Tranexamic acid for intracranial meningioma

Tranexamic acid for intracranial meningioma

Based upon Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA), Wijaya et al. from the Universitas Pelita Harapan, Tangerang, BantenIndonesia, Cedars-Sinai Medical Center, Los Angeles, CES University, El Poblado, Medellín, Antioquia, Colombia. collected fully published English literature on the administration of tranexamic acid for patients undergoing intracranial meningioma surgery using the keywords [“tranexamic acid” and “meningioma”] and its synonyms from Cochrane Central Register of Controlled Trials Database, the WHO International Clinical Trials Registry Platform (ICTRP),, and PubMed. The primary outcome of the current study was total blood loss. The secondary outcomes include individuals requiring blood transfusionanesthesia duration, surgical duration, and complication rate. Each included study’s quality was assessed using the JADAD scale.

For qualitative and quantitative data synthesis, they included five RCTs (n = 321) with a mean age was 47.5 ± 11.9 years for the intervention group and 47.2 ± 11.9 years for the control group. The meta-analysis showed that the administration of TXA is associated with decreased total blood loss of standardized mean difference (SMD) of -1.40 (95% CI [-2.49, -0.31]), anesthetic time SMD -0.36 (95% CI [-0.63, -0.09]), and blood transfusion requirements RR 0.58 (95% CI [0.34, 0.99]).

The current study showed that TXA was associated with reduced intraoperative blood loss and intraoperative and postoperative blood transfusion. However, the studies are small. More RCT studies with a greater sample size are favorable 1).

Patients with supratentorial meningiomas and deemed suitable for surgical resection will be recruited in the trial. Patients will be randomized to receive either a single administration of 20 mg/kg TXA or a placebo of the same volume with a 1:1 allocation ratio after anesthesia induction. The primary endpoint is the cumulative incidence of early postoperative seizures within 7 days after craniotomy. Secondary outcomes include the incidence of non-seizure complications, changes in hemoglobin level from baseline, intraoperative blood loss, erythrocyte transfusion volume, Karnofsky Performance Status, all-cause mortality, length of stay, and total hospitalization cost.

Ethics and dissemination: This trial is registered at and approved by the Chinese Ethics Committee of Registering Clinical Trials (ChiECRCT20200224). The findings will be disseminated in peer-reviewed journals and presented at national or international conferences relevant to the subject fields.

Trial registration number: NCT04595786 2).

conducted a prospective, randomized double-blind clinical study. The patient scheduled to undergo excision of intracranial meningioma were randomly assigned to receive intraoperatively either intravenous TXA or placebo. Patients in the TXA group received an intravenous bolus of 20 mg/kg over 20 min followed by an infusion of 1 mg/kg/h up to surgical wound closure. Efficacy was evaluated based on total blood loss and transfusion requirements. Postoperatively, thrombotic complications, convulsive seizure, and hematoma formation were noted.

Ninety-one patients were enrolled and randomized: 45 received TXA (TXA group) and 46 received placebo (group placebo). Total blood loss was significantly decreased in the TXA group compared to the placebo (283 ml vs. 576 ml; P < 0.001). Transfusion requirements were comparable in the two groups (P = 0.95). The incidence of thrombotic complications, convulsive seizure, and hematoma formation were similar in the two groups.

TXA significantly reduces intraoperative blood loss but did not significantly reduce transfusion requirements in adults undergoing resection of intracranial meningioma 3).

Thirty patients aged 18-65 years undergoing elective meningioma resection surgery were given either tranexamic acid or placebo (0.9% saline), tranexamic acid at a loading dose of 20 mg/kg, and infusion of 1 mg/kg/h during surgery. The intraoperative blood loss, coagulation profile, and the surgical field using the Likert scale were assessed.

The patients in the tranexamic group had significantly decreased intraoperative blood loss compared to the placebo group (616.42 ± 393.42 ml vs. 1150.02 ± 416.1 ml) (P = 0.02). The quality of the surgical field was better in the tranexamic group (median score 4 vs. 2 on Likert Scale) (P < 0.001). Patients in the tranexamic group had an improved coagulation profile and decreased blood transfusion requirement (p=0.016). The blood collected in the closed suction drain in 24 h postsurgery was less in the tranexamic acid group compared to the placebo group (84.7 ± 50.4 ml vs. 127.6 ± 62.2 ml) (P = 0.047).

Tranexamic acid bolus followed by infusion reduces perioperative blood loss by 46.43% and blood transfusion requirement with improved surgical field and coagulation profile in patients undergoing intracranial meningioma resection surgery 4).

In the Department of Neurosurgery, All India Institute of Medical Sciences (AIIMS), New Delhi, India, Sixty adults undergoing elective craniotomy for meningioma excision were randomized to receive either tranexamic acid or placebo, initiated prior to skin incision. Patients in the tranexamic acid group received an intravenous bolus of 20mg/kg over 20min followed by an infusion of 1mg/kg/h till the conclusion of surgery. Intraoperative blood loss, transfusion requirements, and estimating surgical hemostasis using a 5-grade scale were noted. Postoperatively, the extent of tumor excision on CT scan and complications were observed. Demographics, tumor characteristics, amount of fluid infusion, and duration of surgery and anesthesia were comparable between the two groups. The amount of blood loss was significantly less in the tranexamic acid group compared to the placebo (830mlvs 1124ml; p=0.03). The transfusion requirement was less in the tranexamic acid group (p>0.05). The patients in the tranexamic acid group fared better on a 5-grade surgical hemostasis scale with more patients showing good hemostasis (p=0.007). There were no significant differences between the groups regarding the extent of tumor removal, perioperative complications, hospital stay, or neurologic outcome. To conclude, the administration of tranexamic acid significantly reduced blood loss in patients undergoing excision of meningioma. Fewer patients in the tranexamic acid group received blood transfusions. Surgical field hemostasis was better achieved in patients who received tranexamic acid 5).

A man in his 40s with a history of coronary artery disease previously treated with a drug-eluting stent presented for elective craniotomy and resection of an asymptomatic but enlarging meningioma. During his craniotomy, he received desmopressin and tranexamic acid for surgical bleeding. Postoperatively, the patient developed chest pain and was found to have an ST-elevation myocardial infarction (MI). Because of the patient’s recent neurosurgery, standard post-MI care was contraindicated and he was managed symptomatically in the intensive care unit. The echocardiogram on a postoperative day 1 demonstrated no regional wall motion abnormalities and an ejection fraction of 60%. His presentation was consistent with the thrombosis of his diagonal stent. He was transferred out of the intensive care unit on postoperative day 1 and discharged home on postoperative day 3 6).

