ABSTRACT
Background
Given the association between spontaneous cerebrospinal fluid (sCSF) leak and idiopathic intracranial hypertension (IIH), and the association of IIH and venous sinus stenosis (VSS), we sought to determine the prevalence of VSS in sCSF leak and the role of venous sinus stenting for sCSF leak.
Methods
A protocol was registered in PROSPERO [CRD42024568270]. A search was conducted in four electronic databases: Medline (Ovid), Embase, CINAHL, Web of Science, and Cochrane CENTRAL. Two reviewers independently screened citations and extracted data. Methodological quality was assessed using the Joanna Briggs Institute's critical appraisal tool. Data were pooled using a random effects model to calculate overall prevalence and relative risk (RR).
Results
Fifteen studies met the final inclusion criteria, with a total of 372 patients presenting with sCSF leak. The pooled prevalence of VSS in patients with sCSF leak was 0.71 (95% CI: 0.56–0.83, I 2 = 74%). VSS was three‐fold greater in patients with sCSF leak compared to those without, although this was not statistically significant (RR = 3.11; 95% CI: 0.64–15.27, I 2 = 87%). Ninety percent of patients with VSS who underwent venous sinus stenting as adjunctive therapy to surgical repair of sCSF leak or for medically refractive IIH demonstrated resolution of symptoms without sCSF leak recurrence at last follow‐up.
Conclusion
VSS is common in patients with sCSF leak, and adjunctive venous sinus stenting after surgical leak repair may benefit a subset of patients. Further studies are needed to clarify the role of venous sinus stenting in conjunction with surgical repair of leaks.
Keywords: idiopathic intracranial hypertension, spontaneous CSF leak, venous sinus stenosis, venous sinus stent
1. Introduction
Spontaneous cerebrospinal fluid (sCSF) leaks, characterized by bone‐dura defects at the skull base in the absence of a history of trauma, surgery, or other identifiable causes, are frequently presumed to be associated with idiopathic intracranial hypertension (IIH) [1, 2, 3, 4]. However, identifying raised intracranial pressure (ICP) in the presence of sCSF leak remains challenging as sCSF leaks function as a natural shunt, which may relieve intracranial hypertension and mask typical signs and symptoms of raised ICP. Consequently, traditional IIH diagnostic criteria may not be met, resulting in reduced sensitivity for detecting IIH in these patients. Indeed, the prevalence of IIH in sCSF leak in the literature is highly variable ranging from 20% to 72% [5, 6].
The primary approach for managing sCSF leaks is through surgical repair, which reduces the risk of intracranial complications such as meningitis [7]. While postoperative management of elevated ICP with acetazolamide or CSF shunting has been shown to improve the success rate of endoscopic repair of CSF leaks [8], the necessity of such interventions remains debated. Some studies argue that not all patients with sCSF leaks benefit from aggressive ICP management, citing concerns with medication side effects or shunt‐related complications, and must be considered on an individual basis [4, 9].
Venous sinus stenosis (VSS) is a commonly observed feature among patients with IIH, and is thought to cause a relative obstruction of venous outflow with elevated proximal venous pressures, ultimately leading to increased ICP [10, 11, 12]. Venous sinus stenting was described for the first time by Higgins et al. in 2002 and is currently a therapeutic option in VSS management in patients with symptomatic IIH [13]. In a previous meta‐analysis, venous sinus stenting compared favorably with those of CSF diversion procedures, demonstrating greater improvement of symptoms and reduced complications and need for additional intervention [14].
Several studies have noted an association between sCSF leaks and VSS, with some studies reporting underlying VSS in approximately 80% of patients with sCSF leaks compared to 10%–40% in controls without sCSF leak [15, 16]. This raises the possibility of finding a correctable underlying cause of sCSF leaks. Indeed, a recent systematic review and meta‐analysis by Rasmussen and colleagues highlights the evolving role of venous sinus stenting in managing sCSF leaks, reporting failure rates of 18.6%–26.4% with VSS alone and lower rates of 5.5%–12.2% when combined with surgical repair [17]. Notably, 88.7% of patients experienced resolution of IIH‐related symptoms post‐stenting; however, the overall prevalence of VSS in sCSF leak patients and the potential indications for stenting were not elucidated. The objective of this study is to systematically review the literature to identify the prevalence and risk of VSS in patients with sCSF leaks, and to investigate the indications and role of venous sinus stenting in this patient population.
2. Methods
2.1. Protocol
A protocol was constructed and registered with the International Prospective Register of Systematic Reviews (PROSPERO) [CRD42024568270] in accordance with the Preferred Reporting Items for Systematic Reviews and Meta‐Analyses (PRISMA) reporting guidelines [18]. A Population, Intervention, Comparison, Outcome (PICO) statement was followed to assess reviewed studies for inclusion and exclusion. PICO criteria are as follows:
Population: Adult patients ≥18 years of age presenting with spontaneous cerebrospinal fluid leak.
Intervention: Definitive or adjunctive venous sinus stenting or not applicable. Definitive is defined as venous sinus stenting in the absence of surgical sCSF leak repair. Adjunctive is defined as concurrent or successive venous sinus stenting with surgical sCSF leak repair.
Comparison: Not applicable.
Outcomes: Prevalence and relative risk of venous sinus stenosis and/or resolution of sCSF leak and complications secondary to venous sinus stenting.
