Preface

Intracranial tumors represent a vast group of heterogeneous diseases, with complex and often challenging management, requiring specialized interdisciplinary teams in reference centers. Working with these professionals, focused on the most up-to-date behavior possible, is essential to alleviate patients' anxiety and discomfort.

The first successful removal of a brain tumor was described in 1879 by William Macewen. With the arrival of the 20th century, the foundations of modern neurosurgery were established by Cushing and incorporated the surgical microscope in intracranial operations, with House (in 1961 in acoustic tumors) and Kurze (in 1963), and improvements from Yasargil in the following decades. Also in the 1960s, dexamethasone was introduced in the treatment of tumor swelling and became one of the hallmarks for better patient survival.

In the 1970s, computed tomography and magnetic resonance imaging allowed intracranial structures to be visualized directly. Until then, tumors were diagnosed indirectly through invasive and dated examinations. They were delayed diagnoses and, invariably, patients presented with very severe conditions. At the same time, brain irradiation was incorporated in the treatment of malignant or unresectable tumors.

The 1980s and 1990s were decisive in the development of better imaging methods, surgical techniques, and estereotatic navigation for deep lesions. In the late 1990s, Stupp demonstrated the role of temozolamide in the treatment of glioblastomas, one of the most aggressive incurable cancers in humans. Improved monitoring conditions, neuroanesthesia, intensive care, and the increasing incorporation of technology in the service of medicine have made the management of brain tumors somewhat worthy of science fiction films. The current paradigms involve the application of tumor-treating fields, molecular analyses, biological markers, and advanced imaging techniques, all in continuous transformation, and trying to offer definitive solutions for the well-being of patients.

Such knowledge is like a regular polygon gaining more sides with each new discovery, trying to become a perfect "circle," although there are new questions that continuously arise the more we understand each disease. No matter how new divisions and classifications are created for a huge range of tumors, we can always improve the diagnostic methods, the surgery, and the adjuvant treatments.

This book presents specific and important topics about the most frequent primary intracranial tumors, highlighting the relevant contemporary literature and the

**II**

**Chapter 6 87**

**Chapter 7 97**

**Chapter 8 113**

Vestibular Schwannomas: Diagnosis and Surgical Treatment

*by Gustavo Jung and Ricardo Ramina*

The Systemic Treatment of Glioma

Role of Radiotherapy in High Grade Glioma

*by Johnny Camargo*

*by Henrique Balloni*

experience of the services involved. They are fundamental information that, we hope, becomes out of date quickly, given the intensity with which one seeks to make the "polygon of knowledge" a "circle".

> **Erasmo Barros Da Silva Junior** Neurological Institute Of Curitiba, Brazil

#### **Jerônimo Buzetti Milano**

**1**

Section 1

Introduction

Neurological Institute Of Curitiba, Brazil

Section 1 Introduction

**3**

**Chapter 1**

**Abstract**

**1. Introduction**

Treatment

Atypical and Anaplastic

acquired in the experience of our department.

seizures and/or intracranial hypertension.

fluorescence-guided surgery, magnetic resonance imaging

Meningiomas: Diagnosis and

*Erasmo Barros da Silva Jr, Gustavo Simiano Jung,* 

*Joseph Franklin Chenisz da Silva and Ricardo Ramina*

**Keywords:** neurosurgical procedures, brain neoplasms, neuronavigation,

Meningiomas originate from specialized meningothelial cells called arachnoid cap cells and correspond about up to 26% of all intracranial lesions. According to the World Health Organization (WHO), meningiomas are grouped in grade I (benign), grade II (atypical), and grade III (anaplastic) [1, 2]. This classification reflects the risk of recurrence and aggressive growth. Although uncommon, atypical corresponds to 4.7 to 20% of all meningiomas, while anaplastic for 1–2.8% [3, 4]. Symptomatology varies according to intracranial location and may be related to

