Gliomas are tumors that originate from glial cells in the brain and are the most common primary intracranial tumors. The 2021 edition of the WHO Classification of Tumors of the Central Nervous System classifies gliomas into grades 1 to 4, with grades 1 and 2 being low-grade gliomas and grades 3 and 4 being high-grade gliomas 1. This guideline focuses on the management of adult high- and low-grade gliomas of astrocytic, oligodendrocytic, and ventricular meningeal cell origin 2, 3.

The annual incidence of glioma in China is 5-8 per 100,000, and the 5-year mortality rate is second only to pancreatic cancer and lung cancer among systemic tumors. The pathogenesis of glioma is unknown, but two risk factors have been identified: exposure to high doses of ionizing radiation and genetic mutations with high epistasis associated with rare syndromes. In addition, carcinogenic factors such as nitrite foods and viral or bacterial infections may also be involved in the development of gliomas.

The clinical manifestations of glioma include increased intracranial pressure, neurological and cognitive deficits, and seizures. At present, clinical diagnosis mainly relies on CT and MRI, diffusion weighted imaging (DWI), diffusion tensor imaging (DTI), perfusion weighted imaging (PWI), magnetic resonance spectroscopy (MRI), and magnetic resonance imaging (MRI). PWI, magnetic resonance spectroscopy (MRS), functional magnetic resonance imaging (FMRI)

(functional magnetic resonance imaging, fMRI), ortho

electron emission tomography (PET) The use of positron emission tomography (PET) is important for the differential diagnosis of glioma and the evaluation of treatment effects.

Diagnosis of glioma requires histopathological and molecular pathological integration of the specimens obtained through tumor resection or biopsy to determine the pathological grade and molecular subtype. The histopathology and molecular pathology are integrated to determine the pathological grade and molecular subtype. Molecular markers are important for the individualized treatment and clinical prognosis of glioma. The treatment of glioma is based on surgical resection, combined with radiotherapy and chemotherapy. Surgery can relieve clinical symptoms, prolong survival, and obtain sufficient tumor specimens for definitive pathological diagnosis and molecular genetic testing. The principle of surgical treatment is to remove the tumor to the maximum extent safely, and new technologies such as conventional neuronavigation, functional neuronavigation, intraoperative neurophysiological monitoring and intraoperative MRI real-time imaging can help to achieve the maximum extent safely. Radiotherapy can kill or suppress tumor cells and prolong patient survival, and conventional fractionated external irradiation is the standard of care for glioma radiation therapy. Postoperative radiotherapy combined with temozolomide synchronized with adjuvant temozolomide chemotherapy for glioblastoma (GBM) has become the standard of care for newly diagnosed GBM in adults.

Treatment of glioblastoma requires a multidisciplinary approach including neurosurgery, neuroimaging, radiation therapy, neuro-oncology, pathology, and neurorehabilitation.

Treatment of glioma requires multidisciplinary collaboration between neurosurgery, neuroimaging

(multi-disciplinary team, MDT), following the principles of evidence-based medicine, individualized and comprehensive treatment, optimization and standardization of treatment protocols. In order to maximize the therapeutic benefit, maximize the progression-free survival time and overall survival time, and improve the quality of survival, the MDT aims to provide patients with the most optimal and comprehensive treatment. In order to achieve optimal comprehensive treatment, physicians need to follow patients closely and manage them throughout the entire process, with regular imaging reviews.

Physicians need to closely follow and manage patients throughout the course of their treatment, taking into account their daily life, social and family activities, nutritional support, pain management, rehabilitation and psychological management.

These are the most important issues in the world.

Routine neuroimaging currently consists of CT and MRI, which provide relatively clear and precise views of brain anatomy and morphological features of brain tumor lesions. These two imaging methods can show the anatomical and morphological characteristics of brain tumors, such as location, size, peripheral edema status, tissue uniformity in the lesion area, occupancy effect, degree of blood-brain barrier disruption, and other combined signs caused by the lesion. MRI is superior to CT in terms of image information; CT mainly shows the density difference between glioma lesions and normal brain tissue, characteristic density features such as calcification, hemorrhage and cystic changes, the location of lesion involvement, edema status and occupancy effect, etc. Conventional MRI mainly shows the difference in signal intensity and occupancy effect of glioma hemorrhage, necrosis and edema tissue, and also shows the extent of lesion invasion. The conventional MRI mainly shows the difference in signal intensity and occupational effect of glioma hemorrhage, necrosis, edema, etc., and can show the extent of lesion invasion. Multimodal MRI can not only reflect the morphological characteristics of glioma, but also the functional and metabolic status of tumor tissue. Conventional MRI scans, which mainly acquire T1-weighted images, T2-weighted images, liquid

Fluid attenuated inversion recovery (FLAIR) sequence imaging and MR contrast enhancement scanning. The glioma is poorly defined and presents as a glioma. Gliomas are poorly defined and exhibit long T1 and T2 signal shadows, which can be heterogeneous, with varying degrees of peripheral edema. The magnitude of the surrounding edema varies. Enhancement scans vary depending on the degree of tumor damage to the blood-brain barrier. Gliomas can occur in all parts of the brain. The MRI of low-grade gliomas shows long T1 and T2 signals with unclear borders, mild peripheral edema, and mild localized occupying signs, which can be caused by adjacent ventricles.

Degree of compression, insignificant midline shift, largely normal brain pool, and few signs of hemorrhage, necrosis, and cystic degeneration in the lesion area. The enhancement scan shows that the lesion rarely shows mild abnormal enhancement. The MRI signal of high-grade glioma is clearly heterogeneous, with mixed T1 and T2 signals and peripheral finger-like edema; the occupancy signs are obvious, with the adjacent ventricles distorted by compression, the midline structures displaced, and the cerebral sulci and brain pools compressed; the enhancement scan shows obvious wreath-like and nodular abnormal enhancement.

