Risk factors for peritumoral edema after radiosurgery for intracranial benign meningiomas: a long-term follow-up in a single institution

Sheng-Han HuangDepartment of Neurosurgery, Chang Gung Memorial Hospital at Linkou, Chang Gung University, Taoyuan;

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Chi-Cheng ChuangDepartment of Neurosurgery, Chang Gung Memorial Hospital at Linkou, Chang Gung University, Taoyuan;

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Chun-Chieh WangDepartment of Radiation Oncology, Chang Gung Memorial Hospital at Linkou, Chang Gung University, Taoyuan; and

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Kuo-Chen WeiDepartment of Neurosurgery, Chang Gung Memorial Hospital at Linkou, Chang Gung University, Taoyuan;

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Hsien-Chih ChenDepartment of Neurosurgery, Chang Gung Memorial Hospital at Keelung, Chang Gung University, Keelung, Taiwan

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Peng-Wei HsuDepartment of Neurosurgery, Chang Gung Memorial Hospital at Linkou, Chang Gung University, Taoyuan;

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OBJECTIVE

Peritumoral edema (PTE) is recognized as a complication following stereotactic radiosurgery (SRS). The aim of this paper was to evaluate the risk of post-SRS PTE for intracranial benign meningiomas and determine the predictive factors.

METHODS

Between 2006 and 2021, 227 patients with 237 WHO grade I meningiomas were treated with Novalis linear accelerator SRS. All patients were treated with a single-fraction dose of 11–20 Gy (median 14 Gy). The median tumor volume was 3.32 cm3 (range 0.24–51.7 cm3).

RESULTS

The median follow-up was 52 months (range 12–178 months). The actuarial local tumor control rates at 2, 5, and 10 years after SRS were 99.0%, 96.7%, and 86.3%, respectively. Twenty-seven (11.9%) patients developed new or worsened post-SRS PTE, with a median onset time of 5.2 months (range 1.2–50 months). Only 2 patients developed post-SRS PTE after 24 months. The authors evaluated factors related to new-onset or worsened PTE after SRS. In univariate analysis, initial tumor volume > 10 cm3 (p = 0.03), total marginal dose > 14 Gy (p < 0.001), preexisting edema (p < 0.0001), tumor location (p < 0.001), parasagittal location (p < 0.0001), superior sagittal sinus (SSS) involvement (p < 0.0001), and SSS invasion (p < 0.015) were found to be significant risk factors. In multivariate analysis, total marginal dose > 14 Gy (HR 3.38, 95% CI 1.37–8.33, p = 0.008), preexisting SRS edema (HR 12.86, 95% CI 1.09–4.15, p < 0.0001), tumor location (HR 2.13, 95% CI 1.04–3.72, p = 0.027), parasagittal location (HR 8.84, 95% CI 1.48–52.76, p = 0.017), and SSS invasion (HR 0.34, 95% CI 0.13–0.89, p = 0.027) were significant risk factors. Twelve (5.3%) patients were symptomatic. Ten of 27 patients had complete resolution of neurological symptoms and edema improvement with steroid treatment. Steroid treatment failed in 2 patients, who subsequently required resection for PTE.

CONCLUSIONS

Radiosurgery is a safe and effective method of treating benign intracranial meningiomas according to long-term follow-up. We also identified total marginal dose > 14 Gy, preexisting PTE, parasagittal location, and SSS invasion as predictors of post-SRS PTE. Risk factors for post-SRS PTE should be considered in meningioma treatment.

ABBREVIATIONS

LCR = local tumor control rate; PTE = peritumoral edema; SRS = stereotactic radiosurgery; SSS = superior sagittal sinus.

OBJECTIVE

Peritumoral edema (PTE) is recognized as a complication following stereotactic radiosurgery (SRS). The aim of this paper was to evaluate the risk of post-SRS PTE for intracranial benign meningiomas and determine the predictive factors.

