Asian Journal of Neurosurgery

CASE REPORT
Year
: 2019  |  Volume : 14  |  Issue : 3  |  Page : 938--942

Collision occurrence of meningioma and astrocytoma: A case report and literature review


Van Tri Truong1, Duc Duy Tri Tran2, Cong Thuan Dang3,  
1 Department of Neurosurgery, Hue University Hospital, Hue University of Medicine and Pharmacy, Hue University, Hue City, Vietnam; Division of Orthopedics, Central Hospital of University of Montreal, University of Montreal, Montreal, Canada
2 Department of Neurosurgery, Hue University Hospital, Hue University of Medicine and Pharmacy, Hue University, Hue City; Department of Neurosurgery, Xuyen A Hospital, Ho Chi Minh City, Vietnam
3 Department of Pathology, Hue University Hospital, Hue University of Medicine and Pharmacy, Hue University, Hue City, Vietnam

Correspondence Address:
Van Tri Truong
Department of Neurosurgery, Hue University Hospital, Hue University of Medicine and Pharmacy, Hue University, 41, Nguyen Hue Street, Hue City; Division of Orthopedics, Centre Hospitalier de l'Université de Montréal, University of Montreal, 1051, Sanguinet Street, Montreal, QC H2X 3E4, Canada

Abstract

A case of collision tumors occurring between two distinct primary brain tumors is reported. A 61-year-old female without history of radiotherapy or phakomatosis presented with progressive ly increasing headache and left hemiparesis. Investigation revealed a meningioma and a Grade II astrocytoma in the right frontal lobe. Simultaneous development of a meningioma and a low-grade glioma at adjacent sites is extremely rare. This is the third case reported in the literature. Some hypotheses are proposed to explain this phenomenon but most likely represent a coincidental event.



How to cite this article:
Truong VT, Tran DD, Dang CT. Collision occurrence of meningioma and astrocytoma: A case report and literature review.Asian J Neurosurg 2019;14:938-942


How to cite this URL:
Truong VT, Tran DD, Dang CT. Collision occurrence of meningioma and astrocytoma: A case report and literature review. Asian J Neurosurg [serial online] 2019 [cited 2020 Dec 3 ];14:938-942
Available from: https://www.asianjns.org/text.asp?2019/14/3/938/263984


Full Text



 Introduction



Glioma and meningioma are the two most common primary intracranial tumors.[1] However, the simultaneous development of these tumors at adjacent sites in the same patient without a history of radiotherapy or phakomatosis is extremely rare.[2],[3],[4],[5],[6] The exact pathogenesis of this condition is still in controversies. Here, we present a case of collision tumors composed of a low-grade glioma and a meningioma. We discuss the challenges in obtaining an accurate preoperative diagnosis for these tumors, as well as review prior reported cases.

 Case Report



A 61-year-old female presented with 3 months of progressive headache. Neurological examination at hospitalization revealed mild left hemiparesis.

Magnetic resonance imaging of the brain showed two lesions in the right frontal lobe. One lesion was isointense on T1-weighted images and T2-weighted images and enhanced intensely after gadolinium injection. The second lesion was composed of nonenhancing cysts with a significant amount of surrounding edema [Figure 1].{Figure 1}

Intraoperatively, the enhancing lesion was found to be an extra-axial tumor attaching to the dura mater and the other lesion was observed to be an intra-axial tumor. Both the lesions were completely removed macroscopically. The patient improved clinically after the surgery and was discharged without any appreciable neurologic deficit. Histological examination of the extra-axial tumor revealed a fibroblastic meningioma [Figure 2] and the intra-axial lesion was diagnosed as a Grade II astrocytoma [Figure 3]. There was no histological invasion between the two tumors.{Figure 2}{Figure 3}

 Discussion



Since the first report in 1938, about 67 cases of simultaneous occurrence of meningioma and glioma have been reported in the literature, but the collision of two different histologic tumors in patients without prior radiation therapy or phakomatosis is extremely rare.[2],[3],[4],[5],[7] The first case of meningioma and glioma collision without a history of radiotherapy or phakomatosis was reported in 1976 by Strong et al.[8] We reviewed the literature and found 18 cases reported since then, including 10 males and 8 females with age ranging 12–87 years. Most of the managements for these cases were one-stage tumor removal. Histologically, most of them had high-grade gliomas. The present case is the third case of meningioma and low-grade glioma collision reported. Details of these cases are described in [Table 1]. Our understanding of intracranial meningioma and astrocytoma collision remains limited, but several hypotheses have been proposed.{Table 1}

Some authors suggest that the initial tumor can act as an oncogenesis agent for the development of the other tumors.[4],[7],[21],[22] The tumor growth in these cases follows the autocrinous mechanism, due to the production of growth factor and receptors for these factors. Platelet-derived growth factor (PDGF) is a likely substance.[21] It is found that three subunits of PDGF, the PDGF-AA, PDGF-BB, and PDGF-AB, are secreted by astrocytomas.[23],[24] PDGF-β-R receptor is present in meningioma, and PDGF-BB acting on these receptors is shown to stimulate meningioma cell division.[21] As a result, astrocytoma may stimulate adjacent meningioma formation in arachnoid cells by production of a common growth factor. However, this hypothesis fails to elucidate why adjacent meningioma formation does not happen in most cases of the astrocytomas.