The PET imaging characteristics of gliomas vary by grade. The widely used tracer is fluorine-18-fluorodeoxyglucose (18F- fluorodeoxyglucose,18F-FDG) and carbon-11 methionine (11C- methionine,11C-MET). The metabolic activity of low-grade gliomas is generally lower than that of normal gray matter, and that of high-grade gliomas can be close to or higher than that of normal gray matter, but the metabolic activity of 18F There is a large overlap in FDG metabolic activity (level 2 evidence)4. Amino acid tumor imaging has good lesion-background contrast and is better than 18F-FDG for grading gliomas, but there is still some overlap.

When a biopsy is proposed for a clinical diagnosis of suspected glioma, PET can be used to identify the areas of highest metabolic activity in the lesion. 18F-FET and 11C-MET has a higher signal-to-noise ratio and lesion contrast than 18F-FDG (level 2 evidence)F-FET has a higher signal-to-noise ratio and lesion contrast than C-MET. span style=”font-size:8pt”>5.PET combined with MRI is more accurate than MRI alone in defining the target area for radiotherapy (level 1 evidence)6. >6. Compared to conventional MRI techniques, amino acid PET can improve the accuracy of outlining tumor biologic volume, detecting potentially tumor cell-infiltrated/invaded brain tissue (which can be found without abnormalities on conventional MRI images), and incorporating it into the patient’s radiotherapy target area (level 2 evidence)7, 8. /span>. 18F-FDG PET due to tumor/cortex

Low contrast and therefore not suitable for adjuvant targeting of radiotherapy (level 2 evidence)9. Neurosurgery clinicians have clear requirements for neuroimaging diagnosis: first

First, localization is required to determine the size and extent of the tumor, its proximity to important surrounding structures (including important arteries, cortical veins, cortical functional areas, and nerve fiber bundles), and morphological features. This is important for the formulation of the surgical plan for glioma; secondly, the diagnostic requirements of the functional status of neuroimaging, such as tumor growth and metabolism, blood supply status and the degree of tumor invasion to the surrounding brain tissues, which is crucial for the comprehensive postoperative efficacy assessment of patients. In addition to conventional MRI sequences such as basal T1, T2, and enhanced T1, multimodal MRI sequences such as DWI, PWI, and MRS can reflect not only the morphological characteristics of glioma, but also the functional and metabolic status of tumor tissues. The elevated choline (Cho) and Cho/N-acetyl-aspartate (NAA) ratios in MRS are positively correlated with tumor grade. fMRI sequences such as DTI and blood oxygenation level dependent (BOLD) can clarify the relationship between tumor and important functional cortical and metabolic areas. The relationship between the tumor and important functional cortical and subcortical structures can provide evidence to support the protection of brain function during surgical resection. Multimodal MRI is important for differential diagnosis of glioma, determination of surgical boundaries, prognosis, monitoring of treatment outcome, and clarification of the presence or absence of recurrence, and is an important complement to morphological imaging diagnosis.

Table 1 Diagnostic imaging points for glioma

Tumor type Characteristic imaging presentation

Low-grade glioma Mainly diffuse astrocytic glioma

3 types of glioma: oligodendroglioma, oligodendroglioma, and oligodendroglioma. Special types also include PXA, third ventricular chordoma-like glioma, and hairy cell astrocytoma.

The MRI signal of diffuse astrocytoma is relatively homogeneous, with long T1, long T2, and FLAIR high signal, mostly without enhancement; oligodendroglioma shows the same pattern as diffuse astrocytoma. PXA is mostly found in the temporal lobe, with superficial location, cystic lesions and wall nodules. Enhanced scans show enhancement of the wall nodules and adjacent meninges. Chordoma-like glioma of the third ventricle is located in the third ventricle. The hairy cell astrocytoma is predominantly solid and commonly found in the suprasellar and cerebellar hemispheres.

Mesenchymal glioma (grade 3)

Majorly including mesenchymal astrocytoma and mesenchymal oligodendroglioma.

When MRI/CT appears to resemble astrocytoma or oligodendroglioma with enhancement, it suggests a high likelihood of mesenchymal glioma.

Grade 4 glioma Glioblastoma tumor; diffuse midline glioma.

Ventricular meningeal tumors Mainly grade 2 and 3 ventricular meningeal tumors. Special types: mucinous papillary ventricular meningioma is grade 1.

Glioblastoma is characterized by irregularly shaped peripheral enhancement and massive central necrosis, with edema visible outside the enhancement. Diffuse midline gliomas often occur in midline structures such as the thalamus and brainstem, and MRI shows long T1 and long T2 signals, with varying degrees of enhancement on enhancement scans.

Ventricular canal tumors are well-defined, mostly located in the ventricles, with mixed signals, and hemorrhage, necrosis, cystic changes, and calcifications can coexist, and tumor enhancement is often evident. Mucinous papillary ventricular tumors are more likely to be found in the spinal cone and cauda equina.

Note:PXA, pleomorphic yellow neoplastic astrocytoma;FLAIR, liquid inhibition inversion recovery sequence.

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• Metastatic lesions in the brain
  

Multiple metastatic lesions are more common in the brain, mostly located in the subcortex, varying in size and degree of edema, with a variety of presentations, most of which are ring-like or node-like enhancing. The 18F-FDG metabolic activity in metastatic lesions in the brain can be lower, nearer, or higher than that in the gray matter; amino acid metabolic activity is generally higher than that in the gray matter. Single metastatic carcinoma needs to be differentiated from high-grade glioma. Imaging can be based on lesion size, lesion involvement, and enhancement performance, combined with medical history, age, and

Related other adjuvant findings can be combined to differentiate. 2. Infectious lesions in the brain

Infectious lesions in the brain, especially brain abscesses, need to be differentiated from high-grade gliomas. Both have edema and occupying signs, and the enhancement is circumferential. Brain abscesses often have smooth walls and no wall nodules, whereas high-grade gliomas tend to have cauliflower-like enhancement with mixed intracapsular signal and may be associated with tumor stroke. The vast majority of high-grade gliomas have significantly higher amino acid metabolic activity than normal brain tissue, whereas brain abscesses are generally hypometabolic.

