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Research—Human—Clinical Studies: Tumor

Stereotactic Radiosurgery Compared With Active Surveillance for Asymptomatic, Parafalcine, and Parasagittal Meningiomas: A Matched Cohort Analysis From the IMPASSE Study

Pikis, Stylianos MD, MSc; Mantziaris, Georgios MD*; Bunevicius, Adomas MD, PhD; Islim, Abdurrahman I. MD§; Peker, Selcuk MD; Samanci, Yavuz MD; Nabeel, Ahmed M. MD, PhD; Reda, Wael A. MD, PhD; Tawadros, Sameh R. MD, PhD; El-Shehaby, Amr M. N. MD, PhD; Abdelkarim, Khaled MD, PhD; Emad, Reem M. MD, PhD; Delabar, Violaine MD‡‡; Mathieu, David MD‡‡; Lee, Cheng-chia MD, PhD‖‖; Yang, Huai-che MD‖‖; Liscak, Roman MD; May, Jaromir MD¶¶; Alvarez, Roberto Martinez MD, PhD; Patel, Dev N. BA***; Kondziolka, Douglas MD, MSc; Bernstein, Kenneth MS; Moreno, Nuria Martinez MD, PhD##; Tripathi, Manjul MCH; Speckter, Herwin MSc§§§; Albert, Camilo MD; Bowden, Greg N. MD, MSc‖‖‖; Benveniste, Ronald J. MD, PhD; Lunsford, L. Dade MD###; Jenkinson, Michael D. MD; Sheehan, Jason MD, PhD

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doi: 10.1227/neu.0000000000001924
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Asymptomatic, World Health Organization grade I meningiomas constitute up to 39% of newly diagnosed meningiomas.1,2 Parafalcine and parasagittal (PFPS) meningiomas account for 17% to 30%3,4 of all intracranial meningiomas and approximately 27% of all asymptomatic ones.4 The optimal management of asymptomatic meningiomas remains controversial. Active surveillance with serial imaging is often preferred to up-front surgery or radiotherapy as the initial management strategy for small and asymptomatic meningiomas. However, after a period of observation, up to 16.4%4,5 of asymptomatic meningiomas will develop symptoms requiring treatment.

PFPS meningiomas that demonstrate clinical and/or radiological progression are usually managed with resection and/or stereotactic radiosurgery (SRS).6-8 In a study of 603 asymptomatic meningiomas, 37% of patients with a follow-up of 5 years or longer experienced tumor growth. Morbidity from surgical resection was higher in patients who were asymptomatic vs symptomatic at the time of a resection and exceeded 6% in those with asymptomatic meningiomas at the convexity or falx.4 SRS has proven to be an effective and lower risk treatment option for asymptomatic meningiomas.9,10 However, its role as up-front treatment of asymptomatic PFPS meningiomas remains to be clarified.

This study included all patients with an asymptomatic PFPS meningioma from an international multicenter matched cohort analysis that reported outcomes of 1117 patients with asymptomatic meningioma managed with either SRS (n = 727) or active surveillance (n = 388).11 It aimed to define the efficacy and safety of SRS as compared with active surveillance for the management of patients with asymptomatic PFPS meningiomas.


Study Population

The current study is a focused analysis of all patients with an asymptomatic PFPS meningioma treated either with SRS or managed with active surveillance from an international, multicenter study that reported outcomes of 1117 patients with asymptomatic meningioma managed with either SRS (n = 727) or active surveillance (n = 388) (Supplemental File 1, The study methods have been previously described in detail elsewhere.11 In brief, 14 centers across 10 countries contributed data for patients treated with SRS for an asymptomatic meningioma. Comparable data were obtained for patients managed with active clinical and radiological surveillance (active surveillance cohort) from a regional health district comprising 18 hospitals. One center contributed patients in both cohorts. Local institutional review boards granted approval for the study and for sharing the deidentified data with the IRRF coordinating office. Data are available from the corresponding author on reasonable request.