The standard treatment of grade II and grade III meningiomas involve total/ radical resection, respecting Simpson score, followed by adjuvant therapy with irradiation and, eventually, chemotherapy [5, 6]. Despite the treatment efforts, the evolution of aggressive meningiomas remains unsatisfactory due to the high rates of local recurrence and/or tumor progression [7]. These patients frequently underwent multiple surgical approaches during the course of the disease, increas-

With the continuous improvement of molecular and immunochemistry analysis, the paradigm for treatment of these tumors has been changing. In this chapter, the current management of aggressive/malignant meningiomas focusing on the new

ing the rates of postoperative complications as infection or CSF leakage.

discovers in genetic/molecular and radiotherapy field is discussed.

The aim of this chapter is to describe the usefulness of surgical technologies such as neuronavigation, intraoperative MRI, fluorescence-guided surgery and intraoperative monitoring as a tool do make neurosurgical procedures to brain tumors more safe and effective. The main topics to be explored are: history of the specific technique, indications and contra indications, description of the technique, real case examples, pros and cons. The focus on the discussion besides practical aspects is going to be relevant literature regarding impact of their use in avoidance of complications, improve in survival rates, cost-effectiveness, some tips and tricks

#### **Chapter 1**

## Atypical and Anaplastic Meningiomas: Diagnosis and Treatment

*Erasmo Barros da Silva Jr, Gustavo Simiano Jung, Joseph Franklin Chenisz da Silva and Ricardo Ramina*

#### **Abstract**

The aim of this chapter is to describe the usefulness of surgical technologies such as neuronavigation, intraoperative MRI, fluorescence-guided surgery and intraoperative monitoring as a tool do make neurosurgical procedures to brain tumors more safe and effective. The main topics to be explored are: history of the specific technique, indications and contra indications, description of the technique, real case examples, pros and cons. The focus on the discussion besides practical aspects is going to be relevant literature regarding impact of their use in avoidance of complications, improve in survival rates, cost-effectiveness, some tips and tricks acquired in the experience of our department.

**Keywords:** neurosurgical procedures, brain neoplasms, neuronavigation, fluorescence-guided surgery, magnetic resonance imaging

#### **1. Introduction**

Meningiomas originate from specialized meningothelial cells called arachnoid cap cells and correspond about up to 26% of all intracranial lesions. According to the World Health Organization (WHO), meningiomas are grouped in grade I (benign), grade II (atypical), and grade III (anaplastic) [1, 2]. This classification reflects the risk of recurrence and aggressive growth. Although uncommon, atypical corresponds to 4.7 to 20% of all meningiomas, while anaplastic for 1–2.8% [3, 4]. Symptomatology varies according to intracranial location and may be related to seizures and/or intracranial hypertension.

The standard treatment of grade II and grade III meningiomas involve total/ radical resection, respecting Simpson score, followed by adjuvant therapy with irradiation and, eventually, chemotherapy [5, 6]. Despite the treatment efforts, the evolution of aggressive meningiomas remains unsatisfactory due to the high rates of local recurrence and/or tumor progression [7]. These patients frequently underwent multiple surgical approaches during the course of the disease, increasing the rates of postoperative complications as infection or CSF leakage.

With the continuous improvement of molecular and immunochemistry analysis, the paradigm for treatment of these tumors has been changing. In this chapter, the current management of aggressive/malignant meningiomas focusing on the new discovers in genetic/molecular and radiotherapy field is discussed.

#### **2. Materials and methods**

In our database, we reviewed all meningiomas operated between 2012 and 2017 in our institution to describe the epidemiologic characteristics of atypical and anaplastic subtypes, as well as an illustrative case focusing on the treatment and long-term follow-up. Also, literature was reviewed based on the WHO (2016) classification guided through genetic/molecular findings.