Other authors hypothesize that meningiomas may irritate astroglial cells surrounding it, causing local cellular proliferation and eventually tumor formation.[5],[19] In fact, this hypothesis is supported by a case of collision convexity meningioma and glioma reported by Vaquero et al. in 1990. In this case, histologically, a transient area between the meningioma and the astrocytoma was observed and two kinds of tumor cells were mixed in some areas.[19] In 2004, Drlicek et al. reported one case with a meningothelial meningioma WHO-Grade I located within the peripheral glioblastoma WHO-Grade IV, also supporting the above hypothesis.[16] Similarly, Prayson reported a meningioma in the sagittal sinus in the frontal lobe and a peripheral glioma invading each other pathologically.[18] However, collision tumors without histological invasion have also been reported. For example, in 2007, Nestler et al. reported a case of collision of a meningioma and a glioma, but the histological examination showed no invasion of the tissue between them.[14] Tugcu also reported a case of collision of a meningioma and a glioblastoma multiforme at the left parietal cortex without parenchymal invasion.[5] We also did not find any histological invasion between the two tumors in our case. This transformation hypothesis fails to explain why adjacent glial formation does not happen in most of the intracranial meningiomas. It also fails to explain the simultaneous occurrence of two distinct tumors in different brain areas.

Genetic factors are also suggested to play a role in the development of collision meningioma and glioma. In fact, a meningioma-associated tumor suppressor gene which is commonly inactivated in clinically aggressive meningiomas was found on the long arm of chromosome 14, identified as the N-myc downstream-regulated gene 2 (NDRG2).[25] A study in 2005 found that this gene was suppressed in glioblastoma tissue but expressed in normal brain tissue.[26] Thus, the suppression of NDRG2 gene may lead to the formation of meningioma and glioblastoma simultaneously. In 2015, Nestler et al. reported three cases of simultaneous of meningioma and glioblastoma, but specimens from two cases were examined for chromosomal aberration by conventional karyotyping as well as comparative genomic hybridization, and no common genetic aberration in tumor cells with a different histology was found.[14]

Therefore, we are in favor of the hypothesis that the association of collision tumors in reported cases may be a coincidental event.[5],[6],[14],[27]

To have an accurate preoperative diagnosis for these tumors is really difficult. The area with hyperintensity T2-weighted images surrounding a meningioma usually represents peritumoral edema and should be distinguished from low-grade glioma in collision tumors involving meningioma and glioma.

It is important to have an appropriate surgical strategy for these patients. Most authors agree that removal of both tumors in one stage usually yields good results.[4],[28] Some authors suggest that the removal of meningioma should be done first to avoid postoperative brain swelling after glioma resection.[4],[5] However, brain swelling after meningioma resection is not uncommon and can worsen the neurological status. Another approach is to remove the symptomatic tumor first.[2],[3] In our case, we removed both the lesions in one section because both tumors were located in the noneloquent area, and the approach was not difficult.

 Conclusion



The occurrence of collision tumors in patients without a history of radiotherapy or phakomatosis is rare. We report the third case of meningioma and low-grade astrocytoma collision in the frontal lobe. No clear explanation was found, and it is most likely a coincidence. Careful preoperative imaging evaluation is very important in these cases so that we may have a correct diagnosis and surgical strategy. In planning for surgery for collision tumors, one-stage resection is likely the best management.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Acknowledgement

The authors would like to thank you very much Dr. Albert Tu for his contribution in sharing his comments and English correction for this manuscript.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

