et al58 reported a much higher incidence of either persistent severe symptoms or delayed symptom recurrence resulting in a poststent LP (54.3%) and ultimately a second procedure (25.9%). However, in 14 of 21 (67%) of these patients, the indication for repeat procedure was ongoing headache FIG. 4. Papilledema outcomes. In 12.1% of cases, outcomes were not reported. Dinkin and Patsalides: J Neuro-Ophthalmol 2023; 43: 451-463 455 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. State-of-the-Art Review FIG. 5. Retinal nerve fiber layer (RNFL) thicknesses by study pre and post stenting. The average RNFL pre and post stenting is reported for 11 studies or case reports in which optical coherence tomography (OCT) was performed serially. The n for each study refers to the number of eyes. Overall mean RNFL was calculated using weighted averages accounting for size of each study. with impairment of the quality of life, with deterioration of vision or ongoing papilledema only present in 7 (33% of those retreated and 9% of the entire cohort). In addition, the authors point out that the majority of patients who relapsed were found to have lower OP after stenting (mean reduction of 8 cm H2O). This discrepancy was attributed to a “reequilibration” phenomenon as patients get used to their lower (but still high) ICP. However, one may also interpret the LP findings as a reflection of the multifactorial nature of headaches in patients with IIH, suggesting that in some of the patients, ongoing or recurrent headaches in the absence of papilledema were not related to intracranial hypertension. High rates of retreatment were similar in another study in which none of the patients who failed had recurrent papilledema,47 although a larger study from the same group showed only a 10% rate of restenosis requiring a second procedure.93 Predicting the patients who will fail stenting for IIH could help us better choose appropriate candidates but remains challenging. El Makataby et al47 identified higher BMI and larger stent diameters (.6 mm)93 as predictors of failure, the latter feature suggesting that greater mechanical deformation of the stented segment might predispose to subsequent stent-adjacent stenosis. Kumpe et al39 suggested that a new stent-adjacent stenosis (SAS) was more likely to occur in those initially treated for extrinsic stenosis, but in our study, neither stent diameter nor extrinsic status predicted the need for retreatment; instead, we found a positive association with prestent LP, with an odds ratio of 1.06 for every 1 cm H2O increase in OP.92 Finally, Raper et al45 observed that SAS was less likely to occur in patients where 456 stenting resulted in a reduction in the TS pressure toward that of the SS as opposed to an increase in the SS pressure closer to that of the TS. This is not surprising because the latter outcome suggests a factor other than the stenosis itself contributing to elevated venous pressures. Complications Numerous complications have been reported and are summarized in Table 1. In-stent thrombosis and stenosis have been reported in 15 (0.92%) and 24 (1.5%) patients, respectively, whereas thrombosis has been reported in the adjacent transverse sinus occurred in an additional 2 (0.12%). Subdural or intracerebral hematomas were reported in 8 patients (0.49%) with good neurological recovery. However, in 2 cases, cerebellar hemorrhage, one presumably related to guidewire vessel perforation,94 and a second occurring contralaterally and remote to procedural manipulation,95 resulted in death. One patient in Ahmed’s large series died from malignant intracranial hypertension and cerebral edema, which was attributed to anesthesia.96 However, a potential mechanism for an acute rise in ICP after stenting would be occlusion of the vein of Labbe (VOL) by the stent struts or by distortion of the venous sinus anatomy. Levitt et al97 found no alterations in VOL flow following stenting in 21 patients. In our cohort of 70 patients, however, impaired drainage (delayed flow, reduced VOL caliber or occlusion) was observed in 9 (13%) immediately after stenting and was associated with a dominant VOL ipsilateral to the stent and stent diameters of $9 mm.98 These patients were treated with a heparin drip for 24 hours to prevent cortical vein thrombosis, and all patients demonstrated normal flow at the 3-month follow-up contrast magnetic resonance Dinkin and Patsalides: J Neuro-Ophthalmol 2023; 43: 451-463 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. State-of-the-Art Review FIG. 6. Visual field results pre and post stenting. The average mean deviation (MD) pre and post stenting is reported for 10 studies in which formal testing was performed serially. The n for each study refers to the number of eyes. Overall mean MD was calculated using weighted averages accounting for size of each study. venogram (MRV). The true incidence of secondary thrombosis or hemorrhage related to VOL alterations is unknown, but we recommend careful monitoring and management of this potential complication. In the report of Liu et al51 of 88 stented patients, there were 2 deaths over the follow-up period, but both were apparently from unrelated causes (glioma and stroke). Importantly, among 107 respondents to a survey of interventional radiologists in 2022, 2 deaths were reported, one due to a periprocedural in-stent thrombosis.99 It is not clear whether the second death was one of the previously reported, but it is likely that the observed mortality rate of 0.37% is an underestimate due to underreporting of cases with such outcomes. treatment and the numbers required for statistical comparison. One, prospective, nonrandomized trial comparing stenting to diet control and maximal medical therapy was carried out in Beijing and published in 2022.19 Among those with intrinsic stenosis, they found a significantly higher rate of complete resolution of headaches (86.7% vs 23.1%), “visual impairment” (71.4% vs 12.5%), and papilledema (86.5% vs 42.9%) in the stented group vs the medical therapy