#### **3. Results**

A total of 170 new diagnosed patients with intracranial meningiomas underwent microsurgical resection at the Neurological Institute of Curitiba (INC) between January 2012 and June 2017. A total of 94 (55%) tumors were classified as skull base tumors, 58 (34%) convexity, 10 (5.8%) parasagittal, and 8 (4.7%) falcine lesions.

In our series, 76.4% (130) of patients were female. Only six (3.5%) patients had atypical/anaplastic tumors with mean age of 53 years (**Table 1**). Simpson grade I resection (total tumor removal including resection of the underlying bone and associated dura mater) was achieved in all patients with malignant histology, and radiotherapy was reserved for progression. Only one patient with atypical meningioma received upfront radiotherapy because of high Ki-67 index. Any case of skull base meningioma exhibited progression to malignant subtypes in this series.


#### **Table 1.**

*Malignant meningioma at INC (2012–2017).*

#### **4. Illustrative case**

58-year-old male has sporadic new onset headache, and magnetic resonance imaging (MRI) evidences enhanced parasagittal homogenous mass tumor with surrounding edema (**Figure 1**). Simpson grade I resection (**Figure 2**) was achieved at surgery, and histopathology confirmed atypical meningioma.

Immunohistochemistry of the first sample proved the trend toward malignant progression, with Ki-67 index of 70% in hot spots. Only focal positiveness for progesterone receptor was seen. Because of high Ki-67 index, adjuvant external beam radiotherapy (EBRT) was added to the treatment.

**5**

**Figure 2.**

**Figure 1.**

introduced without response.

*complete resection of parasagittal meningioma.*

progression to anaplastic meningioma was confirmed.

*Atypical and Anaplastic Meningiomas: Diagnosis and Treatment*

*parasagittal meningioma with partial occlusion of superior sagittal sinus.*

After 1 year follow-up, recurrence at posterior border of previous surgical field was seen, and another gross total resection was necessary (**Figure 3**). The tumor expressed the same imaging characteristics of first analysis, with homogeneous contrast enhancement and peritumoral edema. Histopathological analyses confirmed again an atypical histology. At this time, chemotherapy with octreotide was

*Postoperative MRI with post-gadolinium-DTPA axial T1-weighted gradient echo (FSPGR) sequence exhibiting* 

*(A) Post-gadolinium-DTPA axial and coronal. (B) T1-weighted gradient echo (FSPGR) sequence with large* 

After 2 years from the first surgery, another recurrence was seen. At MRI, changes in previous pattern were seen with heterogeneous contrast enhancement and central necrosis (**Figure 4**). After another Simpson grade I tumor removal,

*DOI: http://dx.doi.org/10.5772/intechopen.81210*

*Atypical and Anaplastic Meningiomas: Diagnosis and Treatment DOI: http://dx.doi.org/10.5772/intechopen.81210*

#### **Figure 1.**

*Primary Intracranial Tumors*

**3. Results**

falcine lesions.

in this series.

**4. Illustrative case**

*Malignant meningioma at INC (2012–2017).*

**Table 1.**

**2. Materials and methods**

In our database, we reviewed all meningiomas operated between 2012 and 2017

A total of 170 new diagnosed patients with intracranial meningiomas underwent microsurgical resection at the Neurological Institute of Curitiba (INC) between January 2012 and June 2017. A total of 94 (55%) tumors were classified as skull base tumors, 58 (34%) convexity, 10 (5.8%) parasagittal, and 8 (4.7%)

In our series, 76.4% (130) of patients were female. Only six (3.5%) patients had atypical/anaplastic tumors with mean age of 53 years (**Table 1**). Simpson grade I resection (total tumor removal including resection of the underlying bone and associated dura mater) was achieved in all patients with malignant histology, and radiotherapy was reserved for progression. Only one patient with atypical meningioma received upfront radiotherapy because of high Ki-67 index. Any case of skull base meningioma exhibited progression to malignant subtypes