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• Demyelinating lesions in the brain
  

A tumor-like demyelinating lesion, which is easily confused with glioma, is seen as a nodular enhancing shadow on enhancement scan and is easily recurring when reviewed after diagnostic treatment. Laboratory tests can help in the differential diagnosis.

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• Lymphoma
  

In immunocompetent patients, the MRI signal of lymphoma is more homogeneous, intra-tumoral hemorrhage and necrosis are rare, and enhancement is markedly homogeneous. 18F-FDG metabolic activity is generally higher and more uniformly distributed than in high-grade gliomas.

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• Other tumors of neuroepithelial origin
  

Including central neuroblastoma. The initial differential diagnosis can be made based on the location of the tumor and its enhancement.

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• Conventional MRI examination
  

With the exception of some grade 2 gliomas (e.g., pleomorphic yellow astrocytoma, third ventricular chordoma-like glioma, and ventricular meningioma), high-grade gliomas

MRI of high-grade gliomas is often enhanced with stroke, necrosis, and cystic changes. The MRI is a very important tool in the development of a patient’s health.

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• Multimodal MRI examination
  

Including DWI, PWI and MRS, etc. High signal areas in DWI suggest high cell density and represent high-grade lesions; high perfusion areas in PWI suggest increased blood volume and are mostly high-grade lesions; elevated Cho and The Cho/NAA ratio is elevated, which correlates positively with tumor grade.

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• PET
  

The tumor-background contrast of metabolic imaging of glioma is low, whereas amino acid tumor imaging has better tissue contrast, therefore, amino acid PET brain imaging is recommended to evaluate Glioma grade (level 2 evidence)10. 11C-MET PET assessment is more accurate than MRI for high-grade glioma 11C-MET metabolic activity is generally higher than that of low-grade gliomas, but there is still some overlap between high-grade and low-grade gliomas (level 2 evidence)11-13 >. The use of 18F-FDG PET dynamic imaging analysis is recommended to improve the imaging grading of gliomas when necessary.

MRI (plain+enhanced) should be reviewed within 24-72 hours after glioma surgery to assess the extent of tumor resection and to use this as a baseline imaging assessment of the brain. This is used as the baseline imaging data for follow-up comparison after glioma surgery. The imaging evaluation of glioma outcome is based on the RANO criteria (Table 2)14.

Table 2 Glioma treatment outcome assessment RANO criteria

The 5th edition of the WHO Classification of Tumors of the Central Nervous System classifies gliomas into 5 groups based on histologic and molecular pathologic features (Table 5): ①Adult type (1) adult-type diffuse gliomas; (2) pediatric-type diffuse low-grade gliomas; (3) pediatric-type diffuse high-grade gliomas; (4) limited astrogliomas; and (5) ventricular meningeal tumors.

Table 5 Recommended molecular pathology tests for glioma

Markers Genetic variants Detection method Diagnostic value Prognostic significance

IDH1 Mutation

(R132H/C/L/S/G)

IDH2 mutation

(R172K/M/G/W)

Immunohistochemistry, Sanger

Sequencing, pyrophosphate sequencing, diphase sequencing

Sanger sequencing, pyrophosphate sequencing, diphase sequencing

Key molecular variants for glioma classification; identifiable

Differentiate WHO grade I glioma from gliosis.

Indicates a relatively good prognosis; often used in clinical trials as

important grouping indicator; closely associated with MGMT promoter methylation; relatively sensitive to radiotherapy and alkylating agents; potential therapeutic target (e.g. Ivosidenib).

Dye body 1p/19q

Co-Deficiency FISH , PCR , Meth

Chemical Microarrays/ Expression Profiling Microarrays/ Second Generation Sequencing Related Methods

Key variants in oligodendroglioma.    Suggests relatively good prognosis; for radiotherapy and alkylating agents ph

Sensitive to radiotherapy and alkylating agents.

H3 K27 mutation

Immunohistochemistry, Sanger diagnosis of diffuse midline glioma with H3K27 mutation

Relatively poor prognosis; could be a potential therapeutic target (ex.

(K27M)

Sequencing, second generation sequencing

Key reference indicators for variant.

e.g. EZH2 inhibitor).

H3 G34 mutation

(G34R/V)

Immunohistochemistry, Sanger diffuse midline glioma, H3K27 mutation sequencing, second generation sequencing type.

Survival is slightly longer than IDH mutant glioblastoma, but shorter than IDH mutant WHO grade 4 glioma.

ATRX mutation Immunohistochemistry Sanger sequencing, second generation sequencing

TP53 mutation immunohistochemical Sanger sequencing, second-generation sequencing

ATRX nuclear expression deletion and/or positive for p53 mutation can be diagnosed as IDH mutant astrocytoma without detecting 1p19q. ATRX nuclear expression deletion and/or positive p53 mutation can be diagnosed as IDH mutant astrocytoma without detection of 1p19q.

ATRX nuclear expression deletion and/or p53 mutation positive, diagnostic of IDH mutant astrocytoma without detection of 1p19q. ATRX nuclear expression deletion and/or positive p53 mutation can diagnose IDH mutant astrocytoma without detecting 1p19q. It can be used to differentiate diffuse or non-diffuse WHO grade 1 gliomas from gliosis.

The prognosis is better than for IDH-mutant glioblastoma.

Note:FISH, fluorescence in situ hybridization;PCR, polymerase chain reaction technology;qPCR, quantitative polymerase chain reaction technology;< span style="font-family:Times New Roman">MLPA, multiplex ligation-dependent probe amplification technology.