Meningiomas were defined as extra-axial, dural-based, and homogenously enhancing lesions on contrast-enhanced T1-weighted brain MRI with or without dural tail. Patients were excluded from the study if age <16 years, had ≥2 lesions compatible with meningiomas, or had any symptoms attributable to the meningioma at diagnosis. All study participants underwent clinical and neuroimaging follow-up according to local institutional protocols. Meningioma progression was defined according to the response assessment in neuro-oncology criteria.12


As previously reported,11 single-session SRS was performed using the Gamma Knife (Elekta AB). SRS used brain MRI and/or computed tomography with contrast to stereotactic targeting, and radiosurgical planning was performed using a multi-isocentric approach. SRS approach and radiation dose were selected by the local treating team according to the clinical need and Gamma Knife model available.


Patients were followed clinically and radiologically in a longitudinal fashion. The primary end point of the study was local tumor control according to the response assessment in neuro-oncology criteria. Local tumor control was defined as meningioma stability (ie, volume change by less than 25% of baseline) or tumor regression ≥25% from baseline. Meningioma progression was defined as volume increase ≥25% from baseline.12 The secondary end point was the development of new neurological deficits defined as any tumor and/or SRS attributable global or focal change in the patient's neurological status compared with the initial diagnosis for the active surveillance cohort and to the preprocedural clinical evaluation in the SRS cohort. Tumor progression-free survival (PFS) was measured in months based on the radiological follow-up.

Statistical Analysis

Statistical analysis was performed using R programming13 in RStudio.14 Baseline patient characteristics and tumor attributes between the observation and the SRS-treated cohort were compared. The Student t test or Mann–Whitney U test was used to compare continues variables, and the Pearson χ2 test was used to compare categorical variables between the 2 cohorts.

To control for confounders of treatment outcomes, the 2 cohorts were matched without replacement in a 1:1 ratio using propensity scores derived from patient age and tumor volume, and matching was performed using the MatchIt package for Rstudio.15 Adequate balance for the matched covariates was considered an absolute standardized difference <0.1 between the 2 cohorts. Univariate and multivariate analyses of the unmatched and matched cohorts were performed for outcome measures using binary logistic regression analysis. Kaplan–Meier was used to perform time-dependent analyses for PFS. Differences between function curves were analyzed using the log-rank test. Statistical significance was defined as P < .05. Missing data were not imputed.


Unmatched Patient and Tumor Characteristics

The unmatched cohorts consisted of 173 SRS-treated patients and 98 patients managed with active surveillance for a PFPS meningioma. The median radiological follow-up was 48 (interquartile range [IQR] 60) months for the SRS-treated cohort and 36 (IQR 35.75) months for the active surveillance cohort (P < .001). The median clinical follow-up for the SRS-treated and the active surveillance cohorts was 48 (IQR 56) and 36 (IQR 35.75) months, respectively (P < .001) (Table 1).

TABLE 1. - Descriptive Statistics for Unmatched Data and Comparison of Baseline Characteristics
Characteristic Total (n = 271) SRS (n = 173) Observe (n = 98) P-value
Age, mean yr (SD) 59.27 (13.73) 56.79 (13.4) 63.66 (13.26) <.001
Male, n (%) 49 (18.08%) 30 (17.34%) 19 (19.39%) .75
Baseline KPS, median (IQR) 90 (10) 90 (10) 100 (10) .03
Diameter, mean mm (SD) 19.25 (8.58) 19.56 (8.57) 18.73 (8.63) .45
Volume, mean cm3 (SD) 4.29 (5.01) 4.46 (4.31) 3.98 (6.07) .48
Margin dose, mean in Gy (SD) 13.1 (1.72)
Maximum dose, mean in Gy (SD) 26.47 (4.99)
Isocenters, median (IQR) 8 (8)
Imaging FU, median in months (IQR) 42 (43) 48 (60) 36 (35.75) <.001
Clinical FU, median in months (IQR) 42 (42.5) 48 (58) 36 (35.75) <.001
No. of patients with tumor progression (%) 39 (14.39%) 1 (0.58%) 38 (38.78%) <.001
No. of patients with new neurological deficits (%) 6 (2.21%) 4 (2.31%) 2 (2.04%) 1.00
Mortality 1 (0.37%) 0 (0%) 1 (1.02%)
FU, follow-up; Gy, Grey; KPS, Karnofsky performance status; IQR, interquartile range; SD, standard deviation; SRS, stereotactic radiosurgery.