METHODS

Between 2006 and 2021, 227 patients with 237 WHO grade I meningiomas were treated with Novalis linear accelerator SRS. All patients were treated with a single-fraction dose of 11–20 Gy (median 14 Gy). The median tumor volume was 3.32 cm3 (range 0.24–51.7 cm3).

RESULTS

The median follow-up was 52 months (range 12–178 months). The actuarial local tumor control rates at 2, 5, and 10 years after SRS were 99.0%, 96.7%, and 86.3%, respectively. Twenty-seven (11.9%) patients developed new or worsened post-SRS PTE, with a median onset time of 5.2 months (range 1.2–50 months). Only 2 patients developed post-SRS PTE after 24 months. The authors evaluated factors related to new-onset or worsened PTE after SRS. In univariate analysis, initial tumor volume > 10 cm3 (p = 0.03), total marginal dose > 14 Gy (p < 0.001), preexisting edema (p < 0.0001), tumor location (p < 0.001), parasagittal location (p < 0.0001), superior sagittal sinus (SSS) involvement (p < 0.0001), and SSS invasion (p < 0.015) were found to be significant risk factors. In multivariate analysis, total marginal dose > 14 Gy (HR 3.38, 95% CI 1.37–8.33, p = 0.008), preexisting SRS edema (HR 12.86, 95% CI 1.09–4.15, p < 0.0001), tumor location (HR 2.13, 95% CI 1.04–3.72, p = 0.027), parasagittal location (HR 8.84, 95% CI 1.48–52.76, p = 0.017), and SSS invasion (HR 0.34, 95% CI 0.13–0.89, p = 0.027) were significant risk factors. Twelve (5.3%) patients were symptomatic. Ten of 27 patients had complete resolution of neurological symptoms and edema improvement with steroid treatment. Steroid treatment failed in 2 patients, who subsequently required resection for PTE.

CONCLUSIONS

Radiosurgery is a safe and effective method of treating benign intracranial meningiomas according to long-term follow-up. We also identified total marginal dose > 14 Gy, preexisting PTE, parasagittal location, and SSS invasion as predictors of post-SRS PTE. Risk factors for post-SRS PTE should be considered in meningioma treatment.

Stereotactic radiosurgery (SRS) has been widely used as a primary treatment for small (< 3 cm) and asymptomatic intracranial benign meningiomas. It has also served as adjuvant treatment when tumors recur or when complete resection is not achievable. SRS for benign meningioma is generally a safe procedure, but the rate of peritumoral edema (PTE) in patients with intracranial meningiomas ranges from 25% to 92%.1,2 New or worsened post-SRS PTE often occurs late in the course. Although the symptoms typically resolve spontaneously, they can be persistent and severe in some cases and need further treatment with glucocorticoids or resection.3,4 The risk factors proposed previously to determine the development of post-SRS PTE include larger tumor size, higher total marginal dose (> 14 Gy), preexisting PTE and convexity, and parasagittal location.57

We report our experience using SRS in the treatment of benign intracranial meningiomas and describe the incidence and risk factors for post-SRS PTE. Several potential risk factors were evaluated. In this study, we emphasized the risk of developing PTE in meningiomas that compressed or even invaded the superior sagittal sinus (SSS). The clinical course and management of post-SRS PTE are also reported. Such information may help clinicians better select the proper candidate for SRS and lower the risk of new and worsened post-SRS PTE in the first place.

Methods

We retrospectively reviewed patients with benign intracranial meningiomas treated with SRS in our institution from March 2006 to May 2021. We extracted data only for those with WHO grade I meningiomas; those with WHO grade II (atypical) and WHO grade III (anaplastic) meningiomas were both excluded. All meningiomas were confirmed after initial evaluation with CT or MRI. All patients were treated with a single-fraction dose of 12–16 Gy with the Novalis linear accelerator SRS (Novalis Medical, LLC) for 1 day. All patients were immobilized with a Brainlab stereotactic frame.