The full protocol is available in Appendix S1.
2.2. Eligibility Criteria
Included studies described adults presenting with sCSF leak without any identifiable underlying cause and investigated for the presence of VSS. Studies that described the use of venous sinus stenting for the treatment of sCSF leak in the presence of VSS were also included. Studies including patients with a history of acute head trauma, congenital malformations, tumor or infection with erosion into the skull base, or other known cause for CSF leak were excluded. Eligible articles were further confined to case reports, case series, cohort studies, uncontrolled intervention studies, randomized, or non‐randomized controlled trials from peer‐reviewed journals. Review articles, textbook chapters, conference abstracts, commentaries, expert opinions, editorials, and other non‐original studies were excluded. Non‐English studies were excluded.
2.3. Information Sources and Search Strategy
A comprehensive search was performed in four electronic databases: Medline (Ovid), Embase, CINAHL, Web of Science, and Cochrane CENTRAL from inception to July 11, 2024, and updated until the date of submission. Combinations of MeSH terms such as “Cerebrospinal fluid leaks,” “Cerebrospinal fluid rhinorrhea,” “Cerebrospinal fluid otorrhea,” “Pseudotumor cerebri,” “Intracranial hypertension,” and “Cranial sinuses, abnormalities,” and key terms related to “cerebrospinal fluid leak,” “CSF leak,” “CSF rhinorrhea,” “CSF otorrhea,” “pseudotumor cerebri,” “idiopathic intracranial hypertension,” “benign intracranial hypertension,” “venous sinus stenosis,” and “cerebral sinus stenosis” were used to identify relevant articles. The full search strategy can be found in Appendix S2. Reference lists of identified articles and grey literature were manually searched for relevant studies. Searches were not limited by geographical region or date of publication.
2.4. Study Selection Process and Data Charting
Following the removal of duplicates, all article titles and abstracts were included according to the above eligibility criteria. The full‐text review was performed independently by study authors J.X. and H.H. for final inclusion of studies into the analysis (Figure 1). Disagreements were resolved through discussion, and any disputes were settled by the senior author (J.L.). The authors were not blinded to journal titles, study authors, or research institutions.
FIGURE 1.
PRISMA flowchart of study selection. PRISMA refers to Preferred Reporting Items for Systematic Reviews and Meta‐Analyses.
Data extraction forms were created by study author J.X. Studies that met the final inclusion criteria were queried by study authors J.X. and H.H. independently for study characteristics, patient demographics, site of CSF leak, presence of VSS, location of VSS, presence of IIH, clinical findings of IIH, management strategies, indication for venous sinus stenting when applicable, outcomes, complications, and length of follow‐up.
2.5. Assessment of Quality of Evidence
Two study authors (J.X. and H.H.) independently conducted the risk‐of‐bias assessment for the final included studies using the Joanna Briggs Institute (JBI) critical appraisal tools for case–control, cohort, case series, and case studies [19]. Each assessed study category was assigned as yes, no, unclear, and not applicable and a total score was assigned out of 10 for case–control and case series, and out of 11 and eight for cohort and case reports, respectively. Two study authors (J.X., H.H., or C.K.) independently judged whether the risk of bias for each study was considered low, moderate, or high based on the total score. Discrepancies were resolved through discussion with the team and senior author (J.L.).
2.6. Meta‐Analysis
RStudio (Version: 2023.12.1+402) software was used for meta‐analysis of the available data. The prevalence of VSS associated with sCSF leak in patients was obtained from five included studies and pooled through a random effects meta‐analysis using the inverse variance method and examined using a forest plot. Case reports and studies that only included sCSF leak patients with VSS and underwent stenting were excluded from prevalence calculations. Comparisons of the presence of VSS between patients with and without sCSF leak were made by pooling data using a random‐effects model and summarized as risk ratios (RR) using the available data from two included studies. Between‐study heterogeneity was assessed using the I 2 statistic and the p‐value for heterogeneity (via the Cochrane's Q test). An I 2 value ≥75% or a p‐value less than 0.05 was considered high between‐study heterogeneity.
3. Results
3.1. Baseline Characteristics
Following the removal of duplicates, 52 studies were identified in the literature search. After initial title and abstract screening, 32 studies were assessed for eligibility (Figure 1). Three studies were identified through screening of reference lists. Ultimately, 15 studies met the final inclusion criteria and were included for analysis. There were seven case series, three case reports, three retrospective cohort studies, and two retrospective case–control studies. A summary of baseline study characteristics is presented in Table 1.
TABLE 1.
Summary of baseline study characteristics.