• Adult-type diffuse glioma and pediatric-type diffuse glioma. For the first time, the new classification divides diffuse gliomas into two categories: adult-type and pediatric-type diffuse gliomas. It is important to note that this diagnostic classification is not based solely on the age of onset of the tumor, but rather on clinical features such as the major molecular variants and the age-specific distribution of these tumors. Adult-type diffuse gliomas are the main type of adult glioma, but can occur in children, while pediatric-type diffuse gliomas occur primarily in children, but can also occur in adults, especially young adults.
  

  Isocitrate dehydrogenase (IDH) mutations are an important diagnostic marker for adult-type diffuse glioma. The IDH mutation in diffuse gliomas with short arm of chromosome 1/long arm of chromosome 19
  

  (1p/19q) combination deletion is diagnosed as “oligodendroglioma, IDH mutation and 1p/19q combination deletion type”; diffuse glioma without 1p/19q combination deletion but with ATRX mutation is diagnosed as “astrocytoma, IDH The CDKN2A/B pure deletion is a graded marker for this type of tumor. Diffuse gliomas that are IDH wild and histone H3 wild are diagnosed as “glioblastoma, IDH wild” if they show necrosis or microvascular proliferation, or if they have one of three molecular variants: EGFR amplification, chromosome 7 amplification/chromosome 10 deletion (+7/-10), or mutations in the TERT promoter region.
  

  Childhood diffuse low-grade gliomas are characterized by MYB/MYBL1 variants and mitogen-activated protein kinase (MAPK) signaling pathway variants. Among them, MYB/MYBL1 gene copy number variants and gene fusions are important molecular markers for the diagnosis of “diffuse astrocytoma, MYB or MYBL1 variant” and “angiocentric glioma”; MAPK signaling pathway-related gene variants are important molecular markers for the diagnosis of “diffuse astrocytoma, MYB or MYBL1 variant” and “angiocentric glioma”.
  

including BRAF, FGFR1, etc., are important diagnostic criteria for “juvenile pleomorphic low-grade neuroepithelial tumors” and “diffuse low-grade glioma, MAPK pathway variant”. Diffuse high-grade gliomas in children are characterized by histone H3 mutations, including “diffuse midline glioma, H3 K27 variant”, which occurs in the midline and has a deletion of H3 K27me3 nuclear expression, and “diffuse hemispheric glioma, H3 G34 mutant”, which occurs in the hemisphere and has H3G34R/V mutations. For diffuse gliomas that lack IDH mutations and H3 variants, often occur in infants, children, and young adults, and have high-grade histologic features, the diagnosis is “diffuse childhood high-grade glioma, H3 wild and IDH wild” or “infantile hemispheric glioma” based on their molecular variants and methylation characteristics.

• Limited astrocytic glioma: The new classification includes hairy cell astrocytoma, hairy cell-like astrocytoma, hairy cell glioma, and hairy cell glioma. The new classification classifies six types of gliomas, including hairy cell astrocytoma, high-grade astrocytoma with hairy cell-like features, pleomorphic yellow astrocytoma, subventricular giant cell astrocytoma, chordoid glioma, and astroblastoma, MN1 variant, as limited astrocytic glioma. The term “limited” refers to their relatively controlled growth pattern, as opposed to “diffuse” tumors, meaning that these gliomas have a more limited growth pattern and are more clearly defined on imaging, but do not represent low grade, and some tumors may be invasive or even disseminated23< span style="font-size:16pt">. Most of these tumors have typical histologic features, such as astrocytic pseudogerminous clusters, biphasic structures and hair-like cells in hairy cell astrocytomas, as well as characteristic molecular variants, such as KIAA1549: BRAF fusion, BRAF V600E mutation, TSC1/TSC2 mutation, and PRKCA D463H mutation.
  

High-grade astrocytomas with hairy cell-like features are a new class of tumors defined in the WHO CNS5, and the diagnosis of these tumors is dependent on DNA methylation profiles; tumors with a typical astroblastoma morphology that carry the MN1 variant can be diagnosed as “astroblast, MN1 variant.

with CNS features and therefore recommends the use of the term “CNSWHO grade” in grading. The term “CNSWHO level” is recommended for grading.

The use of NOS and NEC effectively identifies unclear tumor diagnoses that (1) lack the necessary molecular information or (2) cannot be effectively classified by molecular testing or have negative results. NOS indicates the inability to establish an integrated diagnosis at the histomorphologic and molecular levels, and thus the failure of molecular testing that has not yet been performed by the clinician or for technical reasons. On the other hand, NEC indicates that the necessary diagnostic tests were successfully performed, but the WHO integrated diagnosis could not be made given the mismatch between clinical, histologic, immunohistochemical, and/or genetic features. As with the WHO diagnosis, the NEC and NOS diagnoses should be reported by stratified integration.

Glioma pathology report should be standardized, standardized, and integrated and stratified diagnosis according to the new version of classification. The content should include: (1) integrated diagnosis; (2) histopathological classification; (3) CNSWHO grade; and (4) molecular information, which should indicate details such as specimen type, detection method, and variant type. The pathology report should also include basic clinical information about the patient, tumor site, and notes on special circumstances.

The principle of surgical treatment of gliomas is to maximize safe resection, with the basic goals of relieving occupying The basic objectives include: relieving the signs of occupancy and relieving the symptoms of intracranial hypertension; relieving or alleviating the symptoms associated with glioma, such as secondary epilepsy; obtaining pathologic histology and molecular pathology to clarify the diagnosis; and reducing the tumor load to provide for subsequent comprehensive treatment.

Surgical treatment of glioma can be divided into tumor resection and pathological biopsy.

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• Indications and contraindications for tumor resection.
  

①Indications: CT or MRI suggesting intracranial occupancy; presence of obvious signs of intracranial hypertension and brain herniation; presence of neurological deficits due to tumor occupancy; clear history of seizures; patient voluntarily undergoes surgery.