Radiosurgical treatments were performed using the Novalis system (Brainlab AG), with Brainscan software version 5.31 (Brainlab AG) to design the treatment plan. A 100% isodose line was used to cover the tumor. The tumor volume was calculated using the iPlan Radiotherapy Planning Software (iPlan RT Image 3.0.1, Brainlab AG). A stereoscopic radiograph system combined with an infrared position-tracking system was used to ensure the correct position. After the patient’s head was immobilized with a Brainlab thermoplastic fixation mask and an oral bite, stereotactic imaging (CT and MRI) was performed to obtain precise data on the shape and volume of the tumors. Oral dexamethasone (0.5 mg, 4 times per day for 3 consecutive days) was administered to the patients from the 1st treatment day to prevent acute toxic effects induced by radiosurgery.

The follow-up duration was defined as the time from SRS to the last date of an outpatient clinic visit or MRI session. The period of local tumor control was defined as the time between initial radiosurgery and the date of local tumor recurrence based on the radiological findings. MR images were generally scheduled at 3 months post-SRS and every 12 months thereafter. Earlier evaluation would be arranged if new symptoms developed. The most recent MR images were used to analyze the remaining tumor volume. T2-weighted and fluid-attenuated inversion recovery (FLAIR) images were used to evaluate PTE before and after SRS treatment. Volumetric data sets for tumors and PTE on serial MRI were both calculated using iPlan RT Image (Brainlab AG). Radiographic change in tumor volume was defined as decreased (≤ 90% of initial tumor volume), stable (> 90% and < 110% of initial tumor volume) or increased (≥ 110% of initial tumor volume). The 10% variation in defining tumor stability was based on volumetry error estimation.8 Clinically meaningful post-SRS edema was defined as an increased volume of PTE > 10% as seen on each post-SRS MR image.

All statistical analysis was performed using SPSS software (version 26.0, IBM Corp). Continuous variables of demographic data are presented as median and range, and categorical variables are presented as frequency and percentages. Tumor control rates and post-SRS PTE were calculated by the Kaplan-Meier method using the log-rank test. Cox proportional hazards models were used to analyze the prognostic factors of post-SRS new or worsened PTE, and to assess hazard ratios (HRs). Factors with a p value < 0.05 in univariate analysis were entered into a multivariate analysis. All statistical tests were two-sided, and a p value < 0.05 was considered as the threshold of significance in all tests.

Results

Patient Characteristics

Between March 2006 and May 2021, 227 patients with 237 benign meningiomas were treated with the linear accelerator (Table 1). The median age at initial radiosurgery treatment was 59 years (range 24–84 years), and most patients were female (n = 161, 70.9%). Among the patients, 32.6% had de novo meningioma, 43.6% had postoperative residual tumor, and 23.8% had recurrence from a previous microsurgical resection. Before radiosurgery, 67.4% of patients had undergone microsurgical resection. The median tumor volume at the time of radiosurgery was 3.32 cm3 (range 0.24–51.7 cm3). The median prescription dose was 14 Gy (range 11–20 Gy).

TABLE 1.

Patient and tumor characteristics

CharacteristicValue
No. of patients227
Follow-up, mos52 (12–178)
Age at treatment, yrs59 (24–84)
Female sex161 (70.9)
Male sex66 (29.1)
Vol, cm33.32 (0.24–51.7)
Vol >10 cm323 (10.1)
Margin dose, Gy14 (11–20)
Previous op 153 (67.4)
Radiosurgery strategy
 De novo meningioma74 (32.6)
 Postop residual tumor99 (43.6)
 Postop recurrence54 (23.8)
Location
 Skull base 76 (32.1)
 Parasagittal56 (23.6)
 Falcine/tentorium50 (21.1)
 Convexity40 (16.9)
 Intraventricular15 (6.3)
SSS involvement72 (30.4)
 External compression34 (14.3)
 Partial obstruction36 (15.2)
 Total occlusion2 (0.8)
Involved 3rd of the SSS
 Anterior9 (12.5)
 Middle29 (40.3)
 Posterior34 (47.2)
Brain edema before SRS59 (26.0)

Values are presented as number (%) or median (range).