1Annegers JF, Schoenberg BS, Okazaki H, Kurland LT. Epidemiologic study of primary intracranial neoplasms. Arch Neurol 1981;38:217-9.
2Davis GA, Fabinyi GC, Kalnins RM, Brazenor GA, Rogers MA. Concurrent adjacent meningioma and astrocytoma: A report of three cases and review of the literature. Neurosurgery 1995;36:599-604.
3Lee EJ, Chang CH, Wang LC, Hung YC, Chen HH. Two primary brain tumors, meningioma and glioblastoma multiforme, in opposite hemispheres of the same patient. J Clin Neurosci 2002;9:589-91.
4Spallone A, Santoro A, Palatinsky E, Giunta F. Intracranial meningiomas associated with glial tumours: A review based on 54 selected literature cases from the literature and 3 additional personal cases. Acta Neurochir (Wien) 1991;110:133-9.
5Tugcu B, Kepoglu U, Gunal M, Gunaldi O, Karakaya B, Demirgil BT, et al. Two distinct primary brain tumors, in same region of the same patient: A case report. J Neurooncol 2006;79:219-20.
6Zhang D, Yu J, Guo Y, Zhao S, Shao G, Huang H, et al. An intraventricular meningioma and recurrent astrocytoma collision tumor: A case report and literature review. World J Surg Oncol 2015;13:37.
7Zhang Z, Yang Y, Zhang K, Zhuang J, Shao F, Liu H, et al. Collision tumor of glioblastoma and meningioma: Case report and literature review. World Neurosurg 2018;117:137-41.
8Strong AJ, Symon L, MacGregor BJ, O'Neill BP. Coincidental meningioma and glioma. Report of two cases. J Neurosurg 1976;45:455-8.
9Ruiz J, Capilla E, Díaz JF, Ruiz JA, Andrade J, Hernández T, et al. Secretory meningioma with KLF4 K409Q mutation in collision with glioma. Clin Neuropathol 2015;34:322-9.
10Khalatbari M, Borghei-Razavi H, Shayanfar N, Behzadi AH, Sepehrnia A. Collision tumor of meningioma and malignant astrocytoma. Pediatr Neurosurg 2010;46:357-61.
11Chen G, Gao X, Liao Y, Xu B. A glioblastoma adjacent to a meningioma. Br J Neurosurg 2010;24:718-9.
12Suzuki K, Momota H, Tonooka A, Noguchi H, Yamamoto K, Wanibuchi M, et al. Glioblastoma simultaneously present with adjacent meningioma: Case report and review of the literature. J Neurooncol 2010;99:147-53.
13Mitsos AP, Konstantinou EA, Fotis TG, Lafazanos SA, Kontogeorgos G, Georgakoulias NV, et al. Sphenoid wing meningioma and glioblastoma multiforme in collision - case report and review of the literature. Neurol Neurochir Pol 2009;43:479-83.
14Nestler U, Schmidinger A, Schulz C, Huegens-Penzel M, Gamerdinger UA, Koehler A, et al. Glioblastoma simultaneously present with meningioma – Report of three cases. Zentralbl Neurochir 2007;68:145-50.
15Maiuri F, Cappabianca P, Iaconetta G, Esposito F, Messina A. Simultaneous presentation of meningiomas with other intracranial tumours. Br J Neurosurg 2005;19:368-75.
16Drlicek M, Aichholzer M, Wurm G, Bodenteich A, Fischer J. Collisiontumour composed of glioblastoma and meningioma-a case report. Pathologe 2004;25:402-5.
17Goyal A, Singh AK, Sinha S, Tatke M, Singh D, Gupta V, et al. Simultaneous occurrence of meningioma and glioma in brain: Report of two cases. J Clin Neurosci 2003;10:252-4.
18Prayson RA, Chowdhary S, Woodhouse S, Hanson M, Nair S. Collision of a syncytial meningioma and malignant astrocytoma. Ann Diagn Pathol 2002;6:44-8.
19Vaquero J, Coca S, Martínez R, Jiménez C. Convexity meningioma and glioblastoma in collision. Surg Neurol 1990;33:139-41.
20Marra A, Ramponi G, Grimaldi G. Simultaneous occurrence of right supratentorial meningioma and glioblastoma multiforme. Case report. Acta Neurochir (Wien) 1977;36:83-91.
21Black PM, Carroll R, Glowacka D, Riley K, Dashner K. Platelet-derived growth factor expression and stimulation in human meningiomas. J Neurosurg 1994;81:388-93.
22Esiri M. Russell and Rubinstein's pathology of tumors of the nervous system. Sixth edition J Neurol Neurosurg Psychiatry 2000;68:538D.
23Hermanson M, Funa K, Hartman M, Claesson-Welsh L, Heldin CH, Westermark B, et al. Platelet-derived growth factor and its receptors in human glioma tissue: Expression of messenger RNA and protein suggests the presence of autocrine and paracrine loops. Cancer Res 1992;52:3213-9.
24Maxwell M, Naber SP, Wolfe HJ, Galanopoulos T, Hedley-Whyte ET, Black PM, et al. Coexpression of platelet-derived growth factor (PDGF) and PDGF-receptor genes by primary human astrocytomas may contribute to their development and maintenance. J Clin Invest 1990;86:131-40.
25Lusis EA, Watson MA, Chicoine MR, Lyman M, Roerig P, Reifenberger G, et al. Integrative genomic analysis identifies NDRG2 as a candidate tumor suppressor gene frequently inactivated in clinically aggressive meningioma. Cancer Res 2005;65:7121-6.
26Deng Y, Yao L, Chau L, Ng SS, Peng Y, Liu X, et al. N-myc downstream-regulated gene 2 (NDRG2) inhibits glioblastoma cell proliferation. Int J Cancer 2003;106:342-7.
27Iyer VR, Sanghvi DA, Shenoy A, Goel A. Three distinct co-existent primary brain tumors in a patient. J Cancer Res Ther 2009;5:293-6.
28Maiuri F, Cappabianca P, Iaconetta G, D'Acunzi G. Meningiomas associated with brain metastases. Zentralbl Neurochir 2002;63:111-5.