②Contraindications: patients with severe cardiac, pulmonary, hepatic, renal dysfunction and recurrence, poor general condition that cannot tolerate surgery; other contraindications that are not suitable for neurosurgical craniotomy.

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• Indications and contraindications for pathologic biopsy.
  

Indications: Tumor located in the dominant hemisphere, extensive infiltrative growth or invasion of bilateral hemispheres; tumor located in functional cortical, deep white matter or brainstem areas that cannot be satisfactorily resected; need to identify the nature of the lesion.

There are contraindications: severe cardiac, pulmonary, hepatic, and renal dysfunction and recurrence, poor general condition that cannot tolerate surgery, and other contraindications that make the patient unsuitable for neurosurgery.

• Pathologic biopsy procedure: Biopsies can be divided into two categories: stereotactic or guided biopsies and open surgical biopsies. Stereotactic or guided biopsies are suitable for
  

for lesions that are more deeply located; whereas open biopsy is indicated for lesions that are superficially located or close to the functional cortex. The lesions are more superficial or close to the functional cortex. Cranial biopsy can obtain more tumor tissue than stereotactic biopsy, which is beneficial for the determination of results. The diagnostic accuracy of biopsy is higher than that of imaging, but there is still a misdiagnosis rate due to the heterogeneity of the tumor and target selection.

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• Perioperative management.
  

Preoperative management: If there are obvious symptoms of intracranial hypertension before surgery, dehydrating drugs should be given to relieve intracranial hypertension; if there is obvious hydrocephalus, ventriculoperitoneal shunt or ventriculostomy can be considered first. If there is significant hydrocephalus, ventriculoperitoneal shunts or ventriculoperitoneal external drainage may be considered.

Post-operative management: dehydration medication should be used to lower the cranial pressure according to the intracranial pressure, and hormones should be used to stabilize the patient. The patient’s neurological status should be stabilized with appropriate hormones. If postoperative fever occurs, lumbar puncture should be performed in a timely manner to collect cerebrospinal fluid for laboratory examination and actively prevent intracranial infection.

• Use of new surgical adjuncts: The use of new surgical adjuncts helps to determine the extent of surgical resection and tumor boundaries as well as the intraoperative period. The use of new surgical adjuncts helps to determine the extent of surgical resection and tumor borders and to preserve intraoperative function.
  

  Recommendations: neuroimaging navigation, functional neuroimaging navigation (level 2 and 3 evidence) 23, intraoperative neurophysiological monitoring techniques (e.g., functional cortical localization and subcortical nerve conduction bundle localization) (level 3 evidence)24 =”font-size:16pt”>and intraoperative MRI real-time image neuronavigation (level 3 evidence)25. Multimodal neuronavigation combined with intraoperative cortical and subcortical localization can further improve surgical safety and protect neurological function,.
  

Benefits Maximum range of safe resection (level 3 evidence)26.

Recommendable: fluorescence-guided microsurgery (level 2 evidence)27 and intraoperative ultrasound imaging for real-time localization.

• Determination of the extent of surgical resection of glioma: review within 24-72 hours after glioma surgery is highly recommended MRI is recommended for high-grade gliomas and T2-FLAIR for low-grade gliomas, and this image is used as a baseline for determining the efficacy of subsequent treatment or tumor progression. The extent of resection is thus classified into 4 levels according to the volume of the resected tumor: total resection, subtotal resection, partial resection, and biopsy, and the specific criteria are not yet uniform.
  
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  • High-grade glioma
    

  Highly recommended for maximum safe resection (level 2 and 3 evidence)28, 29. The goals of surgery include: alleviating symptoms caused by high cranial pressure and compression; reducing steroid drug use and maintaining better survival; reducing tumor cell load and creating conditions for adjuvant radiotherapy/chemotherapy; prolonging survival; and obtaining an accurate pathologic diagnosis. Removing as much of the tumor as possible is an important factor in the prognosis of patients with high-grade glioma compared with biopsy alone30. However, due to the infiltrative nature of high-grade gliomas, it is often difficult to achieve complete pathological resection of the tumor. The use of novel surgical adjuvant techniques can help maximize the extent of safe resection of high-grade gliomas. The extent of tumor resection is an independent prognostic factor for high-grade glioma, and complete tumor resection prolongs postoperative tumor recurrence and patient survival (level 2 and 3 evidence)28, 29, 31. .
  

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  • Low-grade glioma
    

  Low-grade gliomas account for approximately 30 percent of gliomas, and the age of onset of patients
  

Younger than high-grade gliomas, often located in or near important functional areas such as motor, language, visual-spatial, and memory The tumors are often located in or near important functional areas such as motor, language, visual space, and memory. For diffuse low-grade gliomas, maximum safe resection of the tumor is strongly recommended (level 2 and 3 evidence)32. Novel surgical adjunct techniques can effectively improve the rate of complete tumor resection on patient imaging and reduce the incidence of permanent postoperative neurological deficits (level 2 and 3 evidence)24, 25. Arousal surgery techniques have expanded the indications for surgery in functional areas of the brain (see the section on “Surgical Treatment of Gliomas in Functional Areas” for more details). For low-grade gliomas in nonfunctional or adjacent functional areas, functional localization techniques can identify cortical and subcortical structures associated with critical brain functions, allowing surgical resection to extend to the critical functional structures at the border of the brain to achieve maximum safe resection of low-grade gliomas33. span>.

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• Recurrent glioma
  

At present, there is a lack of high-level evidence-based evidence for the benefit of surgical treatment of recurrent gliomas. The principle of surgery is to maximize safe resection. The goals of surgery include obtaining histologic and biological information, determining whether the tumor is recurrent or pseudoprogressive, reducing tumor load, relieving symptoms, and allowing for additional postoperative treatment34. Novel surgical adjunct techniques help to achieve maximum safe resection of recurrent gliomas. The surgical treatment of recurrent glioma must be individualized, taking into account the patient’s age, clinical functional status, histologic type, response to initial treatment, type of recurrence (local or diffuse), time interval between first surgery and reoperation, and previous treatment modalities35. span style=”font-size:16pt”>.