Among the 237 meningiomas treated, 76 (32.1%) were skull base meningiomas, 56 (23.6%) were parasagittal meningiomas, 50 (21.1%) were falcine/tentorium meningiomas, 40 (16.9%) were convexity meningiomas, and 15 (6.3%) were intraventricular meningiomas. Imaging revealed that 72 (30.4%) tumors were diagnosed with SSS involvement, including SSS external compression and invasion (including partial obstruction and total occlusion). Moreover, 36 (15.2%) tumors had SSS partial obstruction and 2 (0.8%) had SSS total occlusion. Among the meningiomas with SSS involvement, 9 (12.5%) tumors were located in the anterior third of the SSS, 29 (40.3%) in the middle third, and 34 (47.2%) in the posterior third.

Tumor Control and Neurological Status

The median follow-up time after radiosurgery was 52 months (range 12–178 months). The actuarial local tumor control rates (LCRs) at 2, 5, and 10 years after SRS were 99.0%, 96.7%, and 86.3%, respectively. The majority of tumors (n = 214, 90.3%) presented with stable or decreased tumor volume at the last follow-up. Specifically, 192 (81.0%) tumors were diagnosed with stable lesions and 22 (9.3%) with decreasing lesions. Twenty-three (9.7%) tumors were diagnosed with a progressive lesion (Table 2). The median time between initial treatment and retreatment for recurrence (n = 21) was 4.3 years (range 2.1–9.7 years).

TABLE 2.

Treatment outcome after SRS

OutcomeNo. of Tumors (%)
Tumor outcomes
 Regression22 (9.3)
 Stable192 (81.0)
 Progression23 (9.7)
Edema outcomes
 New7 (3.0)
 Worsened20 (8.4)
 Stable39 (16.5)
 No edema171 (72.2)

Radiation-Induced PTE and Predictors

For the entire study cohort of 237 tumors, 59 (24.9%) tumors had tumor-related edema prior to radiosurgery. After radiosurgical treatment, most of the tumors (n = 171, 72.2%) had no PTE, 39 (16.5%) had stable PTE, 20 (8.4%) had worsened PTE, and 7 (3.0%) tumors developed new PTE on follow-up imaging (Table 2). Figure 1 shows the Kaplan-Meier curves comparing the rates of post-SRS PTE, stratified by total marginal dose > 14 Gy, preexisting edema, parasagittal location, and SSS invasion. A representative case is shown in Fig. 2. The median time to onset of new or worsened edema was 5.2 months (range 1.2–50 months). Only 2 patients developed post-SRS PTE after more than 24 months.

FIG. 1.
FIG. 1.

Kaplan-Meier analysis of freedom from new or worsened post-SRS PTE, stratified by total marginal dose > 14 Gy (A), preexisting edema (B), parasagittal location (C), and SSS invasion (D).

FIG. 2.
FIG. 2.

Images obtained in a patient with parasagittal meningioma treated with SRS. A and B: Pretreatment, postcontrast T1-weighted contrast (A) and FLAIR sequence (B) MR images showing a small amount of focal PTE. C and D: Treatment plan showing 100% isodose line coverage with 15 Gy in one session. E: FLAIR sequence MR image at 9 months posttreatment showing extensive PTE and presentation of new-onset seizure. F: After 2 weeks of oral steroid therapy, FLAIR sequence MR image showing PTE resolution at 21 months of posttreatment follow-up.