| Study | Country | Study type | N | Study period |
Female (%) |
Age (median, IQR) |
BMI (kg/m2) |
HTN (%) |
DM (%) |
OSA (%) |
History of prior sCSF leak/ meningocele, n (%) |
Patients with sCSF leak | Length of follow‐up |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Bedarida 2020 [16] | France | Retrospective matched case–control | 29 | 10 years | 20 (69) | 57 (48–66) |
Median [IQR] Controls: 25 [15–28] Patients: 35 [28–39] |
Controls: 2 (7) Patients: 14 (48) |
Controls: 1 (3) Patients: 5 (17) |
Controls: 0 (0) Patients: 1 (3) |
Not reported | 29 | Not reported |
| Hurel 2023 [21] | France | Retrospective case–control | 64 | 12 years | 23 (36) | 50 (13.01) b |
Mean [SD] Controls: 32.1 [5.46] sCSFL: 29.4 [7.89] |
Not reported | Not reported | Not reported | Not reported | 32 | Not reported |
| Buchowicz 2021 [20] | USA | Retrospective observational cohort | 57 | 6 years | 55 (96) |
Group 1: 46 (39.5–57) Group 2: 51 (46–69.25) |
Median [IQR] Group 1: 35.6 [31.1–45.6] Group 2: 35.6 [29.1–39.6] |
Not reported | Not reported | Not reported | Not reported | 57 |
Mean 27.6 ± 64 weeks (range: 1.6–330 weeks) |
| Labeyrie 2021 [24] | France | Retrospective observational cohort | 200 | 8 years | 186 (93) | 39 (14) b |
Median [IQR] 30 [17–57] |
Not reported | Not reported | Not reported | Not reported | 35 |
3 months post‐stenting, 1 year, then every 2 years |
| Labeyrie 2022 [25] | France | Retrospective observational cohort | 73 | 10 years 9 months | 17 (23) | 58 (45–69) |
Median [IQR] 31 [27–36] |
Not reported | Not reported | Not reported | Not reported | 73 | 2.4 years |
| Asi 2023 [15] | USA | Case series | 25 | 10 years | 22 (88) | 51 (45–62) | BMI >30: 19 (76) | 15 (60) | 7 (28) | 1 (7) | Not reported | 25 | Not reported |
| Bidot 2021 [6] | USA | Case series | 36 | 8 years 4 months | 34 (94) | 50 (45–54) |
Median [IQR] 36.8 [30.5–39.9] |
Not reported | Not reported | Not reported | Not reported | 36 | 8.7 months |
| Iyer 2017 [23] | USA | Case series | 2 | 1 year | 1 (50) | 56.2 (range: 52–61) b |
Patient 1: 26.6 Patient 2: 34.1 |
0 (0) | 0 (0) | 1 (50) | None | 2 | 14–32 months |
| Lenck 2022 [26] | France | Case series | 5 | 6 years | 5 (100) | 39 (15–49) |
Case 1: 32 Case 2: 26 Case 3: 52.2 Case 4: 36.7 Case 5: 36.5 |
Not reported | Not reported | Not reported | 2 (40) | 5 |
12 months (range: 6–63) |
| López‐Hernández 2024 [27] | Spain | Case series | 8 | Not reported | 5 (63) | 52 (46–72) |
Patient 1: 31.6 Patient 2: 30.7 Patient 3: 27.1 Patient 4: 35.2 Patient 5: 45.8 Patient 6: 20.7 Patient 7: 29.8 Patient 8: 32.3 |
Not reported | Not reported | Not reported | Not reported | 8 | 1 year |
| Michael 2022 [28] | USA | Case series | 54 a | 6 years | 44 (81) | 49.1 (15.4) b |
Mean [SD] 32.2 [7.6] |
Not reported | Not reported | Not reported | 6 (11.1) | 54 | Mean 96 ± 55 months (range: 5–196 months) |
| Tosi 2023 [31] | USA | Case series | 13 | Not reported | 10 (77) | 46.4 (24.9–67.8) |
Mean [SD] 34.6 [2.3] |
Not reported | Not reported | Not reported | Not reported | 13 | Mean 26.9 months |
| Ellens 2024 [22] | USA | Case report | 1 | N/A | 1 (100) | Not reported |
Not reported (patient was reported to be “obese”) |
Not reported | Not reported | Not reported | Not reported | 1 | 6 months |
| Owler 2003 [29] | Australia | Case report | 1 | N/A | 1 (100) | 32 | Not reported | Not reported | Not reported | Not reported | 1 (100) | 1 | 11 months |
| San Millán 2019 [30] | Switzerland | Case report | 1 | N/A | 1 (100) | 72 | <25 | Not reported | Not reported | Not reported | Not reported | 1 | 39 months |
Abbreviations: IQR, interquartile range; sCSF leak, spontaneous cerebrospinal fluid leak.
Only 15 sCSF leak patients were imaged for presence of venous sinus stenosis.
Mean (standard deviation).
A total of 372 patients presented with sCSF leak. The most frequently reported sites of defect were the ethmoid (n = 61), sphenoid (n = 58), cribriform plate/ethmoid (n = 18), and frontal sinus (n = 11) (Table 2). Structural abnormalities such as encephaloceles and meningoceles were reported in 87 patients (23%). All patients who were diagnosed with VSS underwent computed tomography (CT) venogram, magnetic resonance (MR) venogram, digital subtraction angiography (DSA), and/or venous manometry. The most commonly documented features of IIH were VSS (n = 248), partial/empty sella (n = 74), enlarged Meckel's cave (n = 42), optic nerve tortuosity (n = 26), and optic nerve sheath dilation/enlargement (n = 24). Lumbar puncture opening pressure (LPOP) was documented in seven studies, and ranged from 6 cmH2O to a mean of 32.2 cmH2O. Pressure gradient across the site of VSS was documented in seven studies, and ranged from 2 to 14 mmHg. Presence of arachnoid granulations was identified in three studies (n = 18).
TABLE 2.