Raghavendra et al. report the intraoperative use of tranexamic acid to secure complete hemostasis as a rescue measure in intracranial meningioma resection in uncontrollable bleeding 7).

Three of 13 patients with intracranial meningiomas showed the pre-and postoperative elevation of tissue-type plasminogen activator (t-PA) related fibrinolytic activity in euglobulin fractions (EFA). During the operation, two of these three patients showed a significant elevation of the level of fibrinogen degradation products and oozing in the operating field. However, oozing was not observed in the third patient who had been given tranexamic acid preoperatively. Fibrin autography revealed that a broad lytic band of mol wt 50-60 kDa, probably free t-PA, appeared in the plasma obtained from two of the three patients after the operation when EFA elevated significantly. In all patients studied, the t-PA antigen levels were normal preoperatively but increased both during and after the operation, and correlated mainly with the intensities of a lytic band of mol wt 110 kDa, probably t-PA complexed with its major inhibitor (PAI-1). These results suggest that excessive fibrinolysis can induce local hemorrhagic diathesis during operation and may be related to t-PA function in plasma 8).


Wijaya JH, July J, Quintero-Consuegra M, Chadid DP. A systematic review and meta-analysis of the effects of tranexamic acid in surgical procedure for intracranial meningioma. J Neurooncol. 2023 Jan 12. doi: 10.1007/s11060-023-04237-2. Epub ahead of print. PMID: 36633801.

Li S, Yan X, Li R, Zhang X, Ma T, Zeng M, Dong J, Wang J, Liu X, Peng Y. Safety of intravenous tranexamic acid in patients undergoing supratentorial meningiomas resection: protocol for a randomized, parallel-group, placebo control, non-inferiority trial. BMJ Open. 2022 Feb 2;12(2):e052095. doi: 10.1136/bmjopen-2021-052095. PMID: 35110315; PMCID: PMC8811564.

Rebai L, Mahfoudhi N, Fitouhi N, Daghmouri MA, Bahri K. Intraoperative tranexamic acid use in patients undergoing excision of intracranial meningioma: Randomized, placebo-controlled trial. Surg Neurol Int. 2021 Jun 14;12:289. doi: 10.25259/SNI_177_2021. PMID: 34221620; PMCID: PMC8247750.

Ravi GK, Panda N, Ahluwalia J, Chauhan R, Singla N, Mahajan S. Effect of tranexamic acid on blood loss, coagulation profile, and quality of the surgical field in intracranial meningioma resection: A prospective randomized, double-blind, placebo-controlled study. Surg Neurol Int. 2021 Jun 7;12:272. doi: 10.25259/SNI_296_2021. PMID: 34221603; PMCID: PMC8247710.

Hooda B, Chouhan RS, Rath GP, Bithal PK, Suri A, Lamsal R. Effect of tranexamic acid on intraoperative blood loss and transfusion requirements in patients undergoing excision of intracranial meningioma. J Clin Neurosci. 2017 Mar 7. pii: S0967-5868(16)31491-6. doi: 10.1016/j.jocn.2017.02.053. [Epub ahead of print] PubMed PMID: 28283245.

Westfall KM, Ramcharan RN, Anderson HL 3rd. Myocardial infarction after craniotomy for asymptomatic meningioma. BMJ Case Rep. 2022 Dec 29;15(12):e252256. doi: 10.1136/bcr-2022-252256. PMID: 36581354; PMCID: PMC9806024.

Raghavendra H, Varsha KS, Reddy MA, Kumar SS, Sunanda G, Nagarjuna T, Latha S. Rescue Measure in Giant Intracranial Meningioma Resection by Tranexamic Acid. J Neurosci Rural Pract. 2017 Aug;8(Suppl 1):S127-S129. doi: 10.4103/jnrp.jnrp_198_17. PMID: 28936089; PMCID: PMC5602238.

Tsuda H, Oka K, Noutsuka Y, Sueishi K. Tissue-type plasminogen activator in patients with intracranial meningiomas. Thromb Haemost. 1988 Dec 22;60(3):508-13. PMID: 3149049.

Trigone ventricular meningioma

Trigone ventricular meningioma

Thirty patients with trigone meningiomas were enrolled in this retrospective study. Conventional MRI was performed in all patients; SWI (17 cases), dynamic contrast-enhanced PWI (10 cases), and dynamic susceptibility contrast PWI (6 cases) were performed. Demographics, conventional MRI features, SWI- and PWI-derived parameters were compared between different grades of trigone meningiomas.

On conventional MRI, the irregularity of tumor shape (ρ = 0.497, P = 0.005) and the extent of peritumoral edema (ρ = 0.187, P = 0.022) might help distinguish low-grade and high-grade trigone meningiomas. On multiparametric functional MRI, rTTPmax (1.17 ± 0.06 vs 1.30 ± 0.05, P = 0.048), Kep, Ve, and iAUC demonstrated their potentiality to predict World Health Organization grades I, II, and III trigone meningiomas.

Conventional MRI combined with dynamic susceptibility contrast and dynamic contrast-enhanced can help predict the World Health Organization grade of trigone meningiomas 1).

A 65-year-old female refers to a speech disorder (slowed speech and stuttering) for months of evolution, the reason for which an MRI study was performed. Refers to impaired reading (blurred vision of some letters) associated.

Brain MRI:

In the left hemisphere, a rounded tumor of 28 mm in greater diameter is located inside the lateral ventricle. It is a tumor slightly hypointense on T1, slightly hyperintense on Flair, and practically isointense on T2. The lesion uptakes contrast intense and relatively uniform way. The posterior horn of the ventricle appears dilated and there is a modification of the signal intensity of the adjacent tissue. However, the midline does not appear displaced. the ventricle right lateral and third ventricles are dilated

General anesthesia. Right lateral decubitus position with Mayfield skull clampIncision and craniotomy location with craniometric points (intraparietal point). Left parietal craniotomy with the high-speed motor. U-shaped dural opening with a sagittal sinus base. The postcentral sulcus and intraparietal sulcus are visualized in the cortex. Location of the atrium and tumor with intraoperative ultrasound. Approach through the intraparietal sulcus in its lower portion until the ventricle was opened and a pinkish-colored tumor with a rubbery consistency visible, macroscopically compatible with meningioma. Dissection of the edges at the intraventricular level, separating the choroid plexus and coagulating and sectioning several nutrient arteries. Tumor dissection with CUSA until leaving a small fragment that is dissected from the medial wall of the ventricle and excised. Macroscopically complete resection. Careful hemostasis and abundant washing. Dural closure is almost hermetic and sealed with TachosilBone replacement with titanium trephine plates and plugs. Cutaneous closure by planes. Stapled skin. The sample is sent to pathology.