We evaluated the factors related to new-onset or worsened edema after SRS (Table 3). Tumor locations were categorized into four groups: parasagittal, falcine/tentorium, convexity, and skull base. In univariate analysis, initial tumor volume > 10 cm3 (p = 0.03), total marginal dose > 14 Gy (p < 0.001), preexisting edema (p < 0.0001), tumor location (p < 0.001), parasagittal location (p < 0.0001), SSS involvement (p < 0.001), and SSS invasion (p < 0.015) were significantly related to post-SRS edema formation. In multivariate analysis, new-onset or progressive edema was associated with a total marginal dose > 14 Gy (HR 3.38, 95% CI 1.37–8.33, p = 0.008), preexisting SRS edema (HR 12.86, 95% CI 1.09–4.15, p < 0.0001), tumor location (HR 2.13, 95% CI 1.04–3.72, p = 0.027), parasagittal location (HR 8.84, 95% CI 1.48–52.76, p = 0.017), and SSS invasion (HR 0.34, 95% CI 0.13–0.89, p = 0.027).

TABLE 3.

Univariate and multivariate analyses for factors associated with new or worsened post-SRS PTE

FactorUnivariate p ValueMultivariate
HR95% CIp Value
Age >65 yrs0.694
Female sex0.427
Tumor vol >10 cm30.03*1.980.77–5.120.156
Total marginal dose >14 Gy<0.001*3.381.37–8.330.008*
Prior op0.111
Preexisting edema<0.0001*12.861.09–4.15<0.0001*
Location<0.001*2.131.04–3.720.027*
Parasagittal location<0.0001*8.841.48–52.760.017*
SSS involvement<0.0001*2.200.51–9.430.288
SSS invasion0.015*0.340.13–0.890.027*
SSS total occlusion0.135
Involved 3rd of the SSS0.680

Statistically significant (p < 0.05).

Location grouped as parasagittal/falcine and tentorium/convexity/skull base.

Clinical Outcomes of Post-SRS PTE

Of the 27 (11.9%) patients who developed new or worsened post-SRS PTE, 12 (5.3% of the entire cohort) patients were symptomatic. The neurological symptoms associated with PTE included a new motor deficit in 4 patients, visual deficits in 2 patients, new or worsened seizures in 3 patients, new-onset moderate to severe headache in 9 patients, and poor memory in 3 patients. All 12 patients with new-onset neurological symptoms were started on dexamethasone (4 mg per oral every 6 hours); the 15 asymptomatic patients were managed conservatively and merely followed with serial MR images. The doses and periods of corticosteroid treatment were titrated according to the clinical symptoms and neurological deficits. Ten patients had complete resolution of neurological symptoms and edema improvement with a course of glucocorticoids, with a median time to resolution of symptoms of 6 weeks (range 2–37 weeks). Two patients required an antiepileptic agent for increased seizure frequency until the end of follow-up. Steroid treatment failed for 2 patients in our cohort; they subsequently required resection for PTE.

Discussion

In the present study, the overall incidence of new or worsened PTE post-SRS was 11.9%. This rate is consistent with the previously reported incidence of 13.8%–23.6% of patients.2,4,9,10 In our series, total marginal dose > 14 Gy, preexisting PTE, parasagittal location, and SSS invasion were significant risk factors for post-SRS PTE. SRS should be used with caution in these settings. In general, LCRs decreased slightly when the observation period was prolonged. We found a 10-year LCR of 86.3%, which is very similar to that of a previous 10-year follow-up study.11,12 While SRS achieves excellent long-term control for benign meningiomas, this must be balanced with the risk of post-SRS PTE.

The time course of edema development appears to occur late, and our study was in line with this trend. Since most of the post-SRS PTEs were asymptomatic, the time of detection would be highly associated with the follow-up protocol followed at different institutions. In a study by Cai et al., the median time to develop symptomatic edema after SRS was 2.5 months (range 1.5–48 months).2 In another study by Kondziolka et al., post-SRS PTE occurred from 1 to 23 months after treatment and peaked at 6 to 8 months after treatment.7 Most cases of post-SRS PTE resolved within 2 years, a result that is similar to those in the present study.3