group. Similar results were demonstrated for those with extrinsic stenosis in terms of headache (90/9% vs 40%), “visual impairment” (80% vs 45.5%), and papilledema (90.9% vs 36.8%). LIMITATIONS OF THIS METANALYSIS SPECIAL CIRCUMSTANCES There are numerous limitations inherent in this review of the literature. There was significant variability in methodology, follow-up periods, imaging techniques, and most importantly, neuro-ophthalmic assessment, among studies. Many articles were authored without contributions by neuro-ophthalmologists, and visual assessment was limited to the presence or absence of blurry vision or visual symptoms. In some studies in which objective ophthalmic assessment was performed, visual acuities (which are often minimally affected by papilledema) were reported without visual field data. Notably, we cannot be sure that all groups published their most severe complications, so that we may be underestimating serious risks of the procedure. Keeping all of this in mind, the data collated in this review should be interpreted with caution, with large, multicenter, prospective studies needed to better understand the safety and efficacy of venous stenting in IIH. Encephaloceles and Venous Sinus Stenosis HEAD-TO-HEAD TRIALS Numerous barriers to comparative prospective trials include a strong patient preference for one type of surgical Dinkin and Patsalides: J Neuro-Ophthalmol 2023; 43: 451-463 Rarely, brain parenchyma, typically from the temporal lobe or cerebellum, may herniate into a large arachnoid granulation forming an encephalocele. Although such encephaloceles may occur spontaneously, in cases of IIH, they are felt to be a consequence of elevated ICP.100 Distinguishing these from AG without encephaloceles can be challenging but is abetted by high-resolution 3-dimensional fluid-attenuated inversion recovery imaging and gradient echo T1 imaging.101 Drocton et al85 found 3 cases in which they retrospectively identified such encephaloceles following venous stenting for medically refractory IIH. There were no periprocedural complications in the 2 cases where the stent was placed contralateral to the encephalocele or in the patient in whom the stent was placed ipsilaterally. Clinical follow-up was only available in 2 cases, both of which demonstrated a significant improvement in papilledema and symptoms. The authors suggest that the location of the encephalocele should not alter the decision to stent the dominant sinus. It is not surprising that stenting of these patients would still be effective in improving venous outflow and reducing CSF pressure. 457 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. State-of-the-Art Review TABLE 1. Complications of venous sinus stenting Complication Ipsilateral headache Stent thrombosis Transient heading loss In-stent stenosis Stent-adjacent stenosis Allergy to contrast Anaphylaxis Extravasation Vision loss Stent migration DVT Transverse sinus thrombosis Subdural/intracranial hematoma Ataxia Groin hematoma Groin abscess/sepsis Arteriotomy bleed Retroperitoneal hematoma Femoral pseudoaneurysm Urinary tract infection Ruptured ovarian cyst Syncope Hair loss Neck hematoma Melena Menorrhagia Epistaxis AVF Labbe Vasovagal Seizure Death # % 185/1,626 15/1,626 4/1,626 24/1,626 40/1,626 2/1,626 2/1,626 2/1,626 1/1,626 1/1,626 3/1,626 2/1,626 8/1,626 1/1,626 14/1,626 1/1,626 1/1,626 2/1,626 9/1,626 1/1,626 2/1,626 1/1,626 1/1,626 2/1,626 1/1,626 1/1,626 3/1,626 1/1,626 1/1,626 2/1,626 2/1,626 6/1,626 11.38 0.92 0.25 1.48 2.46 0.12 0.12 0.12 0.06 0.06 0.18 0.12 0.49 0.06 0.86 0.06 0.06 0.12 0.55 0.06 0.12 0.06 0.06 0.12 0.06 0.06 0.18 0.06 0.06 0.12 0.12 0.37 AVF, formation of an arteriovenous malformation; DVT, deep venous thrombosis. Venous Sinus Stenting in the Setting of CSF Leaks A subset of patients with IIH may develop spontaneous CSF leaks, presumably due to chronic skull-based erosion due to localized CSF pressure, and act in a compensatory fashion. In such cases, OP may be normal or low, and papilledema may be absent. Repairing CSF leaks is important to prevent secondary meningitis but may result in decompensation of IIH. Buchowicz et al102 looked at 57 patients who underwent repair of CSF leak. Of the 19 who subsequently developed either papilledema, a recurrent CSF leak or required CSF shunting, 79% had venous sinus stenosis. Of the 38 who experienced none of those complications after repair, only 35% had VSS. Thus, it appeared that in the presence of a CSF leak, VSS strongly suggests that the underlying etiology is IIH and that repairing the leak may lead either to an IIH exacerbation or a new compensatory leak. Labeyrie et al65 compared 10 patients treated with prophylactic stenting after CSF repair with 18 patients 458 who were followed conservatively and found that those who underwent stenting had a reduced chance of leak recurrence (0% vs 38%) or need for secondary leak repair, providing preliminary evidence that patients with VSS should be considered for stenting after CSF leak repair, even if they are asymptomatic. Larger prospective studies of stenting in leak patients are necessary to confirm these findings. Stenosis Within Variant Venous Outflow Rarely, anomalous venous outflow may serve as an alternative means of drainage in the setting of bilateral hypoplastic transverse sinuses. In such cases, when IIH supervenes, stenosis along this pathway may occur. Al Balushi et al103 published a case of IIH in which a persistent enlarged occipital sinus demonstrated severe distal stenosis, with hypoplastic right and aplastic left transverse sinuses. Stenting of the stenotic segment resulted in the resolution of papilledema and normalization of ICP. Alvarado et al86 described a similar case of IIH in which multiple arachnoid granulations caused a focal stenosis within a persistent occipital margin sinus (POMS), with bilateral hypoplastic transverses sinuses. Placement of 2 overlapping stents led to the resolution of the stenosis and papilledema, while flow through the hypoplastic vessels ceased. These