Yang X, Xiao Z, Xing Z, Lin X, Wang F, Cao D. Grading Trigone Meningiomas Using Conventional Magnetic Resonance Imaging With Susceptibility-Weighted Imaging and Perfusion-Weighted Imaging. J Comput Assist Tomogr. 2022 Jan-Feb 01;46(1):103-109. doi: 10.1097/RCT.0000000000001256. PMID: 35027521.

Somatostatin analogs in meningioma

Somatostatin analogs in meningioma

Meningiomas are associated with several sex hormones-related risk factors and demonstrate a predominance in females. These associations led to investigations of the role that hormones may have on meningioma growth and development. While it is now accepted that most meningiomas express progesterone and somatostatin receptors, the conclusion for other receptors has been less definitive.

Miyagishima et al. performed a review of what is known regarding the relationship between hormones and meningiomas in the published literature. Furthermore, they reviewed clinical trials related to hormonal agents in meningiomas using MEDLINE PubMedScopus, and the NIH clinical trials database.

They identified that all steroid-hormone trials lacked receptor identification or positive receptor status in the majority of patients. In contrast, four out of five studies involving somatostatin analogs used positive receptor status as part of the inclusion criteria.

Several clinical trials have recently been completed or are now underway using somatostatin analogs in combination with other therapies that appear promising, but a reevaluation of hormone-based monotherapy is warranted. Synthesizing this evidence, they clarified the remaining questions and present future directions for the study of the biological role and therapeutic potential of hormones in meningioma and discuss how the stratification of patients using features such as grade, receptor status, and somatic mutations, might be used for future trials to select patients most likely to benefit from specific therapies 1)

Jensen et al. performed an individual patient data (IPD) meta-analysis. Main outcomes were toxicity, best radiological response, progression-free survival, and overall survival. They applied multivariable logistic regression models to estimate the effect of SSA on the probability of obtaining radiological disease control. The predictive performance was evaluated using area under the curve and Brier scores. They included 16 studies and compiled IPD from 8/9 of all previous cohorts. Quality of evidence was overall ranked “very low.” Stable disease was reported in 58% of patients as best radiological response. Per 100 mg increase in total SSA dosage, the odds ratios for obtaining radiological disease control was 1.42 (1.11 to 1.81, P = 0.005) and 1.44 (1.00 to 2.08, P = 0.05) for patients treated with SSA as monodrug therapy vs SSA in combination with everolimus, respectively. Low quality of evidence impeded exact quantification of treatment efficacy, and the association between response and treatment may represent reverse causality. Yet, the SSA treatment was well tolerated, and beneficial effect cannot be disqualified. A prospective trial without bias from inconsistency in study designs is warranted to assess somatostatin analog therapy for well-defined meningioma subgroups 2).

Between January 1996 and December 2010, 13 patients harboring a progressive residual meningioma (as indicated by MR imaging criteria) following operative therapy were treated with a monthly injection of the SST analog octreotide (Sandostatin LAR [long-acting repeatable] 30 mg, Novartis). Eight of 13 patients had a meningioma of the skull base and were analyzed in the present study. Postoperative tumor enlargement was documented in all patients on MR images obtained before the initiation of SST therapy. All tumors were benign. No patient received radiation or chemotherapy before treatment with SST. The growth of residual tumor was monitored by MR imaging every 12 months.

Results: Three of the 8 patients had undergone surgical treatment once; 3, 2 times; and 2, 3 times. The mean time after the last meningioma operation (before starting SST treatment) and tumor enlargement as indicated by MR imaging criteria was 24 months. A total of 643 monthly cycles of Sandostatin LAR were administered. Five of the 8 patients were on SST continuously and stabilized disease was documented on MR images obtained in these patients during treatment (median 115 months, range 48-180 months). Three of the 8 patients interrupted treatment: after 60 months in 1 case because of tumor progression, after 36 months in 1 case because of side effects, and after 36 months in 1 case because the health insurance company denied cost absorption.

Conclusions: Although no case of tumor regression was detected on MR imaging, the study results indicated that SST analogs can arrest the progression of unresectable or recurrent benign meningiomas of the skull base in some patients. It remains to be determined whether a controlled prospective clinical trial would be useful 3).


Miyagishima DF, Moliterno J, Claus E, Günel M. Hormone therapies in meningioma-where are we? J Neurooncol. 2022 Nov 23. doi: 10.1007/s11060-022-04187-1. Epub ahead of print. PMID: 36418843.

Jensen LR, Maier AD, Lomstein A, Graillon T, Hrachova M, Bota D, Ruiz-Patiño A, Arrieta O, Cardona AF, Rudà R, Furtner J, Roeckle U, Clement P, Preusser M, Scheie D, Broholm H, Kristensen BW, Skjøth-Rasmussen J, Ziebell M, Munch TN, Fugleholm K, Walter MA, Mathiesen T, Mirian C. Somatostatin analogues in treatment-refractory meningioma: a systematic review with meta-analysis of individual patient data. Neurosurg Rev. 2022 Oct;45(5):3067-3081. doi: 10.1007/s10143-022-01849-6. Epub 2022 Aug 19. PMID: 35984552.

Schulz C, Mathieu R, Kunz U, Mauer UM. Treatment of unresectable skull base meningiomas with somatostatin analogs. Neurosurg Focus. 2011 May;30(5):E11. doi: 10.3171/2011.1.FOCUS111. PMID: 21529167.

Foramen magnum meningioma

Foramen magnum meningioma

Foramen magnum meningiomas (FMMs) are slow growing, posterior fossa meningiomas most often intradural and extramedullar. They are those arising anteriorly from the inferior third of the clivus to the superior edge of the C2 body, laterally from the jugular tubercle to the C2 laminae, and posteriorly from the anterior border of the occipital squama to the spinous process of C2 1) 2) 3).

They represent 2% of all meningioma4).

The mean age of the patients with these lesions at the time of diagnosis is approximately 55 years old, but these tumors have been reported in patients of almost every age 5) 6) 7) 8) 9).