Increasing tumor volume has long been recognized as a risk factor for PTE. Since tumor growth was a main force in destroying the tumor-brain contact interface, tumor volume showed a significant relationship to PTE.2 Meningiomas > 10 cm3 in volume increased the risk for developing new or worsened post-SRS PTE.13,14 However, post-SRS PTE in our study was not significantly associated with tumor volume in multivariate analysis, which echoes the results of some previous studies. Cai et al.2 suggested that the significant risk factor for post-SRS PTE is not tumor volume, but a large meningioma-brain contact interface. A single dose > 14 Gy has been recognized as a predictor of symptomatic post-SRS PTE.6 Fractionation may offer some reduction in the risk of posttreatment PTE formation while maintaining satisfactory tumor control.15 Kollová et al.16 suggested that patients with preexisting PTE had a higher risk of worsened PTE post-SRS, which is almost consistent with the present study. Hasegawa et al.17 documented that 4 of 6 patients with preexisting PTE developed severe panhemispheric edema after Gamma Knife surgery and 2 patients required craniotomy.

Development of PTE in meningiomas is considered to be strongly related to those tumors that have a greater pial blood supply because of stronger expression of vascular endothelial growth factor.18 Convexity, parasagittal, and falcine meningiomas have a broader pial interface and greater pial blood supply than skull base meningiomas surrounded by cistern.17 Therefore, convexity, parasagittal, and falcine meningiomas are more likely to develop post-SRS PTE than skull base meningiomas.10,19,20 Sheehan et al.13 reported a multicenter study of meningiomas with parasagittal and parafalcine locations with 45.3% edema before SRS. Patil et al.4 reviewed 102 patients who had undergone CyberKnife radiosurgery for supratentorial meningiomas and found that parasagittal tumors were 4 times more likely to develop PTE post-SRS.

Parasagittal meningiomas are still considered a microsurgical challenge, especially when the SSS is invaded.5 Although many recent studies have demonstrated a marked evolution in the microsurgical management of parasagittal meningioma with major sinus invasion, Simpson grade I resection can only be achieved in fewer than 25% of patients, and considerable surgical morbidity has been noted.13 Those patients with partially resected tumors without any radiotherapy have worse LCRs.21 Thus, the value of radiosurgery has emerged in recent years. Some studies have described post-SRS progression-free survival rates not inferior to those of patients who underwent Simpson grade I resection.22 Gatterbauer et al. reported that, in benign meningiomas, the Simpson resection grade did not have a significant impact on time to recurrence or progression.23 Hence, radiosurgery is a safe and effective treatment for small residual tumors after subtotal resection or for those tumors being monitored radiologically until their progression. In our opinion, microsurgery, radiotherapy, and radiosurgery are complementary treatment options for parasagittal meningiomas.

Once symptomatic post-SRS PTE develops, corticosteroids are the first line of treatment. In our experience, the symptoms of PTE resolved with corticosteroid treatment in most of our patients, if given sufficient time. Only 0.9% of the patients (n = 2) required resection after steroid treatment failure. Vascular endothelial growth factor inhibitors, such as bevacizumab, are an emerging treatment of choice and have been shown to reduce edema following radiosurgery.13,24 We also had another 3 patients with WHO grade III meningioma, not included in the present study, who experienced severe post-SRS PTE and for whom steroid treatment (bevacizumab) failed. After three courses of bevacizumab treatment (each course: 5 mg/kg intravenous every 2 weeks), all 3 patients had great improvement in PTE. However, to date, we have no experience with bevacizumab use in post-SRS PTE in those with benign meningiomas.

This study has several limitations. First, it is retrospective in nature, and therefore conclusions should be confirmed in further larger prospective series. Considering that WHO grade I meningiomas are slowly progressive, the relatively short follow-up period can be another limitation of the current study, in that it may lack sensitivity to detect progression. Further studies with longer follow-up and larger sample sizes are needed for further evaluation. Second, not all tumors detected by imaging were confirmed histologically to be benign meningiomas prior to treatment. Higher grade must be suspected when loss of integrity of the arachnoid layer is found by heterogeneous contrast enhancement.25 There is the potential that some radiographic benign meningiomas were actually higher grade. Another study of ours confirmed this idea, showing that patients without histological confirmation showed a trend toward decreased actuarial LCR compared with patients with histological confirmation.26

Conclusions

Radiosurgery is a safe and effective method of treating benign intracranial meningiomas on long-term follow-up. We identified total marginal dose > 14 Gy, preexisting PTE, parasagittal location, and SSS invasion as predictors of post-SRS PTE. Risk factors for post-SRS PTE should be considered when selecting patients for radiosurgery.