cases demonstrate that venous stenosis contributing to IIH is not limited to the transverse-sigmoid sinus junction but may occur in alternative locations and even within anomalous congenital vessels. As long as that stenosis is limiting venous outflow, stenting appears to improve the clinical outcome. TECHNICAL CONSIDERATIONS AND ADVANCES Imaging Intravascular ultrasound (IVUS) is a catheter-based technique that allows real-time 360° visualization of the vessel lumen and wall in 3 dimensions, avoiding some of the errors that may result from variable contrast using angiography. Using IVUS as a gold standard, Boddu et al104 demonstrated an overestimation of the vessel lumen using contrast MRV, due to vessel wall enhancement, but not with time of flight (TOF) MRV, in a group of 20 patients. Accurate estimations of the vessel lumen are important in choosing the right stent size because underestimation may result in residual stenosis or stent migration and overestimation may lead to greater dural stretching and poststent headache. Yan et al53 used IVUS not only as a secondary means to measure the degree of stenosis but also to characterize the vessel lumen and to differentiate varied causes of the stenosis. In their group of 12 patients, 3 (25%) had intraluminal thrombosis, 1 (8.3%) had a giant arachnoid granulation, 2 (16.7%) intravenous compartments, and 6 (50%) had vessel wall thickening, which they equate to simple ICP-induced extrinsic stenosis. Although many Dinkin and Patsalides: J Neuro-Ophthalmol 2023; 43: 451-463 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. State-of-the-Art Review would argue that those with thrombosis are not true IIH patients, it is likely that some patients felt to have IIH with stenosis harbor chronic thrombosis that could be identified by IVUS. The authors argued that IVUS allowed a more accurate deployment of the stent, allowed for better apposition of the stent to the vessel wall, and permitted them to screen for the presence of postprocedure stent-adjacent stenosis at the time of stenting. Importantly, IVUS could help the practitioner identify small venous channels and avoid guide wire placement through them, which might otherwise lead to wall rupture and intracranial hemorrhage. Color Doppler IVUS can also be used to estimate velocity through a stenotic segment. The authors make the argument that use of IVUS helped them achieve success without any cases of restenosis, but given rates of restenosis as low as 13%, a relatively small number of patients (12) and a follow-up as short as 12 months in some patients, it is not clear that such results would not have occurred in the absence of IVUS. Kishore et al105 used a 3dimensional MRV overlay while performing angiography and reported a greater confidence in detecting the ostia of draining cortical veins. Contralateral Approach In some cases, placement of a stent or even the guide wire and catheter in the stenotic segment proves challenging or impossible due to anatomical factors. These can include large arachnoid granulations, septa, trabeculae, an acute angle at the stenosis, or an adjacent cortical vein, the latter of which could predispose to avulsion of the guidewire and hemorrhage. To solve this problem, Gordon et al demonstrated stent placement using the contralateral approach in 4 patients, a feat that required traversing a hypoplastic and stenotic sinus.55 Symptomatic improvement was reported in 3 of the 4 cases, and there were no complications. This technique may allow the interventionalist to avoid aggressive maneuvers on the ipsilateral side that could lead to serious complications. to control ICP (vs 2% in the stenting group). In light of these results, we do not recommend primary angioplasty for medically refractory IIH patients unless other surgical options have been exhausted or as a temporizing measure, analogous to placement of a lumbar drain. Stent Type With no Food and Drug Administration–approved stents yet available specifically for VSS, the majority of procedures use carotid stents off label,107 such as the PrecisePro stent (Cordis), which is a self-expanding, nitinol stent with a single-layer, V-pattern, open-cell design. The open cells provide larger spaces between nitinol wiring, which might reduce thrombogenicity and lessen the chance of cortical vein occlusion by the stent. However, it also provides more stent rigidity, which in turn could theoretically make traversing tortuous or stenotic segments more challenging and dangerous. Other commonly off-label used stents include the Zilver stent (Cook Medical, Bloomington, IN), also a self-expandable, open-cell design stent, and the Carotid Wallstent (Boston Scientific, Marlborough, MA), a selfexpandable, braided stent. The choice of stents is operator dependent, and there has been no major study demonstrating a clear benefit of one stent over another. Belachew et al62 compared their experience using the Casper stent (Terumo, Somerset, NJ) (n = 10 patients), against the Precise Pro stent (n = 5 patients) in a retrospective study of patients with IIH. The Casper stent is a relatively new duallayer, closed-cell stent, and according to the authors, it was easier to navigate and deliver than the Precise Pro stent; however, there was similar safety and efficacy in symptom improvement. The difference in navigation and delivery of the stent was attributed to the greater flexibility of the closed-cell stent design. However, follow-up beyond 6 months was not provided to evaluate the rate of long-term failure of each type. The Casper stent is not yet approved for use in the United States. Stents Designed for the Venous Sinus Venoplasty Without Stenting As venous stenting carries with it certain risks, including bleeding complications from dual antiplatelet therapy and in-stent thrombosis, there is value in consideration of angioplasty of the stenotic segment without stenting. Carter et al106 described a 15-year-old who was treated with venoplasty alone, with the resolution of papilledema at discharge and