Functional-zone glioma is a tumor involving the brain according to preoperative magnetic resonance imaging.

and sensorimotor areas (precentral gyrus, premotor area, supplementary motor area, and sensory area), language areas (including: posterior superior temporal gyrus of the dominant hemisphere, posterior temporal gyrus of the dominant hemisphere, posterior temporal gyrus of the dominant hemisphere, and posterior temporal gyrus of the dominant hemisphere), and language areas. and sensorimotor areas (precentral gyrus, premotor, supplementary motor, and sensory areas), language areas (including: posterior superior temporal gyrus, posterior middle and inferior temporal gyrus, posterior inferior frontal gyrus, posterior middle frontal gyrus, superior limbic gyrus, angular gyrus, etc.), cortical and subcortical structures such as the basal ganglia or internal capsule, thalamus, and talar visual cortex of the dominant hemisphere 36. Modern cognitive neuroscience considers the distribution of functional areas of the brain as a highly complex topological network structure37, and gliomas in functional areas often invade key nodes or connections of the topological network structure, which can The glioma may cause direct or indirect neurological impairment in motor, language, cognition, and memory. The surgical approach and surgical technique for functional glioma surgery is unique.

• Surgical approach: Currently, intraoperative awakening is recommended for patients with functional glioma. Intraoperative arousal with intraoperative functional brain localization 38-42is recommended to improve the extent of tumor resection and removal while effectively avoiding permanent postoperative sexual dysfunction.
  

  Indications include: patients with glioma involving functional areas of the brain; subjective willingness to cooperate with functional positioning; and voluntary acceptance of wake-up anesthesia.
  

  In addition to contraindications to craniotomy under conventional general anesthesia, contraindications should include 43: patients with severe preoperative intracranial hypertension or existing brain herniation with no improvement in function with conventional preoperative dehydration medications; presence of impaired consciousness or severe cognitive impairment; clear psychiatric history; communication impairment, severe neurological deficits, or difficulty cooperating with intraoperative testing tasks; and The anesthesiologist and surgeon have no experience with wake surgery; the patient refuses to undergo wake anesthesia; the patient is younger than 18 years of age (a relative contraindication) and is mentally retarded; the patient is not able to grow
  

Tolerance of fixed position for a long time, etc.

• Preoperative evaluation: The three main components are imaging, neurological assessment, and preoperative education.
  

  ①Preoperative imaging assessment: MRI T1, T2, T2-FLAIR, T1 enhancement, task state BOLD-fMRI, DTI, 3D-T1WI are highly recommended. MRS, resting-state functional magnetic resonanceimaging (Rs-fMRI), PWI are recommended.
  

  T1, T2, T2-FLAIR, T1-enhanced MRI sequences: can determine the extent of the lesion, edema and malignancy. The distance between the tumor invasion area and the functional area correlates with the functional status of the patient. BOLD-fMRI technique is commonly used to localize the motor and language functional areas of the extremities (level 3). However, when the tumor is close to the functional area (e.g., when the tumor is close to the hand motor area cortical<4mm), the accuracy of localization is reduced by the tumor (level 3 evidence)45, 46. 47, and it is recommended to use ZOOMit sequence for functional localization, which can effectively improve the localization accuracy.
  

  (Level 3 evidence)48. The preoperative localization of the functional area by fMRI allows the operator to determine the extent of tumor resection intraoperatively, effectively avoiding permanent functional impairment after surgery (level 3 evidence)49. Rs-fMRI is an imaging method that does not require the patient to complete the task during the examination and is recommended as a complementary examination (level 3 evidence)50. It should be used in patients who are unable to cooperate with a completed BOLD-fMRI examination.DTI and fiber bundle tracking: strongly recommended in patients with glioma whose tumors invade functional brain areas to improve the extent of tumor resection while protecting the patient’s neurological function (level 3 evidence)51. span style=”font-size:16pt”>. Meanwhile.
  

This technique is recommended to be widely used in patients with non-functional gliomas to understand the tumor and surrounding neurofibrillary anatomy.

Preoperative neurological assessment: The objective neuropsychological scale is used to assess the patient’s functional status before surgery to help the surgeon develop a surgical and postoperative treatment plan. The preoperative neuropsychological scales are used to assess the functional status of the patient and to assist the operator in formulating the surgical and postoperative treatment plan. The scale should include normal range reference values and be reproducible.

Highly recommended: Kanofsky performance score (KPS), Edinburgh Leigh hand check.

Recommended (depending on the functional areas of the brain involved in the tumor): Wechsler Adult Intelligence Scale, Western Aphasia Suite Chinese version, Chinese Aphasia Suite The Wechsler Adult Intelligence Scale, the Chinese version of the Western Aphasia Battery, the Chinese Language Aphasia Battery, and neglect assessments (e.g., line segment equating test).

Recommendable: Wada Test, China Rehabilitation Research Center Aphasia Screening Method, Language Task Standard Atlas (2021SR0231666) ), Montreal Cognitive Assessment Scale (MoCA), Depression Self-Rating Inventory, Anxiety Self-Rating Inventory, Symptom Self-Rating Inventory.

③ Preoperative epilepsy assessment: the four aspects of the patient’s epilepsy history, symptoms of seizures, degree of seizures, and medication control are highly recommended Objective assessment. The International League Against Epilepsy (ILAE) Guidelines for the Treatment of Epilepsy 1981, 1990 Revision, and 2013 Edition52,

53, Clinical Guidelines for the Management of Diffuse Glioma-Associated Epilepsy in Adults (English version)

54.