Matched Patient and Tumor Characteristics

After propensity score matching, there were 98 patients in each cohort. In the SRS-treated cohort, the mean patient age was 63.02 (SD ± 13.4) years, and in the active surveillance cohort, it was 63.66 (SD ± 13.26) years (P = .72). The median Karnofsky performance status (KPS) at presentation was 90 (IQR 10) for both cohorts (P = .29). The mean tumor volume was 4.14 (SD ± 3.56) cm3 and 3.98 (SD ± 6.07) cm3 (P = .82) in the SRS-treated and active surveillance cohorts, respectively. The median radiological follow-up was 43 (IQR 50.25) months for the SRS cohort and 36 (IQR 35.75) months for the observation cohort (P = .04). The median clinical follow-up for the SRS and observation cohorts were 44 (IQR 53.75) and 36 (IQR 35.75) months, respectively (P = .01). The mean SRS margin dose was 13.26 (SD ± 1.91) Gy (Table 2).

TABLE 2. - Descriptive Statistics for Matched Data and Comparison of Baseline Characteristics
Characteristic Total (n = 196) SRS (n = 98) Observe (n = 98) P value
Age, mean yr (SD) 63.34 (12.54) 63.02 (13.4) 63.66 (13.26) .72
Male, n (%) 35 (17.86%) 16 (16.33%) 19 (19.39%) .71
Baseline KPS, median (IQR) 90 (10) 90 (10) 90 (10) .29
Diameter, mean mm (SD) 18.88 (8.68) 19.03 (8.78) 18.73 (8.63) .81
Volume, mean cm3 (SD) 4.06 (4.96) 4.14 (3.56) 3.98 (6.07) .82
Margin dose, mean in Gy (SD) 13.26 (1.91)
Maximum dose, mean in Gy (SD) 26.88 (5.31)
Isocenters, median (IQR) 9 (7)
Imaging FU, median in months (IQR) 38.5 (37.75) 43 (50.25) 36 (35.75) .04
Clinical FU, median in months (IQR) 40.5 (44.25) 44 (53.75) 36 (35.75) .01
No. of patients with tumor progression (%) 38 (19.39%) 0 (0%) 38 (38.78%) <.001
No. of patients with new neurological deficits (%) 5 (2.55%) 3 (3.06%) 2 (2.04%) 1.00
Mortality 1 (0.51%) 0 (0%) 1 (1.02%)
FU, follow-up; Gy, Grey; KPS, Karnofsky performance status; IQR, interquartile range; SD, standard deviation.

Radiological and Neurological Outcomes for Unmatched Cohorts

At the last follow-up, the primary study end point was reached in 99.4% SRS-treated patients and in 61.2% patients managed with active surveillance (P < .001). New neurological deficits associated with the tumor or treatment were observed in 2.0% of patients in the active surveillance cohort and 2.3% of SRS-treated patients (P = 1.0). All SRS-associated deficits were transient. The 4-year radiological PFS for the unmatched SRS-treated and active surveillance cohorts were 99.3% and 64.6%, respectively (Figure 1).

Radiological progression-free survival for the unmatched cohorts. SRS, stereotactic radiosurgery.

In multivariate analysis, active surveillance was associated with an increased risk of meningioma progression during follow-up (odds ratio [OR] = 109.88; 95% CI [22.82-1977.36]; P < .001) while higher KPS at diagnosis was associated with superior tumor control (OR = 0.91; 95% CI [0.85-0.96], P = .005) (Table 3).