a sustained resolution of symptoms of high ICP at 1 year. However, Martinez-Gutierrez et al64 compared 53 stented patients with 9 who underwent only balloon angioplasty and found a lower rate of improvement in papilledema (44% vs 93%), headache (44% vs 92%), and visual disturbance (50% vs 92%) at 6 weeks in the angioplasty group. The mean change in OP was only 6 cm H2O (vs 13 in the stented group), and 44% ultimately required a VPS Dinkin and Patsalides: J Neuro-Ophthalmol 2023; 43: 451-463 The greatest technical challenge for venous sinus stenting is the lack of a stent system specifically designed for the challenges of venous sinus anatomy. The turn from the internal jugular vein to the sigmoid sinus can be sharp and difficult to navigate using a stiffer stent. Another anatomic challenge is navigating the stent system across the stenosis, especially in patients with severe intrinsic stenosis. A third challenge is the length of the stenosis. In many patients, especially with extrinsic stenosis, the length of stenosis exceeds the length of the currently used stents. Thus, 2 overlapping stents are often needed to treat the stenosis, which increases the manipulation of the venous sinuses and predisposes to compromised flow of the cortical veins and the VOL, due to the increased metal coverage at the zone of stent overlap. 459 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. State-of-the-Art Review The River stent (Serenity Medical) is the first stent specifically designed for the venous sinus system. The River stent is an open-cell stent designed to achieve smooth navigation in the venous sinus system, with a variable diameter that allows it to conform to the diameters of the transverse and sigmoid venous sinuses. It has a length equal to 70 mm to treat long-segment stenosis without the need for an additional stent and hopefully reduce the occurrence of stent-adjacent stenosis. The River trial is a prospective, open-label, single-arm, multi-center trial evaluating the safety and benefit in patients with IIH who present with vision loss and/or severe headaches. Enrollment has been completed, and the patients are now in the follow-up period.108 WHEN TO STENT? No agreed on criteria have been adapted as to when to send a patient with IIH for stenting of a venous sinus. However, based on the data available and personal experience, we recommend that patients be sent for consideration of stenting only when certain conditions apply. Once a patient is diagnosed with IIH by the modified Dandy criteria, and MRV or CTV demonstrates venous sinus stenosis, stenting may be considered when conventional venography confirms the stenosis and demonstrates that it is hemodynamically significant and certain clinical circumstances exist: 1. The patient has papilledema with associated visual field loss AND the neuro-ophthalmic examination was refractory to medical therapy with increasing doses of an ICPlowering medication such as acetazolamide or topiramate OR the patient could not tolerate medical therapy. The question of exactly how many weeks one should wait, and to what dose of medication should be trialed will differ among practitioners and will depend on the degree of visual threat, but we recommend a failed trial of increasing over 4 weeks to at least 1,000 mg twice a day of acetazolamide before referral. 2. In cases of “fulminant papilledema,” in which there is severe neurogenic visual field loss, often associated with a significant drop in visual acuity in one or both eyes, it is reasonable to send the patient for a surgical procedure such as stenting, without a trial of increasing medical therapy because the inherent delay in such cases is more likely to result in irreversible vision loss. 3. Patients with IIH without papilledema, or in whom prior therapy has reversed papilledema, will on occasion be referred for consideration of stenting for severe and intractable headaches. In general, the risk–benefit ratio in such cases is not favorable because they are at low risk for vision loss and there may be contributors to headache that will not respond to stenting. In very rare cases, if headaches are clearly positional, without any migrainous features, are medically refractory and 460 are so severe as to be debilitating AND a recent LP confirms unequivocally elevated ICP, then stenting may be considered. Regardless of the clinical scenario, patients should be counseled on alternative surgical therapies, including shunting and optic nerve sheath fenestration, and be made aware of the potential risks and benefits of the options. Specifically, the potential risk of serious neurological complications and the risk of death from stenting should be explained clearly. We have found that some patients are surprised to hear about serious complications because of a perception that interventional radiological procedures are inherently safer than conventional surgery. By convention, although many groups use a TSG of 8 mm of Hg as a cutoff to proceed with stenting, one recent study demonstrated similar benefits with lower pressures.109 CONCLUSIONS Venous stenting for patients with IIH has come a long way since its first use in 2002, with a review of published patients demonstrating efficacies for improvement in symptoms, papilledema, and visual function similar or better than CSF shunting and ONSF.110 Despite several reports of severe neurological complications, including rare mortalities, the safety profile appears similar to or better than CSF shunting. Yet, questions remain regarding the true risk of complications and the risk and predictors of failure or recurrence—questions that would be best answered by head-to-head prospective trials. The Intervention to Preserve Vision in Idiopathic Intracranial Hypertension (IPVIIH),111 Stenting vs Neurosurgical Treatment of Idiopathic Intracranial Hypertension (HYDROPTIC),112 and Operative Procedures vs Endovascular Neurosurgery for Untreated Pseudotumor Trial (OPEN-UP)113 trials will hopefully offer us more rigorous data to support the expansive use of this treatment for patients in need of nonmedical therapy for IIH. STATEMENT OF AUTHORSHIP Conception and design: M. J. Dinkin, A. Patsalides; Acquisition of data: M. J. Dinkin; Analysis and interpretation of data: M. J. Dinkin, A. Patsalides. Drafting the manuscript: M. J. Dinkin, A. Patsalides; Revising the manuscript for intellectual content: M. J. Dinkin, A. Patsalides. Final approval of the completed manuscript: M. J. Dinkin, A. Patsalides. REFERENCES 1. Quincke H. Meningitis serosa. Sammi Klin Vortr, Leipzig, No 67. InnMed. 