Acknowledgments

Chang Gung Memorial Hospital provided financial support (grant no. CMRPG3K1841), as did the Ministry of Science and Technology, Taiwan (grant no. 110-2314-B-182A-078). The sponsors had no role in the design or conduct of this research.

Disclosures

The authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper.

Author Contributions

Conception and design: Hsu, Wang. Acquisition of data: Hsu, Huang. Analysis and interpretation of data: Chuang. Drafting the article: Huang. Critically revising the article: Wang, Wei. Reviewed submitted version of manuscript: Chuang, Wei. Study supervision: Chen.

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    Rogers L, Mehta M. Role of radiation therapy in treating intracranial meningiomas. Neurosurg Focus. 2007;23(4):E4.

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    Chan RC, Thompson GB. Morbidity, mortality, and quality of life following surgery for intracranial meningiomas. A retrospective study in 257 cases. J Neurosurg. 1984;60(1):5260.

    • Crossref
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  • 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):10001005.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 23

    Gatterbauer B, Gevsek S, Höftberger R, et al. Multimodal treatment of parasagittal meningiomas: a single-center experience. J Neurosurg. 2017;127(6):12491256.

    • Crossref
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    • Export Citation
  • 24

    Lou E, Sumrall AL, Turner S, et al. Bevacizumab therapy for adults with recurrent/progressive meningioma: a retrospective series. J Neurooncol. 2012;109(1):6370.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 25

    Spille DC, Adeli A, Sporns PB, et al. Predicting the risk of postoperative recurrence and high-grade histology in patients with intracranial meningiomas using routine preoperative MRI. Neurosurg Rev. 2021;44(2):11091117.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 26

    Huang SH, Wang CC, Wei KC, et al. Treatment of intracranial meningioma with single-session and fractionated radiosurgery: a propensity score matching study. Sci Rep. 2020;10(1):18500.

    • Crossref
    • Search Google Scholar
    • Export Citation
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    FIG. 1.

    Kaplan-Meier analysis of freedom from new or worsened post-SRS PTE, stratified by total marginal dose > 14 Gy (A), preexisting edema (B), parasagittal location (C), and SSS invasion (D).

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    FIG. 2.

    Images obtained in a patient with parasagittal meningioma treated with SRS. A and B: Pretreatment, postcontrast T1-weighted contrast (A) and FLAIR sequence (B) MR images showing a small amount of focal PTE. C and D: Treatment plan showing 100% isodose line coverage with 15 Gy in one session. E: FLAIR sequence MR image at 9 months posttreatment showing extensive PTE and presentation of new-onset seizure. F: After 2 weeks of oral steroid therapy, FLAIR sequence MR image showing PTE resolution at 21 months of posttreatment follow-up.

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    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):513522.

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    Kan P, Liu JK, Wendland MM, Shrieve D, Jensen RL. Peritumoral edema after stereotactic radiosurgery for intracranial meningiomas and molecular factors that predict its development. J Neurooncol. 2007;83(1):3338.

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    Gousias K, Schramm J, Simon M. The Simpson grading revisited: aggressive surgery and its place in modern meningioma management. J Neurosurg. 2016;125(3):551560.

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    Girvigian MR, Chen JC, Rahimian J, Miller MJ, Tome M. Comparison of early complications for patients with convexity and parasagittal meningiomas treated with either stereotactic radiosurgery or fractionated stereotactic radiotherapy. Neurosurgery. 2008;62(5 suppl):A19A28.