Characteristics of VSS and sCSF leak.
| Study | Patients with sCSF leak | Patients with VSS | Patients without VSS | Site of defect (no VSS) | Site of defect (VSS) | Site of VSS | Definite IIH | IIH features | Presence of cephaloceles | Presence of arachnoid granulations | LP opening pressure | Pressure gradient across VSS |
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Asi 2023 [15] | 25 | 20 | 5 |
CP: 1 ES: 2 SS: 2 |
CP: 2 ES: 9 SS: 8 FS: 3 SO: 1 |
Not reported | Not reported | Partial/empty sella: 15 | Not reported | Not reported | Not reported | Not reported |
| Bedarida 2020 [16] | 29 | 23 | 6 |
CP/ES: 18 SS: 9 FS: 1 CL: 2 |
Bilateral TVS: 23 | Not reported |
Visual field defect = 3 Bilateral papilledema = 2 Elevated LPOP (>25 mmHg) = 1 |
Not reported | Not reported | Not reported | Not reported | |
| Bidot 2021 [6] | 36 | 17 | 19 |
ES: 10 SS: 10 FS: 2 TB: 14 |
Bilateral TVS: 17 |
5 | Presumed IIH (presumed pre‐existing IIH, previously undiagnosed papilledema (CSF‐OP, 23 cmH2O), previously undiagnosed resolved papilledema (CSF‐OP, 22 cmH2O): 3 | Cephalocele: 26 | Not reported |
Median (IQR): 22.5 cmH2O (16; 27) |
Not reported | |
| Buchowicz 2021 [20] | 57 | 35 | 22 |
ES: 18 SS: 15 FS: 3 TB: 22 |
Bilateral TVS: 35 |
6 |
Partial/empty sella: 49 Optic nerve head protrusion: 4 Scleral flattening: 22 Perioptic cerebrospinal fluid: 21 Optic nerve tortuosity: 25 Enlarged Meckel's cave: 37 |
Cephalocele: 48 | Not reported | Not reported | Not reported | |
| Hurel 2023 [21] | 32 | 27 | 5 |
ES: 20 SS: 11 FS: 1 |
Unilateral or Bilateral TVS: 27 |
Not reported |
At least two features of IIH: 24 Dilation of the optic nerves: 17 Vacuity of the pituitary fossa: 17 Posterior globe flattening: 4 |
Not reported | Yes: 16 | Not reported | Not reported | |
| Ellens 2024 [22] | 1 | 1 | 0 | N/A | Not reported |
Right transverse‐sigmoid sinus stenosis: 1 |
1 | N/A | None | None | 29 cmH2O | 13 mmHg |
| Iyer 2017 [23] | 2 | 2 | 0 | N/A |
SS: 1 T: 1 |
Bilateral TVS: 2 | 2 | Partial/empty sella: 2 | Meningoencepha‐locele: 2 | None |
Patient 1: Mean 25.8 cmH2OPatient 2: Mean 32.2 cmH2O |
Patient 1: Left: 4 mmHg Right: 6.7 mmHg Patient 2: Left: 13.2 mmHg Right: 12.4 mmHg |
| Labeyrie 2021 [24] | 35 | 35 | 0 | N/A | Not reported |
Unilateral or bilateral TVS: 35 |
Not reported for subset of patients | Not reported for subset of patients | Not reported for subset of patients | Not reported for subset of patients | Not reported | Not reported |
| Labeyrie 2022 [25] | 73 | 57 | 16 | Not reported | Not reported |
Unilateral or bilateral TVS: 57 |
Not reported for subset of patients | Not reported for subset of patients | Not reported for subset of patients | Not reported for subset of patients | Not reported | Not reported |
| Lenck 2022 [26] | 5 | 5 | 0 | N/A | CP: 5 | Bilateral TVS: 5 | Not reported |
Empty sella: 4 Optic nerve sheath enlargement: 3 Enlarged Meckel's cave: 4 |
Encephalocele/Meningocele: 3 | None |
Patient 2: 28 cmH2O Patient 4: 17 cmH2O |
Median 6.5 mmHg (range: 3–9 mmHg) |
| López‐Hernández 2024 [27] | 8 | 8 | 0 | N/A |
Nasal: 4 Left ear: 3 Right ear: 1 |
Bilateral TVS: 5 Left TVS: 2 Right TVS: 1 |
Not reported |
Partial/empty sella: 2 Dilation of optic nerve sheath: 3 Headache: 5 |
None | None |
Mean 29.4 cmH2O |
Mean 10 mmHg (n = 3) |
| Michael 2022 [28] | 54† | 3 | 12 |
CP: 13 ES: 11 SS: 23 CL: 2 |
ES: 3 | Not reported | Not reported for subset of patients | Not reported for subset of patients | Not reported for subset of patients | Not reported for subset of patients | Not reported | Not reported |
| Owler 2003 [29] | 1 | 1 | 0 | N/A | ES: 1 | Right TVS: 1 | 1 |
Partial/empty sella: 1 Headache: 1 Visual acuity change: 1 Optic disc pallor: 1 Optic nerve sheath enlargement: 1 Enlarged Meckel's cave: 1 |
None | Yes: 1 | Not reported | 14 mmHg |
| San Millán 2019 [30] | 1 | 1 | 0 | N/A | CP: 1 |
Bilateral TVS: 1 Right sigmoid sinus stenosis: 1 |
1 |
Partial/Empty sella: 1 Enlarged CSF spaces around oculomotor nerves: 1 Middle cranial fossa arachnoid pits: 1 Optic nerve tortuosity: 1 |
Meningocele: 1 | Yes: 1 | 6 cmH2O | 2–3 mmHg |
| Tosi 2023 [31] | 13 | 13 | 0 | N/A |
CP: 2 SS: 4 FS: 1 T: 4 Sigmoid plate: 1 Middle fossa: 1 |
Not reported | Not reported |
Headache: 6 Tinnitus: 9 |
Encephalocele: 7 | None |
Mean 23.3 ± 2.6 cmH2O (n = 10) |
Mean 9.3 ± 1.3 mmHg (n = 10) |
Abbreviations: CL, clival; CP, cribriform plate; ES, ethmoid sinus; FS, frontal sinus; IIH, idiopathic intracranial hypertension; LP, lumbar puncture; sCSF leak, spontaneous cerebrospinal fluid leak; SO: supraorbital; SS, sphenoid sinus; T, tegmen; TB, temporal bone; TVS, transverse sinus stenosis; VSS, venous sinus stenosis † only 15 sCSF leak patients were imaged for presence of VSS.