1893;23:655–662. 2. Nonne M. Ü ber falle vom symptomkomplex “tumor cerebri”mitausgang in heilung (pseudotumor cerebri). Dtsch Z Nervenheilkd. 1904;27:169–216. 3. Foley J. Benign forms of intracranial hypertension; toxic and otitichydrocephalus. Brain. 1955;78:1–41. Dinkin and Patsalides: J Neuro-Ophthalmol 2023; 43: 451-463 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. State-of-the-Art Review 4. Buchheit WA, Burton C, Haag B, Shaw D. Papilledema and idiopathic intracranial hypertension. N Engl J Med. 1969;280:938–942. 5. Avisar I, Gaton DD, Dania H, Stiebel-Kalish H. The prevalence of polycystic ovary syndrome in women with idiopathic intracranial hypertension. Scientifica (Cairo). 2012;2012:708042. 6. Westgate CS, Botfield HF, Alimajstorovic Z, et al. Systemic and adipocyte transcriptional and metabolic dysregulation in idiopathic intracranial hypertension. JCI Insight 2021;6:e145346. 7. Grech O, Mollan SP, Wakerley BR, Alimajstorovic Z, Lavery GG, Sinclair AJ. Emerging themes in idiopathic intracranial hypertension. J Neurol. 2020;267:3776–3784. 8. Farb RI, Vanek I, Scott JN, et al. Idiopathic intracranial hypertension: the prevalence and morphology of sinovenous stenosis. Neurology. 2003;60:1418–1424. 9. Biousse V, Ameri A, Bousser MG. Isolated intracranial hypertension as the only sign of cerebral venous thrombosis. Neurology. 1999;53:1537–1542. 10. Marvin E, Synkowski J, Benko M. Tumor cerebri: metastatic renal cell carcinoma with dural venous sinus compression leading to intracranial hypertension; a case report. Surg Neurol Int. 2017;8:175. 11. King JO, Mitchell PJ, Thomson KR, Tress BM. Cerebral venography and manometry in idiopathic intracranial hypertension. Neurology. 1995;45:2224–2228. 12. Hedjoudje A, Piveteau A, Gonzalez-Campo C, Moghekar A, Gailloud P, San Millán D. The occipital emissary vein: a possible marker for pseudotumor cerebri. AJNR Am J Neuroradiol. 2019;40:973–978. 13. Rohr A, Dörner L, Stingele R, Buhl R, Alfke K, Jansen O. Reversibility of venous sinus obstruction in idiopathic intracranial hypertension. AJNR Am J Neuroradiol. 2007;28:656–659. 14. King JO, Mitchell PJ, Thomson KR, Tress BM. Manometry combined with cervical puncture in idiopathic intracranial hypertension. Neurology. 2002;58:26–30. 15. Bono F, Giliberto C, Mastrandrea C, et al. Transverse sinus stenoses persist after normalization of the CSF pressure in IIH. Neurology. 2005;65:1090–1093. 16. Lenck S, Radovanovic I, Nicholson P, Hodaie M, Krings T, Mendes-Pereira V. Idiopathic intracranial hypertension: the veno glymphatic connections. Neurology. 2018;91:515–522. 17. Iliff JJ, Nedergaard M. Is there a cerebral lymphatic system? Stroke. 2013;44:S93–S95. 18. Gailloud P, Muster M, Khaw N, et al. Anatomic relationship between arachnoid granulations in the transverse sinus and the termination of the vein of Labb’e: an angiographic study. Neuroradiology. 2001;43:139–143. 19. Liu R, Huo X, Yang H, et al. Characteristics and outcomes of the idiopathic intracranial hypertension treatment in intrinsic and extrinsic stenosis: a single-center experience in China. Neurol Ther. 2021;10:1029–1044. 20. Patsalides A, Oliveira C, Wilcox J, et al. Venous sinus stenting lowers the intracranial pressure in patients with idiopathic intracranial hypertension. J Neurointerv Surg. 2019;11:175– 178. 21. Ahmed RM, Wilkinson M, Parker GD, et al. Transverse sinus stenting for idiopathic intracranial hypertension: a review of 52 patients and of model predictions. AJNR Am J Neuroradiol. 2011;32:1408–1414. 22. Riggeal BD, Bruce BB, Saindane AM, et al. Clinical course of idiopathic intracranial hypertension with transverse sinus stenosis. Neurology. 2013;80:289–295. 23. Fargen KM, Garner RM, Kittel C, Wolfe SQ. A descriptive study of venous sinus pressures and gradients in patients with idiopathic intracranial hypertension. J Neurointerv Surg. 2020;12:320–325. 24. Higgins JN, Owler BK, Cousins C, Pickard JD. Venous sinus stenting for refractory benign intracranial hypertension. Lancet. 2002;359:228–230. Dinkin and Patsalides: J Neuro-Ophthalmol 2023; 43: 451-463 25. Radvany MG, Solomon D, Nijjar S, et al. Visual and neurological outcomes following endovascular stenting for pseudotumor cerebri associated with transverse sinus stenosis. J Neuroophthalmol. 2013;33:117–122. 26. Dinkin MJ, Patsalides A. Venous sinus stenting in idiopathic intracranial hypertension: results of a prospective trial. J Neuroophthalmol. 2017;37:113–121. 27. Liu KC, Starke RM, Durst CR, et al. Venous sinus stenting for reduction of intracranial pressure in IIH: a prospective pilot study. J Neurosurg. 2017;127:1126–1133. 28. Higgins JN, Cousins C, Owler BK, Sarkies N, Pickard JD. Idiopathic intracranial hypertension: 12 cases treated by venous sinus stenting. J Neurol Neurosurg Psychiatry. 2003;74:1662–1666. 29. Donnet A, Metellus P, Levrier O, et al. Endovascular treatment of idiopathic intracranial hypertension: clinical and radiologic outcome of 10 consecutive patients. Neurology. 2008;70:641–647. 30. Bussière M, Falero R, Nicolle D, Proulx A, Patel V, Pelz D. Unilateral transverse sinus stenting of patients with idiopathic intracranial hypertension. AJNR Am J Neuroradiol. 2010;31:645–650. 31. Albuquerque FC, Dashti SR, Hu YC, et al. Intracranial venous sinus stenting for benign intracranial hypertension: clinical indications, technique, and preliminary results. World Neurosurg. 2011;75:648–652; discussion 592–595. 