TABLE 3. - Univariate and Multivariate Analysis With Binary Logistic Regression for Tumor Progression
Unmatched Matched
Univariate Multivariate Univariate Multivariate
Increasing age P = .86 OR = 1.03; 95% CI (1-1.06) P = .03 P = .33
Male sex P = .64 P = .71
Increasing KPS OR = 0.88; 95% CI (0.82-0.94), P < .001 OR = 0.91; 95% CI (0.85-0.96), P = .005 OR = 0.9; 95% CI (0.84-0.97), P = .005 OR = 0.94; 95% CI (0.87-1), P = .002
Increasing diameter P = .66 P = .74
Increasing volume P = .65 P = .79
Laterality P = .94 P = .86
Increasing imaging FU P = .34 P = .06 P = .46
Increasing clinical FU P = .29 P = .07 P = .88
Observation cohort OR = 108.93; 95% CI (22.84-1954.53), P < .001 OR = 109.88 95% CI (22.82-1977.36), P < .001 OR = 199.09 95% CI (24.04-1253), P < .001 OR = 156.3 95% CI (25.26-1026.23), P < .001
FU, follow-up; KPS, Karnofsky performance status; OR, odds ratio.

Radiological and Neurological Outcomes for Matched Cohorts

All SRS-treated patients reached the primary end point while in the active surveillance cohort, tumor progression was noted in 38.8% of patients (P < .001) (Table 2). In the SRS-treated cohort, new treatment-related transient neurological deficits because of peritumoral edema were observed in 3.1% of patients (n = 3) within 6 months of SRS. These patients were managed successfully with oral corticosteroids. At the last follow-up, tumor stability was noted in 2 patients and tumor regression in 1 patient.

In the active surveillance cohort, 2.1% of patients (n = 2) developed neurological symptoms because of tumor progression (P = 1.0) resulting in death of 1 patient 7.5 years after diagnosis (1%). The first patient developed contralateral upper extremity weakness 12 months after meningioma diagnosis, which resolved after resection. The second patient experienced a generalized tonic-clonic seizure 78 months after meningioma diagnosis. After the seizure, the patient was operated for systemic malignancy and developed decompensated liver cirrhosis. Clinical progression of the meningioma was also noted, and 7 months after the seizure, the patient was wheelchair bound because of hemiparesis. Because of comorbidities, surgical resection was deemed inappropriate. The patient subsequently died from hospital-acquired pneumonia after admission for a secondary generalized tonic-clonic seizure 90 months after initial diagnosis and 12 months after the first seizure. Moreover, 6 patients underwent resection because of radiological tumor progression. Postoperative complications related to resection were noted in 2 patients. The first patient experienced stroke manifesting with focal seizures and right lower limb paresis. At the last follow-up, seizures were controlled medically and paresis was improved. The second patient suffered from right-sided hemiparesis that resolved 30 days after the operation. The 4-year radiological PFS rates for the matched SRS-treated and active surveillance cohorts were 100% and 64.6%, respectively (Figure 2).

Progression-free survival for the matched cohorts. SRS, stereotactic radiosurgery.

In univariate analysis, increasing age (OR = 1.03; 95% CI [1.0-1.06], P = .03) and active surveillance (OR = 199.09; 95% CI [24.04-1253] P < .001) were associated with tumor progression. Higher KPS at diagnosis (OR = 0.9; 95% CI [0.84-0.97], P = .005) was correlated with local tumor control. In multivariate analysis, active surveillance was associated with a higher probability of local tumor progression (OR = 156.3; 95% CI [25.26-1026.23], P < .001), and higher initial KPS was associated with local tumor control (OR = 0.94; 95% CI [0.87-1.0], P = .002) (Table 3). Multivariate analysis in the active surveillance cohort revealed radiological follow-up (OR = 1.06, 95% CI [1.04-1.09], P < .001) to be associated with tumor progression.


Key Results

This retrospective multicenter study evaluated the clinical and radiological outcomes of 271 patients with an asymptomatic PFPS meningioma managed either with up-front SRS (n = 173) or with active surveillance (n = 98). In a matched analysis, which included 98 patients from each cohort, tumor progression was noted in 39% of patients in the active surveillance cohort but in none of the SRS-treated patients. Higher initial KPS at diagnosis and active surveillance were associated with tumor control and progression, respectively. Three patients (3%) in the SRS-treated cohort experienced transient SRS-related neurological deficits requiring oral corticosteroid treatment. In the active surveillance cohort, 2 patients (2%) suffered symptomatic tumor progression which resulted in death of 1 patient. Up-front SRS treatment for asymptomatic PFPS afforded statistically significant better tumor control than active surveillance with a nonstatistically significant lower risk of permanent morbidity and no mortality.