58-year-old male has sporadic new onset headache, and magnetic resonance imaging (MRI) evidences enhanced parasagittal homogenous mass tumor with surrounding edema (**Figure 1**). Simpson grade I resection (**Figure 2**) was achieved

Immunohistochemistry of the first sample proved the trend toward malignant progression, with Ki-67 index of 70% in hot spots. Only focal positiveness for progesterone receptor was seen. Because of high Ki-67 index, adjuvant external beam

at surgery, and histopathology confirmed atypical meningioma.

radiotherapy (EBRT) was added to the treatment.

in our institution to describe the epidemiologic characteristics of atypical and anaplastic subtypes, as well as an illustrative case focusing on the treatment and long-term follow-up. Also, literature was reviewed based on the WHO (2016) clas-

sification guided through genetic/molecular findings.

**4**

*(A) Post-gadolinium-DTPA axial and coronal. (B) T1-weighted gradient echo (FSPGR) sequence with large parasagittal meningioma with partial occlusion of superior sagittal sinus.*

#### **Figure 2.**

*Postoperative MRI with post-gadolinium-DTPA axial T1-weighted gradient echo (FSPGR) sequence exhibiting complete resection of parasagittal meningioma.*

After 1 year follow-up, recurrence at posterior border of previous surgical field was seen, and another gross total resection was necessary (**Figure 3**). The tumor expressed the same imaging characteristics of first analysis, with homogeneous contrast enhancement and peritumoral edema. Histopathological analyses confirmed again an atypical histology. At this time, chemotherapy with octreotide was introduced without response.

After 2 years from the first surgery, another recurrence was seen. At MRI, changes in previous pattern were seen with heterogeneous contrast enhancement and central necrosis (**Figure 4**). After another Simpson grade I tumor removal, progression to anaplastic meningioma was confirmed.

#### **Figure 3.**

*One-year-follow-up. (A) MRI. Axial post-gadolinium-DTPA T1-weighted gradient echo (FSPGR). (B) Flair sequences evidencing tumor recurrence adjacent to previous resection with the same features of original tumor.*

#### **Figure 4.**

*Axial post-gadolinium-DTPA. (A) T1-weighted gradient echo (FSPGR) showing irregular contrast enhancement and tumoral necrosis. (B) Axial FLAIR magnetic resonance evidencing extensive peritumoral edema with changes in radiological aspect from original tumor.*

In comparative analyses, immunohistochemistry evidenced an increase in Ki-67 index from 70 to 90% of the cells. The epithelial membrane antigen (EMA), focal positive at first analysis, now expressed diffuse negativeness. Reduction in progesterone receptor expression was also documented.

Later, there was tumor progression again in two more occasions in an interval of 8 months. Progressive neurological impairment and seizures due to motor cortex/ eloquent area involvement/gliosis were seemed, and tumor resection with extensive dural removal was performed both times (**Figures 5** and **6**). The patient underwent salvage irradiation, as the last recurrence was far from the original lesion. Two months after adjuvant treatment, the patient evolved with neurological worsening, dying due to clinical complications.

**7**

**5. Discussion**

**Figure 6.**

**Figure 5.**

*multiple sites.*

About 90% of meningiomas are benign grade I tumors. Atypical meningiomas

are uncommon (4.7–20% of all meningiomas), while anaplastic meningiomas

*Axial post-gadolinium-DTPA. (A) T1-weighted gradient echo (FSPGR) showing tumor progression in* 

account for only 1–2.8% of all meningiomas [1–4].