They have traditionally been said to involve the lower third of the clivus and the C1 C2 area. However, the last categorizations are arbitrary.

There are some tumors that involve the entire clivus, and others that involve the mid and lower third of the clivus. (The upper clivus is the area above the trigeminal root, the mid-clivus extends to the level of the glossopharyngeal nerve, and the lower clivus is the region below the glossopharyngeal nerve).

The indolent clinical course of FMMs and their insidious onset of symptoms are important factors that contribute to delayed diagnosis and relative large size at the time of presentation. Symptoms are often produced by compression of surrounding structures (such as the medulla oblongata, upper cervical spinal cord, lower cranial nerves, and vertebral artery) within a critically confined space

Matsoukas S, Oemke H, Lopez LS, Gilligan J, Tabani H, Bederson JB. Suboccipital Craniectomy for an Anterior Foramen Magnum Meningioma-Optimization of Resection Using Intraoperative Augmented Reality: 2-Dimensional Operative Video. Oper Neurosurg (Hagerstown). 2022 Nov 1;23(5):e321. doi: 10.1227/ons.0000000000000373. Epub 2022 Aug 8. PMID: 36103323.

Emerson SN, Toczylowski M, Al-Mefty O. Dejerine Syndrome Variant Due to Medullary Perforating Artery Ischemia During Foramen Magnum Meningioma Resection: 2-Dimensional Operative Video. Oper Neurosurg (Hagerstown). 2022 Jul 1;23(1):e52-e53. doi: 10.1227/ons.0000000000000211. Epub 2022 Apr 20. PMID: 35726936. Danish B, Costello MC, Patel NV, Higgins DMO, Komotar RJ, Ivan ME. Commentary: Dejerine Syndrome Variant Due to Medullary Perforating Artery Ischemia During Foramen Magnum Meningioma Resection: 2-Dimensional Operative Video. Oper Neurosurg (Hagerstown). 2022 Sep 1;23(3):e205-e206. doi: 10.1227/ons.0000000000000336. Epub 2022 Jul 11. PMID: 35972118.

Danish B, Costello MC, Patel NV, Higgins DMO, Komotar RJ, Ivan ME. Commentary: Dejerine Syndrome Variant Due to Medullary Perforating Artery Ischemia During Foramen Magnum Meningioma Resection: 2-Dimensional Operative Video. Oper Neurosurg (Hagerstown). 2022 Sep 1;23(3):e205-e206. doi: 10.1227/ons.0000000000000336. Epub 2022 Jul 11. PMID: 35972118.

Medina EJ, Revuelta Barbero JM, Porto E, Garzon-Muvdi T, Henriquez O, Solares CA, Pradilla G. Exoscopic and Microscopic Combined Far Lateral Retrocondylar Approach for Resection of a Ventral Foramen Magnum Lesion: 2-Dimensional Operative Video. Oper Neurosurg (Hagerstown). 2022 Aug 1;23(2):e126. doi: 10.1227/ons.0000000000000250. Epub 2022 May 9. PMID: 35838470.

Jeelani Y, Ibn Essayed W, Al-Mefty O. Extended Transcondylar Approach With C-1 Lateral Mass Resection for the Removal of a Calcified Ventral “Spinocranial” Meningioma: 2-Dimensional Operative Video. Oper Neurosurg (Hagerstown). 2022 Aug 1;23(2):e117-e118. doi: 10.1227/ons.0000000000000278. Epub 2022 May 9. PMID: 35838463.

Essayed W, Aboud E, Al-Mefty O. Foramen Magnum Meningioma-The Attainment of the Intra-Arachnoidal Dissection: 2-Dimensional Operative Video. Oper Neurosurg (Hagerstown). 2021 Nov 15;21(6):E518-E519. doi: 10.1093/ons/opab317. PMID: 34498699.

Campero A, Baldoncini M, Villalonga JF, Paíz M, Giotta Lucifero A, Luzzi S. Transcondylar Fossa Approach for Resection of Anterolateral Foramen Magnum Meningioma: 2-Dimensional Operative Video. World Neurosurg. 2021 Oct;154:91-92. doi: 10.1016/j.wneu.2021.07.058. Epub 2021 Jul 21. PMID: 34303002.


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Suisa H, Soustiel JF, Grober Y. IgG4-related pachymeningitis masquerading as foramen magnum meningioma: illustrative case. J Neurosurg Case Lessons. 2021 Dec 6;2(23):CASE21398. doi: 10.3171/CASE21398. PMID: 36061082; PMCID: PMC9435580.

Uramaru K, Sakata K, Shimohigoshi W, Kawasaki T, Manaka H. Primary Meningeal Melanocytoma Located in the Craniovertebral Junction: A Case Report and Literature Review. NMC Case Rep J. 2021 Jun 25;8(1):349-354. doi: 10.2176/ PMID: 35079487; PMCID: PMC8769411.

Anaplastic meningioma

Anaplastic meningioma

Anaplastic meningioma (also known as malignant meningiomas) is defined by several criteria including:

1) Invasion of adjacent brain parenchyma or skull. (see invasive meningioma)

2) Numerous mitosis (> 5/high-powered field)

3) Elevated proliferative index (>3%) as assessed by either 5-bromodeoxyuridine or KI-67 staining

4) Necrosis

5) Increased cellularity

6) Nuclear pleomorphism

7) metastases

Anaplastic meningiomas are uncommon, accounting for only ~1% of all meningiomas 1).

Generally, it is not possible to confidently distinguish benign (WHO grade I) and atypical (WHO grade II) from anaplastic (WHO grade III) meningiomas on general morphology. The most reliable feature in suggesting a non-grade I tumour is the presence of lower ADC values (reflecting higher cellularity) 2) 3).

Importantly presence of vasogenic oedema in adjacent brain parenchyma is not a predictor of atypical or anaplastic histology 4).

Brain invasion, although by definition denoting at least a grade II tumour, is also surprisingly difficult to predict on MRI.

There are, some CT or MRI trends that point in favor of malignant meningioma:

1) the absence of visible calcium aggregates 5).

2) “mushrooming” or the presence of a prominent pannus of tumor extending well away from the globoid mass 6) 7) 8).

Ki-67 index >10% was associated with a trend toward worse PFS. Given the long-term survival, high recurrence rates, and efficacy of salvage therapy, patients with atypical and malignant meningiomas should be monitored systematically long after initial treatment 9).

Older age, male gender, distant metastasis, and radiotherapy were significantly related to poor prognosis; and the extent of resection did not affect survival 10).