3.2. Venous Sinus Stenosis in sCSF Leak
Data from five out of 15 studies (n = 211) reported the proportion of patients with sCSF leak who were also found to have VSS, allowing for the calculation of VSS frequency within this study‐defined cohort (Table 2) [6, 15, 16, 20, 21]. Across individual studies, the frequency of VSS in patients with sCSF leak ranged from 47% to 84% [6, 21]. The pooled proportion of VSS in patients with sCSF leak was 0.71 (95% confidence interval [CI]: 0.56–0.83, I 2 = 74%) (Figure 2). In two studies that compared the frequency of VSS in patients with and without sCSF leak, meta‐analysis suggested that VSS was more commonly observed in patients with sCSF leak (RR = 3.11; 95% CI: 0.64–15.27, I 2 = 87%) (Figure 3), though this difference did not reach statistical significance [16, 21]. There was high heterogeneity amongst studies, likely due to considerable variability in study populations or methodologies, limiting the reliability of these pooled estimates. In Buchowitz et al., the presence of bilateral transverse VSS increased the risk of being in a patient group with postoperative papilledema, recurrent CSF leak, or need for CSF shunting after surgical sCSF leak repair by 4.2 times [20].
FIGURE 2.
Forest plot showing individual study and pooled proportion of venous sinus stenosis (VSS) in sCSF leak patients, with 95% confidence interval (CI).
FIGURE 3.
Forest plot showing relative risk of venous sinus stenosis (VSS) in patients with spontaneous cerebrospinal fluid (sCSF) leak (+sCSFL) versus patients without sCSF leak (−sCSFL), with 95% confidence interval (CI).
3.3. Role of Venous Sinus Stenting in sCSF Leak
Eighty‐six patients across 10 studies underwent venous sinus stenting for the management of sCSF leak in patients with underlying IIH and VSS (Table 3) [22, 23, 24, 25, 26, 27, 28, 29, 30, 31]. The overall primary success rate of venous sinus stenting as an adjunctive or definitive treatment of sCSF leak was 90% (77 out of 86 patients). Indications for stenting included medically refractory symptomology defined by persistent sCSF leak despite medical management, intolerable side effects of medication, and surgically inaccessible leaks for definitive treatment. Time from surgical repair‐to‐stenting ranged from 15 days to 1.5 years. Dual antiplatelet therapy initiation prior to stenting was reported in seven studies (n = 79).
TABLE 3.
Venous sinus stenting indications, outcomes, and complications.
| Study | Procedure | Repair approach | Time between repair and stenting | Indication(s) for stenting | Resolution of sCSF leak and/or IIH (%) | Anticoagulation use | Complications |
|---|---|---|---|---|---|---|---|
| Ellens 2024 [22] | Surgical repair + stenting | Not reported | Not reported | Patient unable to tolerate medical therapy due to side effects. | 0 (0) | Not reported |
Development of a Borden type 1 dAVF 3 months post‐stenting Transarterial embolization was performed with venous remodeling Symptomatic resolution was achieved Required LP shunt placement due to persistent elevated ICP |
| Iyer 2017 [23] | Surgical repair + stenting |
Endonasal: 1 Transcranial: 1 |
1 year: 1 9 months: 1 |
Acetazolamide side effects and overall risks of long‐term acetazolamide Bilateral VSS with persistent, medically refractory symptomatology |
2 (100) |
ASA + clopidogrel (latter stopped 6 months post‐stenting) |
None |
| Labeyrie 2022 [25] | Surgical repair + stenting | Endonasal: 22 | 1.5 years | Stenting was considered after leak repair in patients with VSS criteria | 21 (95) | Dual antiplatelet for 3 months, followed by ASA only for 1 year |
Groin puncture hematoma requiring blood red cell transfusion: 1 Headache (self‐limited): 6 |
| López‐Hernández 2024 [27] | Surgical repair + stenting |
Endonasal: 1 Transmastoid: 2 |
>1 month | Medically refractory to acetazolamide with TVS and pressure gradient exceeding 6 mmHg | 3 (100) | Not reported | Not reported |
| Michael 2022 [28] | Surgical repair + stenting | Endonasal: 3 | Not reported | Not reported | 3 (100) | Not reported | Not reported |
| Owler 2003 [29] | Surgical repair + stenting | Transcranial: 1 | 2 months | LP shunt was poorly tolerated | 1 (100) | Clopidogrel for 1 month and ASA | None |
| Tosi 2023 [31] | Surgical repair + stenting (n = 13) |
Endonasal: 8 Transcranial: 5 |
15–192 days | Not reported | 12 (92) b | Dual antiplatelet therapy |
Meningitis (resolved with antibiotics): 1 Postoperative intracranial hemorrhage causing seizures (managed expectantly): 1 |
| Labeyrie 2021 [24] |
Stenting (n = 18), Surgical repair + stenting (n = 17) |