*Intraoperative image showing the skull after multiple craniotomies.*

*Atypical and Anaplastic Meningiomas: Diagnosis and Treatment*

*DOI: http://dx.doi.org/10.5772/intechopen.81210*

*Atypical and Anaplastic Meningiomas: Diagnosis and Treatment DOI: http://dx.doi.org/10.5772/intechopen.81210*

**Figure 5.**

*Primary Intracranial Tumors*

**Figure 3.**

**Figure 4.**

*original tumor.*

**6**

In comparative analyses, immunohistochemistry evidenced an increase in Ki-67 index from 70 to 90% of the cells. The epithelial membrane antigen (EMA), focal positive at first analysis, now expressed diffuse negativeness. Reduction in proges-

*Axial post-gadolinium-DTPA. (A) T1-weighted gradient echo (FSPGR) showing irregular contrast enhancement and tumoral necrosis. (B) Axial FLAIR magnetic resonance evidencing extensive peritumoral* 

*One-year-follow-up. (A) MRI. Axial post-gadolinium-DTPA T1-weighted gradient echo (FSPGR). (B) Flair sequences evidencing tumor recurrence adjacent to previous resection with the same features of* 

Later, there was tumor progression again in two more occasions in an interval of 8 months. Progressive neurological impairment and seizures due to motor cortex/ eloquent area involvement/gliosis were seemed, and tumor resection with extensive dural removal was performed both times (**Figures 5** and **6**). The patient underwent salvage irradiation, as the last recurrence was far from the original lesion. Two months after adjuvant treatment, the patient evolved with neurological worsening,

terone receptor expression was also documented.

*edema with changes in radiological aspect from original tumor.*

dying due to clinical complications.

*Axial post-gadolinium-DTPA. (A) T1-weighted gradient echo (FSPGR) showing tumor progression in multiple sites.*

**Figure 6.** *Intraoperative image showing the skull after multiple craniotomies.*

#### **5. Discussion**

About 90% of meningiomas are benign grade I tumors. Atypical meningiomas are uncommon (4.7–20% of all meningiomas), while anaplastic meningiomas account for only 1–2.8% of all meningiomas [1–4].

#### *Primary Intracranial Tumors*

The WHO (2016) classification included brain invasion to the previous histological characteristic (4–19 mitotic figures and 3 of 5 histologic features): increased cellularity, small cells (tumor clusters with high nuclear/cytoplasmic ratio), prominent nucleoli, and sheeting (loss of whorling or fascicular architecture and spontaneous necrosis) in the diagnosis of atypical meningiomas.

Anaplastic meningiomas are diagnosed with 20 or more mitotic figures and presence of frank sarcomatous or carcinomatous histology [3].

Despite of diagnostics criteria, the exact mechanism through how benign meningiomas progress to malignant subtypes remains unclear. Several molecular and genetic hypotheses have been postulated, but the real significance of these alterations is still speculative [8].

Evidence-based literature suggests that the extent of surgical resection, accordingly to Simpson grade system, is the most important prognostic factor for good outcome among those patients harboring malignant meningioma [9].

In our series those cases, with atypical or anaplastic subtypes at primary surgery, demonstrated better response to Simpson grade I resection and adjuvant radiotherapy than those cases that progressed from grade I subtype. Some genetic alteration related to progression, as previously reported in literature, can probably explain different evolution among tumors expressing the same histology like in these series [8, 10, 11].

Among those with atypical and anaplastic histology, tumor size and female gender have been related to poor outcome and presence of radiological features such as heterogeneous enhancement, peritumoral edema, and cyst formation, and absence of calcification have been implicated with lower median recurrence-free survival [9, 12].

In the illustrative case, the tumor progression was followed by changes in radiological characteristics and immunohistochemical pattern. Possibly, in this case, the first immunohistochemistry analysis evidenced some characteristics of aggressiveness. In this scenario, Czonka et al. have previously published the utility of p53 gene expression and Ki-67 index in predicting meningioma progression [13].

Maximal safe resection with dural margins and bone hyperostosis removal stills the main point in the treatment of meningiomas, possibly reducing rates of progression and/or improving progression-free survival [14].

Radiotherapy is a special topic in the treatment of malignant meningiomas. Increase from 15 to 80% in 5 year progression-free survival was reported when EBRT was added to surgical resection for anaplastic meningioma. No consensus exists for atypical meningiomas, and EBRT has mostly been reserved for recurrence and progression [15, 16].