Malignant progression with the accumulation of mutations in a benign meningioma can result in an atypical meningioma and/or anaplastic meningioma. Both tumors are difficult to manage and have a high recurrence and poor survival rates. The extent of tumor resection and histological grade are the key determinants for recurrence.

Anaplastic meningiomas are aggressive tumors, with a median overall survival time of 15 months 11).

They have a higher rate of recurrence and metastases accompanied by a significantly shorter survival rate compared to benign variants. Meningioma cancer stem cells (CSCs) have been previously shown to be associated with resistance and aggressiveness. However, the role they play in meningioma progression is still being investigated 12).

Maier AD. Malignant meningioma. APMIS. 2022 Nov;130 Suppl 145:1-58. doi: 10.1111/apm.13276. PMID: 36424331.

Baeesa et al. from the Division of Neurosurgery, Department of Surgery, King Abdulaziz University Hospital, Faculty of Medicine, JeddahSaudi Arabia, report a 29-year-old man who underwent a resection of a grade I meningioma in 2011. The patient had multiple local recurrences of the tumor that exhibited an aggressive change in behavior and transformation to grade III meningioma and developed extracranial metastases to the cervical spine. He underwent multiple operations and received radiotherapy. Analysis of the meningioma indicated the presence of CSCs markers before metastases and showed elevated expressions of associated markers in the metastasized tissue. Also, and similar to the patient’s profile, the pharmacological testing of a primary cell line retrieved from the metastasized tissues showed a high level of drug tolerance and a loss of ability to initiate apoptosis.

Malignant progression of grade I meningioma can occur, and its eventuality may be anticipated by detecting CSCs. We included a comprehensive literature review of relevant cases and discussed the clinical, diagnostic and management characteristics of the reported cases 13).

A patient had an intracranial malignant meningioma and developed a symptomatic osteolytic contrast-enhancing lesion in the left C-1 lateral mass suspicious for metastases. The authors performed a minimally invasive posterior resection of the lesion with vertebroplasty of C-1. Histopathology verified metastases of the malignant meningioma. The surgical procedure resulted in prompt and permanent pain reduction until the patient died 18 months later. Given the very limited life expectancy in this case, the authors did not consider occipitocervical fusion because of their desire to preserve the range of motion of the head. Therefore, they suggest minimally invasive tumor resection and vertebroplasty in selected palliative tumor patients 14).


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Toh CH, Castillo M, Wong AM et-al. Differentiation between classic and atypical meningiomas with use of diffusion tensor imaging. AJNR Am J Neuroradiol. 2008;29 (9): 1630-5. doi:10.3174/ajnr.A1170
5) , 8)

Younis GA, Sawaya R, DeMonte F, Hess KR, Albrecht S, Bruner JM. Aggressive meningeal tumors: review of a series. J Neurosurg 1995; 82:17-27.

Mahmood A, Caccamo DV, Tomecek FJ, Malik GM. Atypical and malignant meningiomas: a clinicopathological review. Neurosurgery 1993;33:955-963.

Jaaskelainen J, Haltia M, Servo A. Atypical and anaplastic meningiomas: radiology, surgery, radiotherapy, and outcome. Surg Neurol 1986; 25:233-242.

Kent CL, Mowery YM, Babatunde O, Wright AO, Barak I, McSherry F, Herndon JE 2nd, Friedman AH, Zomorodi A, Peters K, Desjardins A, Friedman H, Sperduto W, Kirkpatrick JP. Long-Term Outcomes for Patients With Atypical or Malignant Meningiomas Treated With or Without Radiation Therapy: A 25-Year Retrospective Analysis of a Single-Institution Experience. Adv Radiat Oncol. 2021 Dec 24;7(3):100878. doi: 10.1016/j.adro.2021.100878. PMID: 35647401; PMCID: PMC9133398.

Zhang GJ, Liu XY, Wang W, You C. Clinical factors and outcomes of malignant meningioma: a population-based study. Neurol Res. 2022 Mar 30:1-9. doi: 10.1080/01616412.2022.2056343. Epub ahead of print. PMID: 35353024.

Modha A, Gutin PH. Diagnosis and treatment of atypical and anaplastic meningiomas: a review. Neurosurgery. 2005 Sep;57(3):538-50; discussion 538-50. Review. PubMed PMID: 16145534.
12) , 13)

Baeesa SS, Hussein D, Altalhy A, Bakhaidar MG, Alghamdi FA, Bangash M, Abuzenadah A. Malignant Transformation and Spine metastases of an Intracranial Grade I Meningioma: In Situ Immunofluorescence analysis of Cancer Stem Cells. World Neurosurg. 2018 Sep 8. pii: S1878-8750(18)32024-2. doi: 10.1016/j.wneu.2018.09.004. [Epub ahead of print] PubMed PMID: 30205223.

Klingler JH, Krüger MT, Kogias E, Brendecke SM, Hubbe U, Scheiwe C. Minimally invasive resection and vertebroplasty for an osteolytic C-1 metastases of malignant meningioma: case report. J Neurosurg Spine. 2015 Jul 17:1-5. [Epub ahead of print] PubMed PMID: 26185898.

Meningioma Systematic Reviews

Meningioma Systematic Reviews

Eight electronic databases/registries were searched to identify eligible meningioma Systematic Reviews with and without meta-analysis published between January 1990 and December 2020Articles concerning spinal meningioma were excluded. Reporting and methodological quality were assessed against the following tools: Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA), A Measurement Tool to Assess systematic Reviews (AMSTAR 2), and Risk Of Bias in Systematic reviews (ROBIS).

116 Systematic Reviews were identified, of which 57 were SRMAs (49.1%). The mean PRISMA score for SRMA was 20.9 out of 27 (SD 3.9, 77.0% PRISMA adherence), and for SR without meta-analysis was 13.8 out of 22 (SD 3.4, 63% PRISMA adherence). Thirty-eight studies (32.8%) achieved greater than 80% adherence to PRISMA. Methodological quality assessment against AMSTAR 2 revealed that 110 (94.8%) studies were of critically low quality. Only 21 studies (18.1%) were judged to have a low risk of bias against ROBIS.

The reporting and methodological quality of meningioma evidence syntheses were poor. Established guidelines and critical appraisal tools may be used as an adjunct to aid methodological conduct and reporting of such reviews, in order to improve the validity and transparency of research that may influence clinical practice 1).

Updated Systematic Review on the Role of Brain Invasion in Intracranial Meningiomas: What, When, Why? 2).