Natural History of PFPS Meningiomas

The natural history of asymptomatic PFPS meningiomas can be variable. A systematic review and meta-analysis of 22 studies reported that during a 4.6-year follow-up period, 13% of the 54 patients with an asymptomatic PFPS experienced symptomatic progression.5 In a series of 273 conservatively managed patients with an asymptomatic meningioma, linear growth was noted in 120 tumors (44%) at a mean follow-up of 3.8 years. Of these, resection was the preferred treatment for 49 tumors (18%) while 23 tumors (8%) were treated with radiotherapy.16 In our study, during 36 months of follow-up, meningioma growth by ≥25% was noted in approximately 39% of the conservatively managed asymptomatic PFPS meningiomas. This resulted in neurological deterioration in 2% of the patients and death in 1%.

Surgical Resection of PFPS Meningiomas

Resection is the treatment of choice for symptomatic or enlarging PFPS meningioma. However, in single-center studies including both symptomatic and asymptomatic PFPS meningiomas, resection was associated with up to 19% complication rate6 and up to 3% mortality rate.17-19 In a series of 100 consecutive patients with meningiomas around the major sinuses, postoperative complications included pulmonary embolism (1%), sepsis (6%), and permanent neurologic deterioration because of venous infarction (8%). Postoperative hematoma requiring evacuation occurred in 3 patients (3%), and the mortality rate was 3%. Tumor recurrence occurred in 4% of the patients.19 In a series of 126 parafalcine meningiomas, reported complications included motor deficit (n = 18), epileptic seizures (n = 12), and acute pancreatitis (n = 4). Postoperative hematoma requiring evacuation occurred in 5 cases, and there was no mortality.17 In a series of 58 patients with PFPS meningiomas, new neurological deficits occurred at a rate of 5.2%, and the total complication rate reported was 8.6%. Tumor growth or recurrence was noted in 3.4% of patients.20

Stereotactic Radiosurgery for Meningiomas

SRS has been established as a safe and effective treatment option for small and medium-sized meningiomas.21,22 Risk factors for post-SRS peritumoral edema include PFPS meningioma location,7,23 high number of isocenters and isocenters outside the target volume,24 pre-existing peritumoral edema, and greater area of tumor–brain interface.25 In addition, to minimize toxicity in patients treated with GKRS for an intracranial meningioma, it was recommended that the conformality index should be <2.0, heterogeneity index <2.0, and gradient index ≥3.0.25 However, GI ≥3 is concerning of suboptimal SRS planning and irradiation of more normal tissue than necessary.

Sheehan et al25 evaluated the incidence, timing, and extent of edema in 212 patients who underwent either up-front (40%) or adjuvant SRS (60%) for PFPS meningiomas. Gradual edema index elevation started 6 months post-SRS and reached a peak 36 months post-SRS. New or worsening post-SRS peritumoral edema was noted in 38% of patients, which subsequentially regressed in 33% of patients. Parasagittal location, tumor volume >10 cc, venous sinus invasion, tumor–brain contact interface area, and greater margin and maximal doses were associated with increasing risk for post-SRS edema.25,26 In addition, dose planning indices including conformality index, heterogeneity index, and gradient index have been linked to radiosurgical outcomes for patients with meningioma.24 In their series of 320 patients managed with SRS for asymptomatic meningiomas,24 Hoe et al reported post-SRS peritumoral edema in 15.3% of patients of whom 8.8% were symptomatic. Hemispheric location, tumor volume >4.2 cc, and pre-SRS peritumoral edema were associated with an increased risk for post-SRS peritumoral edema.23 In another single-center study, which included 65 patients with 90 WHO grade I PFPS meningiomas, post-SRS peritumoral edema was noted in 4 patients (8.2%) and resulted in permanent clinical sequelae in 1 patient (2%). Tumor progression was reported as the cause of death of 2 patients.7 In the unmatched cohorts of our study, 4 patients (2.31%) experienced transient neurological deterioration because of post-SRS peritumoral edema within 6 months of SRS. Conservative management with oral corticosteroids resulted in resolution of symptoms in all patients.