Due to the possibility of margin inclusion in irradiation field with EBRT, radiosurgery is no longer indicated for malignant meningiomas. However, Lubgan et al. have reported excellent results with stereotactic radiotherapy when used as an adjuvant after gross total resection or as definitive treatment regime [17].

In the illustrative case, the lower progesterone receptor expression and higher Ki-67 index could probably predict the chance of progression and help in earlier adjuvant decision.

Several chemotherapy agents have been used for atypical and anaplastic meningiomas refractory to surgery and radiotherapy. In the largest revision, Kaley et al. found 47 publications using different chemotherapy agents (hydroxyurea, temozolomide, irinotecan, interferon-alpha, mifepristone, octreotide analogues, megestrol acetate, bevacizumab, imatinib, erlotinib, and gefitinib) with an average 6 month progression-free survival of 26%, concluding that the available chemotherapy agents provide poor outcomes for refractory malignant meningiomas [18].

**9**

Brazil

**Author details**

Erasmo Barros da Silva Jr1

Curitiba, Paraná, Brazil

de Curitiba, Curitiba, Paraná, Brazil

Curitiba, Curitiba, Paraná, Brazil

and Ricardo Ramina4

provided the original work is properly cited.

\*Address all correspondence to: erasmo-inc@uol.com.br

*Atypical and Anaplastic Meningiomas: Diagnosis and Treatment*

Atypical and anaplastic meningiomas remain challenging diseases, and no effective treatment is current available. Against literature evidence, we presume that the biological signature of this specific tumor is more important for evolution than previously reported prognostic factor. In this scenario, new studies aiming objective analyses of immunohistochemistry patterns and genetic profile of meningiomas are probably the next step for the comprehension of such complex neurosurgical

*DOI: http://dx.doi.org/10.5772/intechopen.81210*

**6. Conclusion**

pathology.

© 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

\*, Gustavo Simiano Jung2

1 Department of Neurosurgery/Division of Neurooncology, Instituto de Neurologia

2 Department of Neurosurgery/Division of Skull Base, Instituto de Neurologia de

3 Neurosurgery Resident, Instituto de Neurologia de Curitiba, Curitiba, Paraná,

4 Head of Department of Neurosurgery, Instituto de Neurologia de Curitiba,

, Joseph Franklin Chenisz da Silva3

### **6. Conclusion**

*Primary Intracranial Tumors*

alterations is still speculative [8].

[8, 10, 11].

survival [9, 12].

and progression [15, 16].

adjuvant decision.

malignant meningiomas [18].

The WHO (2016) classification included brain invasion to the previous histological characteristic (4–19 mitotic figures and 3 of 5 histologic features): increased cellularity, small cells (tumor clusters with high nuclear/cytoplasmic ratio), prominent nucleoli, and sheeting (loss of whorling or fascicular architecture and sponta-

Anaplastic meningiomas are diagnosed with 20 or more mitotic figures and

Despite of diagnostics criteria, the exact mechanism through how benign meningiomas progress to malignant subtypes remains unclear. Several molecular and genetic hypotheses have been postulated, but the real significance of these

Evidence-based literature suggests that the extent of surgical resection, accordingly to Simpson grade system, is the most important prognostic factor for good

In our series those cases, with atypical or anaplastic subtypes at primary surgery, demonstrated better response to Simpson grade I resection and adjuvant radiotherapy than those cases that progressed from grade I subtype. Some genetic alteration related to progression, as previously reported in literature, can probably explain different evolution among tumors expressing the same histology like in these series

Among those with atypical and anaplastic histology, tumor size and female gender have been related to poor outcome and presence of radiological features such as heterogeneous enhancement, peritumoral edema, and cyst formation, and absence of calcification have been implicated with lower median recurrence-free