32. Kumpe DA, Bennett JL, Seinfeld J, Pelak VS, Chawla A, Tierney M. Dural sinus stent placement for idiopathic intracranial hypertension. J Neurosurg. 2012;116:538–548. 33. Ahmed RM, Parker GD, Halmagyi GM. Letters to the editor: stenting and idiopathic intracranial hypertension. J Neurosurg. 2012;117:1205; author reply 1205–1206. 34. He CZ, Ji XM, Wang LJ, et al. Endovascular treatment for venous sinus stenosis in idiopathic intracranial hypertension [in Chinese]. Zhonghua Yi Xue Za Zhi. 2012;92:748–751. 35. Fields JD, Javedani PP, Falardeau J, et al. Dural venous sinus angioplasty and stenting for the treatment of idiopathic intracranial hypertension. J Neurointerv Surg. 2013;5:62–68. 36. Ducruet AF, Crowley RW, McDougall CG, Albuquerque FC. Long-term patency of venous sinus stents for idiopathic intracranial hypertension. J Neurointerv Surg. 2014;6:238– 242. 37. Teleb MS, Cziep ME, Issa M, et al. Stenting and angioplasty for idiopathic intracranial hypertension: a case series with clinical, angiographic, ophthalmological, complication, and pressure reporting. J Neuroimaging. 2015;25:72–80. 38. Elder BD, Goodwin CR, Kosztowski TA, et al. Venous sinus stenting is a valuable treatment for fulminant idiopathic intracranial hypertension. J Clin Neurosci. 2015;22:685– 689. 39. Kumpe DA, Seinfeld J, Huang X, et al. Dural sinus stenting for idiopathic intracranial hypertension: factors associated with hemodynamic failure and management with extended stenting. J Neurointerv Surg. 2017;9:867–874. 40. Smith KA, Peterson JC, Arnold PM, Camarata PJ, Whittaker TJ, Abraham MG. A case series of dural venous sinus stenting in idiopathic intracranial hypertension: association of outcomes with optical coherence tomography. Int J Neurosci. 2017;127:145–153. 41. Aguilar-Pérez M, Martinez-Moreno R, Kurre W, et al. Endovascular treatment of idiopathic intracranial hypertension: retrospective analysis of immediate and longterm results in 51 patients. Neuroradiology. 2017;59:277– 287. 42. Satti SR, Leishangthem L, Spiotta A, Chaudry MI. Dural venous sinus stenting for medically and surgically refractory idiopathic intracranial hypertension. Interv Neuroradiol. 2017;23:186–193. 43. Shazly TA, Jadhav AP, Aghaebrahim A, et al. Venous sinus stenting shortens the duration of medical therapy for increased intracranial pressure secondary to venous sinus stenosis. J Neurointerv Surg. 2018;10:310–314. 461 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. State-of-the-Art Review 44. Matloob SA, Toma AK, Thompson SD, et al. Effect of venous stenting on intracranial pressure in idiopathic intracranial hypertension. Acta Neurochir (Wien). 2017;159:1429–1437. 45. Raper D, Buell TJ, Ding D, Chen CJ, Starke RM, Liu KC. Pattern of pressure gradient alterations after venous sinus stenting for idiopathic intracranial hypertension predicts stent-adjacent stenosis: a proposed classification system. J Neurointerv Surg. 2018;10:391–395. 46. Asif H, Craven CL, Siddiqui AH, et al. Idiopathic intracranial hypertension: 120-day clinical, radiological, and manometric outcomes after stent insertion into the dural venous sinus. J Neurosurg. 2018;129:723–731. 47. El Mekabaty A, Obuchowski NA, Luciano MG, et al. Predictors for venous sinus stent retreatment in patients with idiopathic intracranial hypertension. J Neurointerv Surg. 2017;9:1228– 1232. 48. Koovor JM, Lopez GV, Riley K, Tejada J. Transverse venous sinus stenting for idiopathic intracranial hypertension: safety and feasibility. Neuroradiol J. 2018;31:513–517. 49. Xu Y, Meng R, Rajah GB, et al. Long-term outcomes of cerebral venous sinus stenosis corrected by stenting. Curr Neurovasc Res. 2019;16:77–81. 50. Cappuzzo JM, Hess RM, Morrison JF, et al. Transverse venous stenting for the treatment of idiopathic intracranial hypertension, or pseudotumor cerebri. Neurosurg Focus. 2018;45:E11. 51. Liu X, Di H, Wang J, et al. Endovascular stenting for idiopathic intracranial hypertension with venous sinus stenosis. Brain Behav. 2019;9:e01279. 52. Shields LBE, Shields CB, Yao TL, Plato BM, Zhang YP, Dashti SR. Endovascular treatment for venous sinus stenosis in idiopathic intracranial hypertension: an observational study of clinical indications, surgical technique, and long-term outcomes. World Neurosurg. 2019;121:e165–e171. 53. Yan F, Rajah G, Ding Y, et al. Safety and efficacy of intravascular ultrasound as an adjunct to stenting for cerebral venous sinus stenosis-induced idiopathic intracranial hypertension: a pilot study. J Neurosurg. 2019;132:749– 754. 54. Kulhari A, He M, Fourcand F, et al. Safety and clinical outcomes after transverse venous sinus stenting for treatment of refractory idiopathic intracranial hypertension: single center experience. J Vasc Interv Neurol. 2020;11:6– 12. 55. Gordon W, Abraham M. Contralateral approach to transversesigmoid sinus stenting. Interv Neuroradiol. 2020;26:658– 663. 56. Guo XB, Deng X, Wei S, Li DD, Wei Y, Guan S. Analysis of emergency venous sinus stenting in the treatment of acute visual impairment caused by idiopathic cranial hypertension [in Chinese]. Zhonghua Yi Xue Za Zhi. 2020;100:2288– 2292. 57. Touzé R, Bonnin S, Houdart E, et al. Long-term kinetic papilledema improvement after venous sinus stenting in idiopathic intracranial hypertension. Clin Neuroradiol. 2021;31:483–490. 58. Garner RM, Aldridge JB, Wolfe SQ, Fargen KM. Quality of life, need for retreatment, and the re-equilibration phenomenon after venous sinus stenting for idiopathic intracranial hypertension. J Neurointerv Surg. 2021;13:79–85. 59. Lee KE, Zehri A, Soldozy S, et al. Dural venous sinus stenting for treatment of pediatric idiopathic intracranial hypertension. J Neurointerv Surg. 2021;13:465–470. 60. Schwarz J, Al Balushi A, Sundararajan S, et al. Management of idiopathic intracranial hypertension in children utilizing venous sinus stenting. Interv Neuroradiol. 2021;27:257– 265. 61. Wang W, Jia Q, Fan YM, et al. Evaluation of papilledema and visual improvement in patients with idiopathic intracranial hypertension after venous sinus stenting [in Chinese]. Zhonghua Wai Ke Za Zhi. 2021;59:1012–1017. 