The Emerging Relevance of H3K27 Trimethylation Loss in Meningioma: A Systematic Review of Recurrence and Overall Survival with Meta-Analysis 3).

Seizure prophylaxis in meningiomas: a systematic review and meta-analysis 4).

A systematic review and meta-analysis of the association between cyproterone acetate and intracranial meningiomas 5).

Volumetric growth of residual meningioma – A systematic review 6)

Incidental intracranial meningiomas: a systematic review and meta-analysis of prognostic factors and outcomes 7).


George AM, Gupta S, Keshwara SM, Mustafa MA, Gillespie CS, Richardson GE, Steele AC, Zamanipoor Najafabadi AH, Dirven L, Marson AG, Islim AI, Jenkinson MD, Millward CP. Meningioma systematic reviews and meta-analyses: an assessment of reporting and methodological quality. Br J Neurosurg. 2022 Oct 20:1-8. doi: 10.1080/02688697.2022.2115008. Epub ahead of print. PMID: 36263847.

Brunasso L, Bonosi L, Costanzo R, Buscemi F, Giammalva GR, Ferini G, Valenti V, Viola A, Umana GE, Gerardi RM, Sturiale CL, Albanese A, Iacopino DG, Maugeri R. Updated Systematic Review on the Role of Brain Invasion in Intracranial Meningiomas: What, When, Why? Cancers (Basel). 2022 Aug 27;14(17):4163. doi: 10.3390/cancers14174163. PMID: 36077700; PMCID: PMC9454707.

Lu VM, Luther EM, Eichberg DG, Morell AA, Shah AH, Komotar RJ, Ivan ME. The Emerging Relevance of H3K27 Trimethylation Loss in Meningioma: A Systematic Review of Recurrence and Overall Survival with Meta-Analysis. World Neurosurg. 2022 Jul;163:87-95.e1. doi: 10.1016/j.wneu.2022.04.048. Epub 2022 Apr 16. PMID: 35439620.

Delgado-López PD, Ortega-Cubero S, González Bernal JJ, Cubo-Delgado E. Seizure prophylaxis in meningiomas: a systematic review and meta-analysis. Neurologia (Engl Ed). 2022 Jun 30:S2173-5808(22)00036-0. doi: 10.1016/j.nrleng.2022.03.002. Epub ahead of print. PMID: 35781420.

Lee KS, Zhang JJY, Kirollos R, Santarius T, Nga VDW, Yeo TT. A systematic review and meta-analysis of the association between cyproterone acetate and intracranial meningiomas. Sci Rep. 2022 Feb 4;12(1):1942. doi: 10.1038/s41598-022-05773-z. PMID: 35121790; PMCID: PMC8816922.

Gillespie CS, Taweel BA, Richardson GE, Mustafa MA, Keshwara SM, Babar RK, Alnaham KE, Kumar S, Bakhsh A, Millward CP, Islim AI, Brodbelt AR, Mills SJ, Jenkinson MD. Volumetric growth of residual meningioma – A systematic review. J Clin Neurosci. 2021 Sep;91:110-117. doi: 10.1016/j.jocn.2021.06.033. Epub 2021 Jul 5. PMID: 34373014.

Islim AI, Mohan M, Moon RDC, Srikandarajah N, Mills SJ, Brodbelt AR, Jenkinson MD. Incidental intracranial meningiomas: a systematic review and meta-analysis of prognostic factors and outcomes. J Neurooncol. 2019 Apr;142(2):211-221. doi: 10.1007/s11060-019-03104-3. Epub 2019 Jan 17. Erratum in: J Neurooncol. 2019 Sep;144(2):427-429. PMID: 30656531; PMCID: PMC6449307.

Intraosseous meningioma of the sphenoid bone

Intraosseous meningioma of the sphenoid bone

Some sphenoid wing meningiomas are associated with a significant hyperostosis of the adjacent sphenoid ridge that may even exceed the size of the intradural mass. The decision-making process and surgical planning based on neuroanatomic knowledge are the mainstays of management of this group of lesions. Given their natural history and biologic behavior, many hyperostosing meningiomas at this location require long-term management analogous to a chronic disease. This is particularly true when making initial decisions regarding treatment and planning surgical intervention, when it is important to take into consideration the possibility of further future interventions during the patient’s life span 1).

The relationship of the development of intraosseous meningioma to the entrapment of dura containing arachnoid cells is discussed in considering the cause of such lesions, and it is stressed that calvarial fractures and cranial sutures may contribute to the entrapment of arachnoidal tissue and later the formation of a meningioma 2).

Intraosseous growth is a unique feature of sphenoorbital meningioma. Quantitative assessment of the biological behavior of intraosseous remnants revealed a continuous slow growth rate independent of the soft tumor component of more than half of SOM. According to our data, application of a multimodal image guidance provided high accuracy and significantly increased the resection rate of the intraosseous component of SOM 3)

A 24-year-old woman presented with subdural hemorrhage, and subsequent radiology depicted an osteolytic mass-like lesion in the sphenoid bone. Intraoperatively, a solid and cystic hemorrhagic lesion mimicking an aneurysmal bone cyst was observed in the sphenoid bone with dural tearing. Frozen cytology showed singly scattered or epithelioid clusters of round to elongated cells intermixed with many neutrophils. Tumor cells had bland-looking round nuclei with rare prominent nucleoli and nuclear inclusions and eosinophilic granular to globoid cytoplasm in capillary-rich fragments. Histology revealed intraosseous meningothelial and microcystic meningioma (World Health Organization grade 1) in right lesser wing of the sphenoid bone. Considering its unusual location and cytologic findings, differential diagnoses included chordomachondromachondrosarcoma, and aneurysmal bone cyst. The present case posed a diagnostic challenge due to possible confusion with these entities 4)

A 43-year-old female presented with a 1 year history of headache, peri-orbital pain, proptosis, and severe vision loss. She had previously undergone subtotal resection of a large Simpson Grade 1 spheno-orbital meningioma 3 years prior at an outside institution. Workup at our institution revealed hyperostosis of the left greater wing of the sphenoid bone and narrowing of the optic canal along with bony enhancement concerning for residual tumor. The patient was given the recommendation from outside institutions for radiation, presumably due to the chronicity of her visual loss. Our institution recommended resection of the residual osseous tumor with orbital reconstruction. Less than 2 weeks after surgery, the patient noted significant improvement in orbital pain and vision. At 3 months, she had regained full and symmetric orbital appearance with no orbital pain. Her visual acuity improved to 20/30 with full visual fields. Conclusion Surgical decompression of the optic canal and orbital contents for tumor related sphenoid wing hyperostosis should be strongly considered, despite an extended duration of visual change and loss. This case report shows that vision can be significantly restored even after symptoms have been present for greater than 6 months 5).