In the illustrative case, the tumor progression was followed by changes in radiological characteristics and immunohistochemical pattern. Possibly, in this case, the first immunohistochemistry analysis evidenced some characteristics of aggressiveness. In this scenario, Czonka et al. have previously published the utility of p53 gene

Maximal safe resection with dural margins and bone hyperostosis removal stills the main point in the treatment of meningiomas, possibly reducing rates of progres-

Radiotherapy is a special topic in the treatment of malignant meningiomas. Increase from 15 to 80% in 5 year progression-free survival was reported when EBRT was added to surgical resection for anaplastic meningioma. No consensus exists for atypical meningiomas, and EBRT has mostly been reserved for recurrence

Due to the possibility of margin inclusion in irradiation field with EBRT, radiosurgery is no longer indicated for malignant meningiomas. However, Lubgan et al. have reported excellent results with stereotactic radiotherapy when used as an adjuvant after gross total resection or as definitive treatment regime [17].

In the illustrative case, the lower progesterone receptor expression and higher Ki-67 index could probably predict the chance of progression and help in earlier

Several chemotherapy agents have been used for atypical and anaplastic meningiomas refractory to surgery and radiotherapy. In the largest revision, Kaley et al. found 47 publications using different chemotherapy agents (hydroxyurea, temozolomide, irinotecan, interferon-alpha, mifepristone, octreotide analogues, megestrol acetate, bevacizumab, imatinib, erlotinib, and gefitinib) with an average 6 month progression-free survival of 26%, concluding that the available chemotherapy agents provide poor outcomes for refractory

expression and Ki-67 index in predicting meningioma progression [13].

sion and/or improving progression-free survival [14].

neous necrosis) in the diagnosis of atypical meningiomas.

presence of frank sarcomatous or carcinomatous histology [3].

outcome among those patients harboring malignant meningioma [9].

**8**

Atypical and anaplastic meningiomas remain challenging diseases, and no effective treatment is current available. Against literature evidence, we presume that the biological signature of this specific tumor is more important for evolution than previously reported prognostic factor. In this scenario, new studies aiming objective analyses of immunohistochemistry patterns and genetic profile of meningiomas are probably the next step for the comprehension of such complex neurosurgical pathology.

### **Author details**

Erasmo Barros da Silva Jr1 \*, Gustavo Simiano Jung2 , Joseph Franklin Chenisz da Silva3 and Ricardo Ramina4

1 Department of Neurosurgery/Division of Neurooncology, Instituto de Neurologia de Curitiba, Curitiba, Paraná, Brazil

2 Department of Neurosurgery/Division of Skull Base, Instituto de Neurologia de Curitiba, Curitiba, Paraná, Brazil

3 Neurosurgery Resident, Instituto de Neurologia de Curitiba, Curitiba, Paraná, Brazil

4 Head of Department of Neurosurgery, Instituto de Neurologia de Curitiba, Curitiba, Paraná, Brazil

\*Address all correspondence to: erasmo-inc@uol.com.br

© 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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[3] Komori T, Sasaki H, Yoshida K. Revised WHO classification of tumor of the central nervous system: Summary of the revision and perspective. No Shinkei Geka. 2016;**44**(8):625-635. DOI: 10.11477/mf.1436203347

[4] Komotar RJ, Iorgulescu JB, Raper DM, Holland EC, Beal K, Bilsky MH, et al. The role of radiotherapy following gross-total resection of atypical meningiomas. Journal of Neurosurgery. 2012;**117**(4):679-686. DOI: 10.3171/2012.7.JNS112113

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[9] Nanda A, Bir SC, Konar S, Maiti T, Kalakoti P, Jacobsohn JA, et al. Outcome of resection of WHO grade II meningioma and correlation of pathological and radiological predictive factors of recurrence. Journal of Clinical Neuroscience. 2016;**31**:112-121. DOI: 10.1016/j.jocn.2016.02.021