Endonasal: 17 | Not reported | Adjunctive treatment after endoscopic repair to prevent leak recurrences, or as primary treatment in patients with cryptogenic leaks non‐accessible to repair | 30 (86) | Dual antiplatelet for 3 months, followed by ASA only for 1 year |
a Headache: 42 Groin hematoma requiring blood cell transfusion or surgery: 9 Stent thrombosis: 3 Epistaxis requiring embolization: 2 General seizure: 1 Anaphylactic shock: 1 |
| Lenck 2022 [26] | Stenting | Not reported | Not reported | Medically refractory to acetazolamide in 4 patients | 4 (80) | Dual antiplatelet for 3 months, followed by ASA only for 1 year | Headache (self‐limited): 1 |
| San Millán 2019 [30] | Stenting | Not reported | >1 month |
In the absence of encephaloceles, surgical repair was not thought to be necessary, provided that IIH was corrected Stenting was preferred over CSF shunting as it offered the advantage of treating the cause of IHH |
1 (100) |
ASA + clopidogrel (latter stopped 6 months post‐stenting) |
None |
Abbreviations: ASA, acetylsalicylic acid; ICP, intracranial pressure; IIH, idiopathic intracranial hypertension; LP, lumboperitoneal; sCSF, spontaneous cerebrospinal fluid; TVS, transverse sinus stenosis; VSS, venous sinus stenosis.
Complications of stenting are not limited to sCSF leak patients.
Two patients underwent stenting prior to repair. One patient had a leak recurrence, which resolved with repeat repair and stenting.
Five studies (n = 56) employed the use of venous sinus stenting as an adjunct to surgical repair for prevention of CSF leak recurrence [24, 25, 28, 29, 31]. The primary resolution rate of sCSF leak after stenting was found by Labeyrie et al. to be 86%, although the percentage of patients undergoing adjunctive or definitive therapy was not differentiated [24]. Recurrence of CSF leak was reported in 9% of patients at a median follow‐up of 2.2 years. In a more recent case–control study by the same authors, the overall rate of successful sCSF leak repair with adjunctive stenting was 95% at a median follow‐up of 2.4 years [25]. Furthermore, stenting was associated with significantly less leak recurrence and less need for additional IIH treatment (i.e., pharmacologic therapy, shunting, or diversion procedures) compared to controls without stenting. Similar positive results were reported by Michael et al., where all three patients receiving adjuvant stenting following surgical repair did not experience sCSF leak recurrence at a mean follow‐up of 96 months [28]. In Tosi et al., 12 out of 13 (92%) patients who underwent combined surgical sCSF leak repair and venous sinus stenting demonstrated resolution of sCSF leak and associated symptoms with no CSF leak recurrence at a mean follow‐up of 26.9 months [31]. In a case report by Owler et al., stenting was considered after poor toleration of a lumboperitoneal shunt [29]. Successful deployment of the stent allowed for removal of the shunt, and the patient remained symptom‐free at 11‐month follow‐up.
Three studies (n = 24) employed venous sinus stenting for definitive treatment of sCSF leak [24, 26, 30]. In San Millán et al., venous sinus stenting was used as a stand‐alone treatment for sCSF leak, given that surgical repair of the sCSF leak was deemed unnecessary due to the absence of encephaloceles and provided that the underlying IIH was corrected [30]. Stenting was chosen over CSF shunting due to the underlying VSS. At 9 months post‐stenting, the patient presented with a few episodes of isolated possible rhinorrhea that resolved spontaneously after a few days. There was no sCSF leak recurrence at 39‐month follow‐up. In Lenck et al., all patients with sCSF leak, two (40%) of whom were refractory to surgical repair, failed acetazolamide therapy [26]. sCSF leak resolved in four out of five patients (80%) after stenting.
Three studies (n = 6) investigated the use of venous sinus stenting for medically refractory IIH after sCSF leak repair [22, 23, 27]. In a case series by Iyer et al., both patients underwent stenting due to refractory IIH (persistent headache, elevated opening pressure) after surgical sCSF leak repair. In one patient, IIH symptoms improved with high doses of acetazolamide after surgical sCSF leak repair; however, they were not able to tolerate the side effects and underwent subsequent evaluation for stenting [23]. Acetazolamide was weaned 8–13 months post‐stenting, with no further clinical findings concerning increased ICP or leak recurrence. Most recently, in López‐Hernández et al., all patients who underwent endoscopic repair for sCSF leak with medically refractory IIH demonstrated normal ICP values after stenting, with no leak recurrence at 1‐year follow‐up [27].