462 62. Belachew NF, Baschung S, Almiri W, et al. Casper versus precise stent for the treatment of patients with idiopathic intracranial hypertension. Clin Neuroradiol. 2021;31:853– 862. 63. Su H, Zhang RJ, Cao XY, et al. Endovascular stenting for idiopathic intracranial hypertension with different types of venous sinus stenosis [in Chinese]. Zhonghua Nei Ke Za Zhi. 2021;60:728–733. 64. Martinez-Gutierrez CJ, Kole MJ, Lopez-Rivera V, et al. Primary balloon angioplasty of venous Sinus stenosis in idiopathic intracranial hypertension. Interv Neuroradiol. 2022. doi: 10.1177/15910199221089446. 65. Labeyrie MA, Bedarida V, Vever U, et al. Venous sinus stenting after repair of skull base spontaneous cerebrospinal fluid leaks: a single-center retrospective cohort series with case-control analysis. J Neuroradiol. 2022;49:164–168. 66. Labeyrie MA, Fantoni M, Vever U, et al. Intracranial venous sinus stenting for the treatment of lateral sinus stenoses: an analysis of 200 patients. Diagn Interv Imaging. 2021;102:619–627. 67. Hendrix P, Whiting CJ, Griessenauer CJ, Bohan C, Schirmer CM, Goren O. Neuro-ophthalmological evaluation including optical coherence tomography surrounding venous sinus stenting in idiopathic intracranial hypertension with papilledema: a case series. Neurosurg Rev. 2022;45:2239– 2247. 68. Reid K, Winters HS, Ang T, Parker GD, Halmagyi GM. Transverse sinus stenting reverses medically refractory idiopathic intracranial hypertension. Front Ophthalmol. 2022;2. doi: 10.3389/fopht.2022.885583. 69. Oyemade KA, Xu TT, Brinjikji W, et al. Improved ophthalmic outcomes following venous sinus stenting in idiopathic intracranial hypertension. Front Ophthalmol. 2022;2. doi: 10.3389/fopht.2022.910524. 70. Zehri AH, Lee KE, Kartchner J, et al. Efficacy of dural venous sinus stenting in treating idiopathic intracranial hypertension with acute vision loss. Neuroradiol J. 2022;35:86–93. 71. Ogungbo B, Roy D, Gholkar A, Mendelow AD. Endovascular stenting of the transverse sinus in a patient presenting with benign intracranial hypertension. Br J Neurosurg. 2003;17:565–568. 72. Rajpal S, Niemann DB, Turk AS. Transverse venous sinus stent placement as treatment for benign intracranial hypertension in a young male: case report and review of the literature. J Neurosurg. 2005;102:342–346. 73. Paquet C, Poupardin M, Boissonnot M, Neau JP, Drouineau J. Efficacy of unilateral stenting in idiopathic intracranial hypertension with bilateral venous sinus stenosis: a case report. Eur Neurol. 2008;60:47–48. 74. Crosa R, Marabotto O, Meehroff G, et al. Pseudotumor cerebri: a new door opens for treatment. Interv Neuroradiol. 2007;13:145–151. 75. Arac A, Lee M, Steinberg GK, Marcellus M, Marks MP. Efficacy of endovascular stenting in dural venous sinus stenosis for the treatment of idiopathic intracranial hypertension. Neurosurg Focus. 2009;27:E14. 76. 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;21:927– 929. 77. Spilberg GZ, Wajnberg E, Gasparetto EL, Magalhaes G. Case report: endovascular treatment of idiopathic intracranial hypertension. Pakistan J Radiol. 2010;20:23–26. 78. Lazzaro MA, Darkhabani Z, Remler BF, et al. Venous sinus pulsatility and the potential role of dural incompetence in idiopathic intracranial hypertension. Neurosurgery. 2012;71:877–883. 79. Fargen KM, Velat GJ, Lewis SB, Hoh BL, Mocco J, Lawson MF. Concomitant intracranial pressure monitoring during venous sinus stenting for intracranial hypertension secondary to venous sinus stenosis. J Neurointerv Surg. 2013;5:e22. 80. Ding D, Starke RM, Durst CR, Crowley RW, Liu KC. Venous stenting with concurrent intracranial pressure monitoring for Dinkin and Patsalides: J Neuro-Ophthalmol 2023; 43: 451-463 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. State-of-the-Art Review the treatment of pseudotumor cerebri. Neurosurg Focus. 2014;37:1. 81. Young CC, Morton RP, Ghodke BV, Levitt MR. Retrograde 3D rotational venography (3DRV) for venous sinus stent placement in idiopathic intracranial hypertension. J Neurointerv Surg. 2018;10:777–779. 82. Miyachi S, Hiramatsu R, Ohnishi H, Takahashi K, Kuroiwa T. Endovascular treatment of idiopathic intracranial hypertension with stenting of the transverse sinus stenosis. Neurointervention. 2018;13:138–143. 83. Buell TJ, Raper DMS, Ding D, et al. Concurrent venous stenting of the transverse and occipito-marginal sinuses: an analogy with parallel hemodynamic circuits. J Neurosci Rural Pract. 2019;10:334–338. 84. Morisaki Y, Nakagawa I, Omoto K, Wada T, Kichikawa K, Nakase H. Endovascular treatment of idiopathic intracranial hypertension caused by multiple venous sinus stenoses. Surg Neurol Int. 2019;10:47. 85. Drocton GT, Copelan A, Eisenmenger L, et al. Venous sinus stenting as a treatment approach in patients with idiopathic intracranial hypertension and encephaloceles. Interv Neuroradiol. 2021;27:129–136. 86. Alvarado AM, Nalluri P, Alvarado AM, Reeves A, Abraham MG. Unique variant of idiopathic intracranial hypertension dural sinus stenting. Int J Neurosci. 2021;131:196–198. 87. Mathkour M, Scullen T, Kilgore MD, et al. Complete ophthalmoplegia secondary to idiopathic intracranial hypertension managed successfully with dural sinus stenting: a case and systematic review. Clin Neurol Neurosurg. 2021;209:106910. 88. Mugge L, Dang D, Curry B, Whiting R, Crimmins M. Superior ophthalmic vein flow patterns as a marker of venous sinus stenosis and hypertension in idiopathic intracranial hypertension: a case of emergent transverse sinus stenting as treatment of fulminant idiopathic intracranial hypertension. World Neurosurg. 2022;161:170–178. 89. Boddu S, Dinkin M, Suurna M, Hannsgen K, Bui X, Patsalides A. Resolution of pulsatile tinnitus after venous sinus stenting in patients with idiopathic intracranial hypertension. PLoS One. 2016;11:e0164466. 90. Friedman DI, Quiros PA, Subramanian PS, et al; the NORDIC IIHTT Study Group. Headache in idiopathic intracranial hypertension: findings from the idiopathic intracranial hypertension treatment trial. Headache. 