Limitations of our study include its retrospective design, which may lead to patient selection bias, and the lack of centralized neuroimaging review and standardized clinical follow-up protocols among participating centers. In addition, the duration of the clinical and imaging follow-up intervals between the 2 cohorts was statistically significant which may have biased the results of this study against SRS. Moreover, there were no quality of life and performance status evaluations in this study; therefore, conclusions on functional outcomes could not be drawn.

Interpretation of the Study

The optimal management of asymptomatic PFPS meningiomas remains unclear. Active surveillance is the initial management of choice by many. In the current study, SRS afforded superior local tumor control over active surveillance without an increased risk of new neurological deficits suggesting a role of SRS in the initial management of patients with asymptomatic PFPS meningioma.


Data for patients treated with SRS for an asymptomatic PFPS meningioma were collected from multiple centers in different countries. Therefore, the results of the current study can be readily generalized. However, because single-center data on active surveillance were analyzed in this study, our results may not be generalizable for all patients initially deciding on active surveillance.


Compared with an active surveillance strategy, up-front SRS was associated with superior radiological control of asymptomatic PFPS meningiomas and a lower risk of meningioma related permanent neurological deficit and/or death. In our study, active surveillance was associated with tumor progression. SRS may be offered as an alternative to active surveillance for asymptomatic PFPS meningiomas. If active surveillance is the initial management chosen, early SRS is a safe and effective treatment option when tumor growth is documented on follow-up neuroimaging.


The authors would like to acknowledge Dev N. Patel, who passed away in 2021, for his contribution in preparing this manuscript.


This study did not receive any funding or financial support.


Dr Dade Lunsford is a shareholder in Elekta AB, the manufacturer of some radiosurgical devices. The other authors have no personal, financial, or institutional interest in any of the drugs, materials, or devices described in this article.