A 30-year-old female patient presented to the Emergency Department (ED) with a six-week history of right eye pain, diplopia on lateral gaze, and proptosis. She had reported progressive onset of symptoms over the past 12 months. Her only previous medical issue was asthma. Haematological and biochemical results were all normal.

Non-contrast CT orbits were undertaken to evaluate for intraconal or extraconal masses or collection. Findings demonstrated poorly marginated diffuse right greater sphenoid wing cortical thickening, resulting in mass effect on the lateral rectus muscle. Post-contrast CT orbits did not show lesional or soft-tissue enhancement. A CT thorax/abdomen/pelvis was undertaken to exclude a primary malignancy.

MRI orbits pre-and post-contrast demonstrated low-signal thickening of the right greater sphenoid wing with lesional and adjacent dural enhancement on post-contrast sequences. 6).

Use of an acrylic jig to aid orbital reconstruction after resection of a sphenoid intraosseous meningioma: a technical note 7)

A 50-year-old female presented to the Neurosurgery clinic with dimness of vision and proptosis of her right eye. Maxillofacial CT showed a hyperostotic mass involving the right sphenoid ridgeanterior clinoid processorbital roof, and lateral wall with mass effect on the intraorbital contents and lateral wall of the sphenoid sinus. MRI of the brain and orbit showed a heterogeneous enhancement of underlying dura and right orbital apex extending into the cavernous sinus. The patient underwent a staged resection in which pathological analysis showed an intraosseous meningioma. When a hyperostotic mass of the skull is encountered, meningioma should be considered in the differential diagnosis. Although primary intraosseous meningiomas are rare benign tumors, they can be associated with morbidity secondary to mass effect. 8)

A 40-year-old man treated for systemic hypertension complained of decreased vision and floaters in his right eye. Initial examination revealed decreased visual acuity to 20/50 of the right eye with a slight dyschromatopsia, but a lack of afferent pupillary defect and normal visual fields. Fundus examination showed the presence of a slightly swollen right optic disc and chorioretinal folds. A diagnosis of presumed anterior ischemic optic neuropathy was made. Symptoms persisted and, five months later, right proptosis was noted. Magnetic resonance imaging revealed a diffuse thickening of the parieto-temporal bone and the greater wing of the sphenoid bone on the right side. Radiological differential diagnosis included fibrous dysplasia and metastasis.

Bone biopsy revealed a grade I intraosseous meningioma. Conservative management was chosen because the lesion was too extensive to be resected and radiotherapy is usually not efficient on grade I meningiomas.

Intraosseous meningiomas are benign tumors which are due to meningeal cells entrapment during vaginal delivery. It is a rare tumor of slow progression. Therapy usually consists of resection and cranioplasty and/or radiotherapy. In the present case, decompression of the optic canal remains feasible in case of further visual loss 9).

A 71-year-old woman with a long history of slowly progressive proptosis was found to have an intraosseous meningioma of the right sphenoid bone. Radiologically, the lesion resembled fibrous dysplasia. The key to the diagnosis is irregularity of the inner table of the skull. The histologic appearance is characteristic. Intraosseous meningioma is one part of the spectrum of diseases known as primary extraneuraxial meningioma. In this paper we discuss the theories of cellular origin as well as the radiologic differential diagnosis 10)


Kirollos RW. Hyperostosing sphenoid wing meningiomas. Handb Clin Neurol. 2020;170:45-63. doi: 10.1016/B978-0-12-822198-3.00027-6. PMID: 32586508.

Van Tassel P, Lee YY, Ayala A, Carrasco CH, Klima T. Case report 680. Intraosseous meningioma of the sphenoid bone. Skeletal Radiol. 1991;20(5):383-6. doi: 10.1007/BF01267669. PMID: 1896882.

Maschke S, Martínez-Moreno M, Micko A, Millesi M, Minchev G, Mallouhi A, Knosp E, Wolfsberger S. Challenging the osseous component of sphenoorbital meningiomas. Acta Neurochir (Wien). 2019 Nov;161(11):2241-2251. doi: 10.1007/s00701-019-04015-y. Epub 2019 Aug 1. PMID: 31368053; PMCID: PMC6820812.

Kim NR, Yie GT. Intraoperative frozen cytology of intraosseous cystic meningioma in the sphenoid bone. J Pathol Transl Med. 2020 Nov;54(6):508-512. doi: 10.4132/jptm.2020.05.21. Epub 2020 Jul 1. PMID: 32601263; PMCID: PMC7674761.

Parish JM, Shields M, Jones M, Wait SD, Deshmukh VR. Proptosis, Orbital Pain, and Long-Standing Monocular Vision Loss Resolved by Surgical Resection of Intraosseous Spheno-Orbital Meningioma: A Case Report and Literature Review. J Neurol Surg Rep. 2020 Jan;81(1):e28-e32. doi: 10.1055/s-0040-1708845. Epub 2020 Mar 31. PMID: 32257766; PMCID: PMC7108951.

Williams JV, Parmar JD, Carter LM, Woodhead P, Corns R. Use of an acrylic jig to aid orbital reconstruction after resection of a sphenoid intraosseous meningioma: a technical note. Br J Oral Maxillofac Surg. 2019 Dec;57(10):1156-1157. doi: 10.1016/j.bjoms.2019.08.026. Epub 2019 Oct 6. PMID: 31594717.

Hussaini SM, Dziurzynski K, Fratkin JD, Jordan JR, Hussain SA, Khan M. Intraosseous meningioma of the sphenoid bone. Radiol Case Rep. 2015 Nov 6;5(1):357. doi: 10.2484/rcr.v5i1.357. PMID: 27307848; PMCID: PMC4898218.

Henchoz L, Borruat FX. Intraosseous meningioma: a rare cause of chronic optic neuropathy and exophthalmos. Klin Monbl Augenheilkd. 2004 May;221(5):414-7. doi: 10.1055/s-2004-812812. PMID: 15162295.

Daffner RH, Yakulis R, Maroon JC. Intraosseous meningioma. Skeletal Radiol. 1998 Feb;27(2):108-11. doi: 10.1007/s002560050347. PMID: 9526778.