Complications of venous sinus stenting are presented in Table 3. Labeyrie et al. discussed general complications of venous sinus stenting in patients with and without sCSF leak, including headache (n = 42), groin hematoma (n = 9), stent thrombosis (n = 3), epistaxis (n = 2), seizure (n = 1), and anaphylactic shock (n = 1) [24]. In Tosi et al., one patient developed postoperative meningitis, which resolved with antibiotics, and another patient developed a postoperative intracranial hemorrhage causing seizures, both managed accordingly [31]. In a recent case report, a patient presenting with refractory IIH symptoms following sCSF leak repair was found to have right‐sided VSS. After stenting, she reported a recurrence of symptoms, and subsequent angiography revealed a Borden Type 1 dural arteriovenous fistula (dAVF) along the stent. Following trans‐arterial embolization with venous remodeling, she reported a resolution of symptoms, but ultimately required lumboperitoneal shunt placement due to persistent elevated ICP [22].
3.4. Risk‐of‐Bias Assessment
Critical appraisal of all studies using the JBI tool is summarized in Appendix S3. In three retrospective cohort studies, risk of bias was rated as low by JBI standards; however, none of these studies identified or adjusted for potential confounding variables, which limits the interpretability of their findings, particularly for outcomes related to risk or treatment response [20, 24, 25]. Similarly, two case–control studies were also rated as low risk of bias, but failed to address confounders in their design or analysis [16, 21]. For case series, one study had a moderate risk of bias, with unclear reporting of consecutive and complete inclusion of participants, and did not report site or clinic information [27]. Case reports were uniformly rated as low risk of bias by JBI criteria, but inherently provide limited generalizability [22, 29, 30]. Furthermore, across study designs, important outcome measures—such as postoperative complications, short‐ and long‐term follow‐up data, and treatment durability—were inconsistently reported or absent. In most studies, statistical analyses lacked adjustments for relevant confounders, further limiting confidence in the reported associations.
4. Discussion
The current evidence in the literature supports a strong association between IIH and sCSF leaks [1, 2, 3, 4]. VSS is frequently observed in patients with IIH and is thought to play a role in its pathophysiology by contributing to elevated ICP [10, 11, 12]. Our systematic review and meta‐analysis highlight a significant pooled proportion of VSS in patients with sCSF leaks, with approximately 71% of these patients exhibiting this condition. This finding supports the growing evidence of a relationship between sCSF leaks, IIH, and VSS, suggesting that VSS may be an important factor in the etiology and management of sCSF leaks. However, it is important to note that these findings are limited to a subset of studies that included only patients who were specifically investigated for the presence of VSS and are therefore not representative of the broader sCSF population. The term “prevalence” is not used here in the epidemiological sense, as the included sample does not reflect a large, unselected, or population‐based cohort. Our pooled proportion is slightly lower than that reported in previous single‐center retrospective studies, which found VSS in 79% and 80% of patients with sCSF leaks [15, 16]. These two single‐center studies also noted VSS prevalence rates of 10% and 40% in control populations without sCSF leaks, highlighting the potential role for VSS in patients with sCSF leaks. In the general population, the prevalence of unilateral and bilateral transverse VSS is estimated to be 33% and 5%, respectively [32]. The variation in proportion between our meta‐analysis and single‐center studies may reflect differences in study populations, sample size, diagnostic criteria, and methodologies used to assess VSS in the pooled sample.
VSS is thought to partly obstruct CSF outflow and impair venous drainage from the brain, which leads to a venous pressure gradient across the site of VSS and subsequently to elevated ICP, a key feature of IIH [33, 34]. Biousse et al. proposed a unifying model in which IIH and VSS are intertwined in the form of a vicious positive feedback cycle [35]. In this model, the elevation of ICP causes venous sinus compression, venous hypertension, decreased CSF absorption, and, in turn, worsening intracranial hypertension. This cyclical process suggests that VSS contributes to and is further exacerbated by elevated ICP, thereby increasing the likelihood of sCSF leaks. However, there continues to be debate whether initial VSS is a contributing cause or a consequence of ICP elevation [36, 37]. Furthermore, this model does not account for the observation that weight loss is associated with improvements in IIH in the absence of rectifying potential underlying VSS [38]. In our analysis, there was a low reporting of definite IIH (n = 16, six studies), although a far greater number of patients either experienced symptoms of elevated ICP or had one or more radiological signs of IIH. In the literature, the prevalence of IIH in sCSF remains highly variable. In Bidot et al., only 20% of sCSF leak patients fulfilled the modified Dandy criteria for IIH, whereas in another retrospective study, 72% of patients with beta‐2 transferrin‐proven sCSF leaks also met criteria for IIH [5, 6]. This discrepancy may be attributed to the underdiagnosis of IIH in this population due to subtle or atypical presentations that result in the absence of classic clinical signs such as papilledema. The absence of typical clinical symptoms has been proposed to be due to intermittent improvement of intracranial hypertension by pressure release from the leak, masking the diagnosis of IIH [39].