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    Kondziolka D, Mathieu D, Lunsford LD, et al. Radiosurgery as definitive management of intracranial meningiomas. Neurosurgery. 2008;62(1):5360.

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    Snell JW, Sheehan J, Stroila M, Steiner L. Assessment of imaging studies used with radiosurgery: a volumetric algorithm and an estimation of its error. Technical note. J Neurosurg. 2006;104(1):157162.

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  • 9

    Kobayashi T, Kida Y, Mori Y. Long-term results of stereotactic gamma radiosurgery of meningiomas. Surg Neurol. 2001;55(6):325331.

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    Chang JH, Chang JW, Choi JY, Park YG, Chung SS. Complications after gamma knife radiosurgery for benign meningiomas. J Neurol Neurosurg Psychiatry. 2003;74(2):226230.

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    Lippitz BE, Bartek J Jr, Mathiesen T, Förander P. Ten-year follow-up after Gamma Knife radiosurgery of meningioma and review of the literature. Acta Neurochir (Wien). 2020;162(9):21832196.

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    Cohen-Inbar O, Lee CC, Schlesinger D, Xu Z, Sheehan JP. Long-term results of stereotactic radiosurgery for skull base meningiomas. Neurosurgery. 2016;79(1):5868.

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    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):317324.

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  • 14

    Pollock BE, Stafford SL, Link MJ, Garces YI, Foote RL. Single-fraction radiosurgery for presumed intracranial meningiomas: efficacy and complications from a 22-year experience. Int J Radiat Oncol Biol Phys. 2012;83(5):14141418.

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  • 15

    Unger KR, Lominska CE, Chanyasulkit J, et al. Risk factors for posttreatment edema in patients treated with stereotactic radiosurgery for meningiomas. Neurosurgery. 2012;70(3):639645.

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    Kollová A, Liscák R, Novotný J Jr, Vladyka V, Simonová G, Janousková L. Gamma Knife surgery for benign meningioma. J Neurosurg. 2007;107(2):325336.

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  • 17

    Hasegawa T, Kida Y, Yoshimoto M, Iizuka H, Ishii D, Yoshida K. Gamma Knife surgery for convexity, parasagittal, and falcine meningiomas. J Neurosurg. 2011;114(5):13921398.

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  • 18

    Yoshioka H, Hama S, Taniguchi E, Sugiyama K, Arita K, Kurisu K. Peritumoral brain edema associated with meningioma: influence of vascular endothelial growth factor expression and vascular blood supply. Cancer. 1999;85(4):936944.

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  • 19.

    Kim DG, Kim ChH, Chung HT, et al. Gamma knife surgery of superficially located meningioma. J Neurosurg. 2005;102(suppl):255-258

  • 20

    Rogers L, Mehta M. Role of radiation therapy in treating intracranial meningiomas. Neurosurg Focus. 2007;23(4):E4.

  • 21

    Chan RC, Thompson GB. Morbidity, mortality, and quality of life following surgery for intracranial meningiomas. A retrospective study in 257 cases. J Neurosurg. 1984;60(1):5260.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 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):10001005.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 23

    Gatterbauer B, Gevsek S, Höftberger R, et al. Multimodal treatment of parasagittal meningiomas: a single-center experience. J Neurosurg. 2017;127(6):12491256.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 24

    Lou E, Sumrall AL, Turner S, et al. Bevacizumab therapy for adults with recurrent/progressive meningioma: a retrospective series. J Neurooncol. 2012;109(1):6370.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 25

    Spille DC, Adeli A, Sporns PB, et al. Predicting the risk of postoperative recurrence and high-grade histology in patients with intracranial meningiomas using routine preoperative MRI. Neurosurg Rev. 2021;44(2):11091117.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 26

    Huang SH, Wang CC, Wei KC, et al. Treatment of intracranial meningioma with single-session and fractionated radiosurgery: a propensity score matching study. Sci Rep. 2020;10(1):18500.

    • Crossref
    • Search Google Scholar
    • Export Citation

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