Meningiomas are leptomeningeal neoplasms thought to originate from arachnoid membranes that form the cranial and spinal meninge1).

Written with Louise Eisenhardt and published in 1938Meningiomas is a monograph of incredible description and detail. The meticulous categorization of meningiomas, their presentation, clinical outcome, and surgical therapies are even further supplemented by Cushing‘s personal commentary, questions, and recollections. Cushing’s genius was evident in his ability not only to make insightful clinical observations, but also to synthesize these ideas within the neurosurgical context of his era. As he says in Meningiomas, “Thus the pathological curiosity of one day becomes in its proper time a commonplace… most of which are one and the same disorder–had, for their interpretation, to await the advent of the Neurosurgeon 2).


Meningioma epidemiology.


see Meningioma classification.

Cell lines

see Meningioma cell lines.

Meningioma immune response

Meningioma immune response


see Meningioma etiology.


see Meningioma Pathogenesis.

Clinical features

Meningioma clinical features

Asymptomatic meningiomas

see Asymptomatic meningioma


see Meningioma Diagnosis.

Differential diagnosis

see Meningioma differential diagnosis.


see Meningioma treatment.


see Meningioma outcome.

Meningioma metastases

see Meningioma metastases


see Meningioma recurrence.

Simpson grading system

see Simpson grading system.

The Top 100 Most Cited Articles

In November 2016, Almutairi et al. performed a title-specific search of the Scopus database using “Meningioma” as the search query term without publication date restrictions. The top 100 most cited articles were obtained and reviewed.

The top 100 most cited articles received a mean 198 citations per paper. Publication dates ranged from 1953 to 2013; most articles were published between 1994 and 2003, with 50 articles published during that period. NEUROSURGERY published the greatest number of top cited articles (22 of 100). The most frequent study categories were laboratorial studies (31 of 100) and natural history studies (28 of 100). Non-operative management studies were twice as common as operative management studies in the top cited articles. Neurosurgery as a specialty contributed to 50% of the top 100 list. The most contributing institute was the Mayo Clinic (11%); the majority of the top cited articles originated in the United States (53%).

They identified the top 100 most-cited articles on meningioma that may be considered significant and impactful works, as well as the most noteworthy. Additionally, they recognized the historical development and advances in meningioma research, and the important contributions of various authors, specialty fields, and countries. A large proportion of the most cited articles were written by authors other than neurosurgeons, and many of these articles were published in non-neurosurgery journals 3).

Case series

Meningioma case series.

1) Smith MJ, O’Sullivan J, Bhaskar SS, Hadfield KD, Poke G, Caird J, Sharif S, Eccles D, Fitzpatrick D, Rawluk D, du Plessis D, Newman WG, Evans DG. Loss-of-function mutations in SMARCE1 cause an inherited disorder of multiple spinal meningiomas. Nat Genet. 2013 Mar;45(3):295-8. doi: 10.1038/ng.2552. Epub 2013 Feb 3. PubMed PMID: 23377182.2) Shrivastava RK, Segal S, Camins MB, Sen C, Post KD. Harvey Cushing’s Meningiomas text and the historical origin of resectability criteria for the anterior one third of the superior sagittal sinus. J Neurosurg. 2003 Oct;99(4):787-91. PubMed PMID: 14567620.3) Almutairi O, Albakr A, Al-Habib A, Ajlan A. The Top 100 Most Cited Articles on Meningioma. World Neurosurg. 2017 Aug 10. pii: S1878-8750(17)31318-9. doi: 10.1016/j.wneu.2017.08.021. [Epub ahead of print] Review. PubMed PMID: 28804043.

World Health Organization grade 3 meningioma

World Health Organization grade 3 meningioma

Papillary meningioma

Rhabdoid meningioma

Anaplastic meningioma

Mast cells (MCs) were present in as many as 90 % of all high grade meningiomas mainly found in the perivascular areas of the tumor. A correlation between peritumoral edema and MCs was found.

Accumulation of MCs in meningiomas could contribute to the aggressiveness of tumors and to brain inflammation that may be involved in the pathogenesis of additional disorders 1).

From the available data, surgical resection followed by RT and salvage therapy can lead to extended survival 2).

For a systematic review, studies analyzing the effectiveness of adjuvant radiotherapy and stereotactic radiosurgery in grade 3 (gr. 3) meningioma were reviewed. Thirty studies met the inclusion criteria for qualitative synthesis, and 6 studies were assessed in quantitative analysis. In quantitative analysis, the weighted average of hazard ratios for adjuvant RT in univariate analyses of overall survival (OS) was 0.55 (CI: 0.41; 0.69). The median 5-year OS after adjuvant RT in gr. 3 meningiomas were 56.3%, and the median OS ranged from 24 to 80 months for patients treated with adjuvant RT versus 13 to 41.2 months in patients not treated. For stereotactic radiosurgery, the 3-year progression-free survival was 0% in one study and 57% in another. The 2-year OS ranged from 25 to 75% in 2 studies. The quality of evidence was rated as “very low” in 14 studies analyzed, and considerable allocation bias was detected. Treatment toxicity was reported in 47% of the studies. The severity, according to the CTCAE, ranged from grades I-V and 5.3 to 100% of patients experiencing complications. Adjuvant RT is usually considered the standard of care for WHO grade 3 meningiomas, although supporting evidence was of low quality. Better evidence from registries and prospective trials can improve the evidence base for adjuvant fractionated radiotherapy in malignant meningioma3).


Polyzoidis S, Koletsa T, Panagiotidou S, Ashkan K, Theoharides TC. Mast cells in meningiomas and brain inflammation. J Neuroinflammation. 2015 Sep 17;12(1):170. doi: 10.1186/s12974-015-0388-3. PubMed PMID: 26377554.

Rosenberg LA, Prayson RA, Lee J, Reddy C, Chao ST, Barnett GH, Vogelbaum MA, Suh JH. Long-term experience with World Health Organization grade III (malignant) meningiomas at a single institution. Int J Radiat Oncol Biol Phys. 2009 Jun 1;74(2):427-32. doi: 10.1016/j.ijrobp.2008.08.018. PMID: 19427553.

Bergner A, Maier AD, Mirian C, Mathiesen TI. Adjuvant radiotherapy and stereotactic radiosurgery in grade 3 meningiomas – a systematic review and meta-analysis. Neurosurg Rev. 2022 May 11. doi: 10.1007/s10143-022-01773-9. Epub ahead of print. PMID: 35543810.