The repair of sCSF leaks has evolved significantly over the past 30 years, shifting from craniotomy [40] to the endoscopic endonasal approach first described by Wigand in 1981 [41]. Endoscopic endonasal techniques have since been refined, with reported success rates averaging around 90% and reaching as high as 95% in recent studies and reviews [42, 43, 44, 45, 46]. However, while the primary goal of surgical repair is to close the leak and prevent intracranial complications, managing underlying IIH is crucial for optimizing long‐term surgical outcomes [8]. Traditionally, patients with elevated ICP following surgical repair of sCSF leak have required long‐term treatments such as acetazolamide or CSF diversion to lower ICP. However, prolonged use of acetazolamide can lead to side effects like paresthesia, dysgeusia, fatigue, and metabolic imbalances, and CSF diversion procedures carry risks including shunt migration, infection, acquired Chiari malformation, and intracranial hemorrhage [47, 48]. The emergence of VSS as a common finding in patients with sCSF leaks introduces another therapeutic consideration and opens the possibility of identifying an underlying correctable cause for these leaks, potentially eliminating the need for long‐term pharmacological interventions with possible adverse effects.
Venous sinus stenting has emerged as a promising intervention for patients with VSS, particularly in patients with refractory IIH and persistent sCSF leaks after surgical sCSF leak repair [13, 49]. As a minimally invasive procedure, venous sinus stenting offers an attractive alternative to more invasive CSF diversion procedures, such as shunting, with potentially fewer complications and reduced need for additional interventions. Our review found that most patients who underwent venous sinus stenting alongside surgical repair experienced resolution of symptoms without further leaks, indicating the potential efficacy of this combined approach. Complications of stenting were either mild, transient, or managed expectantly; however, in addition to common complications such as headache, serious complications of stenting, including subdural hematoma, stent thrombosis, cerebellar hemorrhage, and subarachnoid hemorrhage, have been reported in the literature [50, 51].
Several limitations must be acknowledged in this analysis. First, the heterogeneity among the included studies was substantial, with differences in study design, patient selection criteria, imaging modalities, and diagnostic definitions of VSS and IIH. This variability contributes to the high I 2 values observed in the meta‐analyses, which call into question the reliability of pooled estimates derived from such heterogeneous data. Second, while proportions were calculated to describe the frequency of VSS in patients with sCSF leak, these data were drawn from a small subset of studies (n = 211) that investigated for VSS only in patients meeting specific inclusion criteria—namely, adults with sCSF leak without an identifiable cause. This does not represent an unselected or population‐based sample of all sCSF patients, and thus should not be interpreted as an estimate of prevalence in the broader sCSF population. We emphasize that our findings reflect only the frequency of VSS within this narrowly defined, selected cohort. Similarly, while pooled relative risk was calculated in studies comparing patients with and without sCSF leak, the limited number of studies, small sample sizes, and wide confidence intervals undermine the robustness of this analysis. Moreover, substantial heterogeneity further limits the validity of drawing conclusions about risk. Many included studies were retrospective in nature, inherently limiting control over confounding factors and follow‐up consistency. Preoperative imaging protocols were not standardized across studies, raising the possibility that patients with undiagnosed VSS may have been excluded, potentially underestimating the frequency of VSS. Lastly, variation in diagnostic imaging techniques and lack of consistent application of established criteria, such as the modified Dandy criteria for IIH, introduce further inconsistencies in the interpretation of results.
While the literature exploring the relationship between sCSF leak and VSS and the role of venous sinus stenting in this patient population is promising, it remains in its infancy, and further prospective studies with standardized diagnostic and treatment protocols are needed. In addition, investigation into the long‐term outcomes and potential risks of venous sinus stenting, including intracranial hemorrhage, stroke, and risks of postprocedural dual antiplatelet therapy, must be considered. Specifically, an important consideration for venous sinus stenting is the need for anticoagulation for at least 6 months after stenting. Thus, surgical intervention for sCSF leak should be considered prior to venous sinus stenting. At this point, recommending venous sinus stenting for primary treatment of spontaneous CSF leaks is not appropriate to broadly recommend or insinuate, as the risk of meningitis is still present with skull base defects and poor ability to monitor. Identifying specific patient populations that would benefit most from stenting and establishing clear guidelines for its use will be critical for optimizing outcomes. Future studies may also consider capturing information regarding long‐term changes in ICP (via ophthalmologic checks for papilledema or LPOP) to better understand whether patients are indeed controlled via venous sinus stenting.
5. Conclusion
This systematic review and meta‐analysis highlight the substantial prevalence of VSS in patients with sCSF leaks and underscore VSS as a potential therapeutic target. Venous sinus stenting emerges as a promising adjunctive strategy, potentially offering symptom resolution and reduced sCSF leak recurrence rates. Further research is needed to better define the role of venous sinus stenting in this patient population and improve our understanding of the pathophysiological mechanisms linking VSS, IIH, and sCSF leaks.
Conflicts of Interest
John Lee: speaker and advisory board, Sanofi Regeneron, GlaxoSmithKline
Supporting information
Appendix 1: The Association Between Venous Sinus Stenosis and Idiopathic Intracranial Hypertension: A Systematic Review Protocol.
Appendix 2: Search Strategy.
Appendix 3: Risk of Bias Assessment.
Xiao J. B., Khalil C., Hsiao H., et al. “Prevalence of Venous Sinus Stenosis in Spontaneous Cerebrospinal Fluid Leak and the Role for Venous Sinus Stenting: A Systematic Review and Meta‐Analysis.” International Forum of Allergy & Rhinology 15, no. 10 (2025): 1136–1151. 10.1002/alr.70026
Funding: No funding was secured for this study.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Appendix 1: The Association Between Venous Sinus Stenosis and Idiopathic Intracranial Hypertension: A Systematic Review Protocol.
Appendix 2: Search Strategy.
Appendix 3: Risk of Bias Assessment.