1. Islim AI, Mohan M, Moon RDC, et al. Incidental intracranial meningiomas: a systematic review and meta-analysis of prognostic factors and outcomes. J Neurooncol. 2019;142(2):211-221.
2. Kuratsu J, Kochi M, Ushio Y. Incidence and clinical features of asymptomatic meningiomas. J Neurosurg. 2000;92(5):766-770.
3. Mirimanoff RO, Dosoretz DE, Linggood RM, Ojemann RG, Martuza RL. Meningioma: analysis of recurrence and progression following neurosurgical resection. J Neurosurg. 1985;62(1):18-24.
4. Yano S, Kuratsu J. Indications for surgery in patients with asymptomatic meningiomas based on an extensive experience. J Neurosurg. 2006;105(4):538-543.
5. Sughrue ME, Rutkowski MJ, Aranda D, Barani IJ, McDermott MW, Parsa AT. Treatment decision making based on the published natural history and growth rate of small meningiomas: a review and meta-analysis. J Neurosurg. 2010;113(5):1036-1042.
6. Sughrue ME, Rutkowski MJ, Shangari G, Parsa AT, Berger MS, McDermott MW. Results with judicious modern neurosurgical management of parasagittal and falcine meningiomas: clinical article. J Neurosurg. 2011;114(3):731-737.
7. Ding D, Xu Z, McNeill IT, Yen C-P, Sheehan JP. Radiosurgery for parasagittal and parafalcine meningiomas: clinical article. J Neurosurg. 2013;119(4):871-877.
8. Douglas K, John CF, Bernardo P; Gamma Knife Meningioma Study Group. Judicious resection and/or radiosurgery for parasagittal meningiomas: outcomes from a multicenter review. Neurosurgery. 1998;43(3):405-413.
9. Kim KH, Kang SJ, Choi J-W, et al. Clinical and radiological outcomes of proactive Gamma knife surgery for asymptomatic meningiomas compared with the natural course without intervention. J. Neurosurg. 2018;130(5):1740-1749.
10. Pikis S, Bunevicius A, Sheehan J. Outcomes from treatment of asymptomatic skull base meningioma with stereotactic radiosurgery. Acta Neurochir (Wien). 2021;163(1):83-88.
11. Sheehan J, Pikis S, Islim A, et al. An international multicenter matched cohort analysis of incidental meningioma progression during active surveillance or after stereotactic radiosurgery: the IMPASSE study. Neuro Oncol. 2021;24(1):116-124.
12. Huang RY, Bi WL, Weller M, et al. Proposed response assessment and endpoints for meningioma clinical trials: report from the response assessment in Neuro-Oncology Working Group. Neuro Oncol. 2019;21(1):26-36.
13. R Core Team. R: A Language and Environment for Statistical Computing. R Foundation for Statistical Computing; 2020. Accessed July 1, 2021.
14. R Studio Team. RStudio. Integrated Development Environment for R. RStudio, PBC; 2020.
15. Ho D, Imai K, King G, Stuart EA. MatchIt: nonparametric preprocessing for parametric causal inference. J Stat Softw. 2011;42(1):1-28.
16. Oya S, Kim S-H, Sade B, Lee JH. The natural history of intracranial meningiomas: clinical article. J Neurosurg. 2011;114(5):1250-1256.
17. Kong X, Gong S, Lee I-T, Yang Y. Microsurgical treatment of parafalcine meningiomas: a retrospective study of 126 cases. Onco Targets Ther. 2018;11:5279-5285.
18. Raza SM, Gallia GL, Brem H, Weingart JD, Long DM, Olivi A. Perioperative and long-term outcomes from the management of parasagittal meningiomas invading the superior sagittal sinus. Neurosurgery. 2010;67(4):885-893; discussion 893.
19. Sindou MP, Alvernia JE. Results of attempted radical tumor removal and venous repair in 100 consecutive meningiomas involving the major dural sinuses. J Neurosurg. 2006;105(4):514-525.
20. Eichberg DG, Casabella AM, Menaker SA, Shah AH, Komotar RJ. Parasagittal and parafalcine meningiomas: integral strategy for optimizing safety and retrospective review of a single surgeon series. Br J Neurosurg. 2020;34(5):559-564.
21. Kondziolka D, Mathieu D, Lunsford LD, et al. Radiosurgery as definitive management of intracranial meningiomas. Neurosurgery. 2008;62(1):53-60.
22. Pollock BE, Stafford SL, Utter A, Giannini C, Schreiner SA. Stereotactic radiosurgery provides equivalent tumor control to Simpson grade 1 resection for patients with small- to medium-size meningiomas. Int J Radiat Oncol Biol Phys. 2003;55(4):1000-1005.
23. Hoe Y, Choi YJ, Kim JH, Kwon DH, Kim CJ, Cho YH. Peritumoral brain edema after stereotactic radiosurgery for asymptomatic intracranial meningiomas: risks and pattern of evolution. J Korean Neurosurg Soc. 2015;58(4):379-384.
24. The Importance of the Conformality, Heterogeneity, and Gradient Indices in Evaluating Gamma Knife Radiosurgery Treatment Plans for Intracranial Meningiomas | Elsevier Enhanced Reader.
25. Cai R, Barnett GH, Novak E, Chao ST, Suh JH. Principal risk of peritumoral edema after stereotactic radiosurgery for intracranial meningioma is tumor-brain contact interface area. Neurosurgery. 2010;66(3):513-522.
26. Sheehan JP, Cohen-Inbar O, Ruangkanchanasetr R, et al. Post-radiosurgical edema associated with parasagittal and parafalcine meningiomas: a multicenter study. J Neurooncol. 2015;125(2):317-324.

Supplemental Digital Content

Supplemental File 1. Flowchart describing patient selection for the current study.


Meningioma; Parasagittal; Parafalcine; Asymptomatic; Radiosurgery; Active Surveillance

Supplemental Digital Content

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