[10] Bujko M, Machnicki MM, Grecka E, Rusetska N, Matyja E, Kober P, et al. Mutational analysis of recurrent meningioma progressing from atypical to Rhabdoid subtype. World Neurosurgery. 2017;**97**:754.e1-754.e6. DOI: 10.1016/j.wneu.2016.10.047

[11] Yuzawa S, Nishihara H, Tanaka S. Genetic landscape of Meningiomas. Brain Tumor Pathology. 2016;**33**(4):237-247

[12] Jääskeläinen J, Haltia M, Servo A. Atypical and anaplastic meningiomas: Radiology, surgery, radiotherapy, and outcome. Surgical Neurology. 1986;**25**(3):233-242

[13] Csonka T, Murnyák B, Szepesi R, Bencze J, Bognár L, Klekner A, et al. Assessment of candidate immunohistochemical prognostic markers of meningioma recurrence. Folia Neuropathologica. 2016;**54**(2):114-126

[14] Aizer A, Bi W, Kandola M, Lee E, Nayak L, Rinne M, et al. Extent of resection and overall survival for patients with atypical and malignant meningioma. Cancer. 2015;**121**(24):4376-4381

[15] Dziuk TW, Woo S, Butler EB, Thornby J, Grossman R, Dennis WS, et al. Malignant meningioma: An

**11**

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indication for initial aggressive surgery and adjuvant radiotherapy. Journal of Neuro-Oncology. 1998;**37**(2):177-188

[16] Jung GS, Ramina R, da Silva EB Jr, Neto MC. Diagnosis and predictors of treatment outcomes in Meningiomas with atypical or anaplastic histology. Jornal Brasileiro de Neurocirurgia.

[17] Lubgan D, Rutzner S, Lambrecht U, Rössler K, Buchfelder M, Eyüpoglu I, et al. Stereotactic radiotherapy as primary definitive or postoperative treatment of intracranial meningioma of who grade II and III leads to better disease control than stereotactic radiotherapy of recurrent meningioma.

Journal of Neuro-Oncology. 2017;**134**:407-416. DOI: 10.1007/

[18] Kaley T, Barani I, Chamberlain M, McDermott M, Panageas K, Raizer J, et al. Historical benchmarks for medical therapy trials in surgery and radiation refractory meningioma: A RANO review. Neuro-Oncology. 2014;**16**(6):829-840. DOI: 10.1093/

s11060-017-2540-7

neuonc/not330

2016;**27**(2):100-104

*Atypical and Anaplastic Meningiomas: Diagnosis and Treatment DOI: http://dx.doi.org/10.5772/intechopen.81210*

indication for initial aggressive surgery and adjuvant radiotherapy. Journal of Neuro-Oncology. 1998;**37**(2):177-188

[16] Jung GS, Ramina R, da Silva EB Jr, Neto MC. Diagnosis and predictors of treatment outcomes in Meningiomas with atypical or anaplastic histology. Jornal Brasileiro de Neurocirurgia. 2016;**27**(2):100-104

[17] Lubgan D, Rutzner S, Lambrecht U, Rössler K, Buchfelder M, Eyüpoglu I, et al. Stereotactic radiotherapy as primary definitive or postoperative treatment of intracranial meningioma of who grade II and III leads to better disease control than stereotactic radiotherapy of recurrent meningioma. Journal of Neuro-Oncology. 2017;**134**:407-416. DOI: 10.1007/ s11060-017-2540-7

[18] Kaley T, Barani I, Chamberlain M, McDermott M, Panageas K, Raizer J, et al. Historical benchmarks for medical therapy trials in surgery and radiation refractory meningioma: A RANO review. Neuro-Oncology. 2014;**16**(6):829-840. DOI: 10.1093/ neuonc/not330

**10**

*Primary Intracranial Tumors*

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**13**

Section 2

Diagnosis and Treatment

Modalities

### Section 2