• Surgical preparation: incision design: the incision should be designed according to the location of the lesion and the functional area, and in principle should include the tumor and the important functions it involves
  

The brain area (monitoring target area). The following factors are taken into account: (1) Exposure of the lesion and surrounding functional areas for intraoperative monitoring and functional localization protection. The possibility of secondary surgery should be considered for tumors with high recurrence rate (e.g., glioma). (3) Inter-individual variability in the distribution of functional areas. (4) Structural factors such as subcutaneous arteries, venous sinuses, and hairline are often considered.

Positioning: often lateral or supine with a head frame. If supine is used, close attention should be paid to prevent intraoperative aspiration. The position chosen should ensure intraoperative comfort, and the use of a thermal blanket after positioning helps to reduce chills after awakening and the increase in intracranial pressure it causes.

Anesthesia: Current functional area glioma wake surgery includes intraoperative wake anesthesia for cranial functional area tumor resection and supervised anesthesia for the entire procedure. The two types of wake-up surgery include intraoperative wake-up anesthesia for cranial tumor resection and supervised anesthesia for full cranial tumor resection. Sleep-wake-sleep (AAA) anesthesia mode is the most commonly used anesthesia for wake-up surgery, which is a technique of deep anesthesia close to general anesthesia, and requires laryngeal mask, oropharyngeal airway with capsule and other auxiliary airway tools to keep the patient’s airway usual. The advantage of this procedure is that the patient is breathing spontaneously throughout the procedure, without the need for a laryngeal mask or other adjunctive ventilation device, and avoids intracranial pressure increase induced by removal of the mask after intraoperative awakening.

• Intraoperative maneuvers: craniotomy: local infiltrative anesthesia with head frame fixation staples, important scalp nerve blocks (supraorbital and supraglottic nerves, auriculotemporal nerve, lesser occipital nerve, greater occipital nerve, and third occipital nerve) and local infiltration anesthesia for the incision.
  

The incisional anesthesia covers the skin of the operative field, subcutaneously to the periosteum, including the basal part of the flap. The anesthesiologist is told to awaken the patient and to cover the dura with 2lidocaine infiltrated cotton pads for 15 to 20 min. After the patient is awakened and in a stable general condition and mood, the dura is cut and suspended around the dura (without excessive traction) and the epidural is completely hemostatic55.

Intraoperative imaging techniques: Intraoperative neuronavigation system is highly recommended; intraoperative MRI, intraoperative ultrasound, etc. are recommended. ①Neuronavigation system: intraoperative location of surgical resection and depth of resection can be determined based on the position of the navigation stick probe (level 3 evidence)56. ②Intraoperative MRI technique: can assist the operator to determine the volume of residual tumor after tumor resection and improve the final extent of tumor resection (level 3 evidence)57.

③Intraoperative ultrasound imaging: can assist in intraoperative determination of the extent of tumor and resection, and provide blood flow around and within the lesion.

Intraoperative functional brain localization techniques: direct electrical stimulation to localize functional cortical areas is highly recommended (level 2 and 3 evidence)58, 59; somatosensory evoked potentials to localize the central sulcus, continuous transcranial or transcortical motor evoked potentials to monitor motor pathway integrity, direct electrical stimulation to localize cortical and subcortical functional structures, and neuronavigation combined with preoperative fMRI localization images are recommended.

Motor Zone Monitoring: 1) Positive motor zone is indicated by involuntary muscle movements in the contralateral limb or corresponding part of the face, and electromyographic activity can be recorded. The motor area is positive for involuntary movements of the corresponding muscles of the contralateral limb or face. 60-62.

Sensory area monitoring: Positive sensory areas manifest as abnormal sensations in the contralateral limb or head in the form of pulses, mostly numbness; stimulation of sensory areas can also sometimes induce numbness.

Prompting limb movement.

Language area monitoring: the recommended language tasks are: counting and picture naming. Abnormalities during electrical stimulation (including interruptions, dysarthria, naming errors, unresponsiveness, repetition, etc.) suggest that this area is the language center associated with object naming63. Pictures of objects that have been standardized for Chinese language are recommended for picture materials. The important structures to be monitored and protected in the subcortical language areas are the arcuate fasciculus, superior longitudinal fasciculus, inferior occipitofrontal fasciculus, frontal oblique fasciculus, and inferior longitudinal fasciculus 64, 65.

Resection strategy: Select the appropriate surgical approach to remove the lesion as much as possible while preserving important functional structures. The current internationally accepted safe margin of resection should be at least 5 mm from the positive irritation zone (level 3 evidence)66. At the same time, care is taken to protect the normal arteries and important drainage vessels on the brain surface. The patient’s functional status is monitored continuously during resection, and subcortical electrical stimulation is performed immediately to identify and protect important subcortical functional structures when the presence of important subcortical pathways is suspected. After removal of the lesion, intraoperative MRI, intraoperative ultrasound, or tumor fluorescence imaging can be used to observe whether the lesion remains 67, 68.

• Postoperative evaluation and prognosis: MRI within 24-72h postoperatively is highly recommended, and high-grade brain MRI enhancement for high-grade glioma and volumetric quantitative analysis of T2-FLAIR for low-grade glioma are recommended to evaluate the extent of tumor resection. It is recommended to evaluate the KPS score, speech function, motor function and quality of life at 1-3 days, 1 month, 3 months and 6 months after surgery. The evaluation process is recommended to use a combination of neuroimaging and behavioral scales.
  

The use of direct cortical and subcortical electrical stimulation techniques to localize and preserve functional areas during arousal surgery significantly reduces the incidence of permanent postoperative neurological deficits in patients, and temporary postoperative neurological deficits tend to recover within 3 months (level 3 evidence)69 =”font-size:16pt”>.