2017;57:1195– 1205. 91. Alessi G, Levrier O, Conrath J, et al. Optical coherence tomography in following up papilledema in idiopathic intracranial hypertension treated with lateral sinus stent placement. J Fr Ophtalmol. 2010;33:637–648. 92. Kahan J, Sundararajan S, Brown K, Dinkin M, Oliveira C, Patsalides A. Predicting the need for retreatment in venous sinus stenting for idiopathic intracranial hypertension. J Neurointerv Surg. 2021;13:574–579. 93. El Mekabaty A, Pearl MS, Moghekar A, Gailloud P. Midterm assessment of transverse sinus stent patency in 104 patients treated for intracranial hypertension secondary to dural sinus stenosis. J Neurointerv Surg. 2021;13:182–186. 94. Lavoie P, Audet M-È, Gariepy J-L, et al. Severe cerebellar hemorrhage following transverse sinus stenting for idiopathic intracranial hypertension. Interv Neuroradiol. 2018;24:100– 105. 95. Townsend RK, Jost A, Amans MR, et al. Major complications of dural venous sinus stenting for idiopathic intracranial hypertension: case series and management considerations. J Neurointerv Surg. 2022;14:neurintsurg-2021-017361. Dinkin and Patsalides: J Neuro-Ophthalmol 2023; 43: 451-463 96. Ahmed R, Friedman DI, Halmagyi GM. Stenting of the transverse sinuses in idiopathic intracranial hypertension. J Neuroophthalmol. 2011;31:374–380. 97. Levitt MR, Albuquerque FC, Ducruet AF, Kalani MY, Mulholland CB, McDougall CG. Venous sinus stenting for idiopathic intracranial hypertension is not associated with cortical venous occlusion. J Neurointerv Surg. 2016;8:594–595. 98. Boddu SR, Gobin YP, Dinkin M, Oliveira C, Patsalides A. Impaired drainage of vein of Labbé following venous sinus stenting for idiopathic intracranial hypertension. J Neurointerv Surg. 2019;11:300–306. 99. Fargen KM, Kittel C, Amans MR, Brinjikji W, Hui F. A national survey of venous sinus stenting practices for idiopathic intracranial hypertension. J Neurointerv Surg. 2023;15:507–511. 100. Settecase F, Harnsberger HR, Michel MA, Chapman P, Glastonbury CM. Spontaneous lateral sphenoid cephaloceles: anatomic factors contributing to pathogenesis and proposed classification. AJNR Am J Neuroradiol. 2014;35:784–789. 101. Liebo GB, Lane JJ, Van Gompel JJ, et al. Brain herniation into arachnoid granulations: clinical and neuroimaging features. J Neuroimaging. 2016;26:592–598. 102. Buchowicz B, Chen BS, Bidot S, et al; CSF-Leak Study Group. Prediction of postoperative risk of raised intracranial pressure after spontaneous skull base cerebrospinal fluid leak repair. J Neuroophthalmol. 2021;41:e490–e497. 103. Al Balushi A, Oliveira C, Patsalides A. Idiopathic intracranial hypertension with stenosis of a solitary occipital venous sinus treated with stenting. Interv Neuroradiol. 2020;26:664–667. 104. Boddu SR, Gobin P, Oliveira C, Dinkin M, Patsalides A. Anatomic measurements of cerebral venous sinuses in idiopathic intracranial hypertension patients. PLoS One 2018;13:e0196275. 105. Kishore V, Sundararajan SH, Doustaly R, et al. Magnetic resonance venography for 3-dimensional live guidance during venous sinus stenting. CVIR Endovasc. 2020;3:66. 106. Carter LM, Chakraborty AR, McCoy-Stephens TM, Strickland AE, Bohnstedt BN, Gross NL. Venous sinus stenosis treatment in pediatric idiopathic intracranial hypertension: illustrative case and literature review. World Neurosurg. 2021;149:2–7. 107. Leishangthem L, SirDeshpande P, Dua D, Satti SR. Dural venous sinus stenting for idiopathic intracranial hypertension: an updated review. J Neuroradiol. 2019;46:148–154. 108. Venous Sinus Stenting With the River Stent in IIH. Serenity Medical, Inc. Available at: https://clinicaltrials.gov/ct2/ show/NCT03556085. 109. Inam ME, Martinez-Gutierrez JC, Kole MJ, et al. Venous sinus stenting for low pressure gradient stenoses in idiopathic intracranial hypertension. Neurosurgery. 2022;91:734–740. 110. Satti SR, Leishangthem L, Chaudry MI. Meta-analysis of CSF diversion procedures and dural venous sinus stenting in the setting of medically refractory idiopathic intracranial hypertension. AJNR Am J Neuroradiol. 2015;36:1899–1904. 111. Intervention To Preserve Vision In Idiopathic Intracranial Hypertension: Evaluation Of Clinical Effectiveness And Cost Effectiveness. Chief Investigator: A Sinclair. https:// fundingawards.nihr.ac.uk/award/NIHR131211. 112. Stenting Versus Neurosurgical Treatment of Idiopathic Intracranial Hypertension. (HYDROPTIC). PI: Pierre Bourdillon, MD. Available at https://clinicaltrials.gov/ct2/show/ NCT05050864. 113. Operative Procedures vs. Endovascular Neurosurgery for Untreated Pseudotumor Trial (OPEN-UP). PI: Principal Investigator: Felipe C Albuquerque, M. Available at: https:// clinicaltrials.gov/ct2/show/NCT02513914. 463 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |
| Date | 2023-12 |
| Date Digital | 2023-12 |
| References | 1. Quincke H. Meningitis serosa. Sammi Klin Vortr, Leipzig, No 67. InnMed. 1893;23:655-662. 2. Nonne M. Über falle vom symptomkomplex "tumor cerebri"mitausgang in heilung (pseudotumor cerebri). Dtsch Z Nervenheilkd. 1904;27:169-216. 3. Foley J. Benign forms of intracranial hypertension; toxic and otitichydrocephalus. Brain. 1955;78:1-41. 4. Buchheit WA, Burton C, Haag B, Shaw D. Papilledema and idiopathic intracranial hypertension. N Engl J Med. 1969;280:938-942. 5. Avisar I, Gaton DD, Dania H, Stiebel-Kalish H. The prevalence of polycystic ovary syndrome in women with idiopathic intracranial hypertension. Scientifica (Cairo). 2012;2012:708042. |
| Language | eng |
| Format | application/pdf |
| Type | Text |
| Publication Type | Journal Article |
| Source | Journal of Neuro-Ophthalmology, December 2023, Volume 43, Issue 4 |
| Collection | Neuro-Ophthalmology Virtual Education Library: Journal of Neuro-Ophthalmology Archives: https://novel.utah.edu/jno/ |
| Publisher | Lippincott, Williams & Wilkins |
| Rights Management | © North American Neuro-Ophthalmology Society |
| ARK | ark:/87278/s6jfex2e |
| Setname | ehsl_novel_jno |
| ID | 2635249 |
| Reference URL | https://collections.lib.utah.edu/ark:/87278/s6jfex2e |