• Surgical treatment to control glioma-associated epilepsy. Total glioma resection is superior to subtotal resection for postoperative epilepsy control (level 1 evidence)70, 71. Most patients with glioma-associated epilepsy are seizure-free after total glioma resection, and the largest possible lesion resection for postoperative seizure control is performed when safe and feasible (level 2 evidence)72. size:16pt”>. Patients with preoperative glioma with secondary grand mal seizures and tumor calcification had a better prognosis for postoperative epilepsy (level 3 evidence)73. In patients with temporal lobe glioma-associated epilepsy, tumor resection combined with selective resection of the hook gyrus and amygdala and/or anterior temporal cortical resection may improve postoperative seizure control compared with lesion resection alone (level 2 evidence). However, the decision to preserve hippocampal structures should be considered in the context of the patient’s actual needs for memory and learning.
  

  The risk of seizures due to glioma is related to the area of the brain involved in the tumor
  

  (Level 2 evidence)74. Gliomas in functional areas have a relatively limited scope of surgical resection and a relatively high incidence of postoperative seizures, and the existing techniques should be fully utilized to remove as many tumors as possible to reduce postoperative seizures while preserving brain function (level 3 evidence)75.
  

  For patients with glioma with epilepsy, intraoperative skin is recommended as appropriate
  

Intraoperative electroencephalography or deep EEG monitoring is recommended for patients with glioma with epilepsy to guide the extent of resection of epileptic foci to improve the patient’s epilepsy prognosis and improve long-term epilepsy cure rates (level 2 evidence)76.

• Intraoperative seizure control: gliomas involving functional areas of the brain in intraoperative electrical stimulation of functional areas localized with some risk of seizures (level 2 evidence)77, 78, when intraoperative EEG monitoring or symptomatic observation suggests that the patient is experiencing seizures with Local flushing with ice Ringer’s solution or ice saline can control most seizures (level 2 evidence)79. Seizures may be terminated with antiepileptic, sedative, or inotropic medications if persistent seizures remain (Level 4 evidence)
  

  78.
  

Significant survival benefit can be achieved with postoperative radiotherapy for high-grade glioma (level 1 evidence).

• Timing of radiotherapy: survival time in high-grade glioma is strongly correlated with the timing of initiation of radiotherapy . 83, early postoperative radiotherapy is effective in prolonging patient survival, and starting radiotherapy as early as possible after surgery (2-6 weeks postoperatively) is strongly recommended (level 2 evidence).
  
• Radiotherapy techniques: 3D Conformal radiotherapy or conformal modulation techniques, routinely fractionated, are recommended to improve target dose coverage, conformality and protection of normal tissues, reduce unnecessary irradiation volume and complications (level 2 evidence)84. size:16pt”>, pre-radiotherapy image verification is an indispensable part of radiotherapy quality control.
  
• Radiotherapy dose: Recommended radiotherapy The total irradiation dose is 54-60 Gy, routinely fractionated, and the total irradiation dose can be appropriately reduced for larger tumors and/or located in critical functional areas and grade 3 gliomas (level 1 evidence)85. Although 3D conformal radiotherapy or conformal intensity modulation techniques have the ability to increase the conformality of the target area, reduce the amount of normal tissue exposed, minimize the irradiation volume, and give a higher dose to the target area, the efficacy of the increased dose has not been proven, and it is prudent to blindly increase the total dose or fractionated dose.
  
• Target area determination: The target area of radiotherapy for high-grade glioma is still controversial, focusing mainly on the initial clinical target area (the “clinical target area”). The main focus is whether the initial clinical target volume (CTV) needs to include the peritumoral edema area, and the American Society for Therapeutic Oncology
  

  The Radiation Therapy Oncology Group (RTOG) recommends that the CTV1 should include the 2 cm area outside the periampullary edema zone. CTV2 should be outside the gross tumor target volume (GTV) after field reduction.
  

2 cm outside the gross tumor target volume (GTV) and a dose of 14 Gy. cm at a dose of 14 Gy. 2021 US National Comprehensive Cancer Network

(National Comprehensive Cancer Network, NCCN) guidelines recommend MRI T1 enhancement or T2-FLAIR abnormal signal as GTV with 1 to 2 cm of outgrowth to form CTV; if edema area is considered, it is recommended to include it in a course of CTV1

(46Gy/23f), second-pass incremental area (14Gy/7f) CTV2 includes only residual tumor and/or postoperative tumor cavity with appropriate external expansion. Phase II clinical trials confirmed that there was no significant difference in tumor control and survival with or without the inclusion of the edema zone in the target area86, 87, European Organisation for the Research and Treatment of Cancer (EORTC) Organisation for the Research and Treatment of Cancer (EORTC) recommended CTV settings that do not emphasize the need to include all areas of peritumoral edema.

The principle of target area mapping is to ensure that the tumor is illuminated at a dose of 60Gy as much as possible with safety in mind, and that target area mapping should refer to pre/post-operative MRI. In clinical practice, physicians should apply the above recommendations on target area setting flexibly, balancing the relationship between irradiation dose, volume and radiation damage, based on a combination of factors such as target area location, volume, patient age and KPS score.

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• Combination radiotherapy: simultaneous application of radiotherapy and temozolomide.
  

①GBM: radiotherapy combined with temozolomide (75 mg/m2 is strongly recommended for adults with primary treatment “font-size:16pt”>) with concurrent chemotherapy and subsequent 6 cycles of temozolomide (150-200 mg/m2) adjuvant chemotherapy, during and after radiotherapy Temozolomide significantly prolonged patient survival (level 1 evidence)88, and this synergistic effect was most pronounced in patients with methylation of the MGMT promoter region (level 2 evidence)89.

②Grade 3 glioma: For patients with 1p/19q combined deletion on chem/

Radiotherapy is more sensitive (level 1 evidence)90, 91< span style="font-size:16pt">, radiotherapy combined with PCV (methylphenidate + lomustine + vincristine) chemotherapy is the first-line treatment option (level 1 evidence), and temozolomide is now showing preliminary efficacy in grade 3 gliomas (level 2 evidence) with fewer side effects. Two large randomized clinical trials examining the relationship between temozolomide, radiotherapy, and 1p/19q combination deletion are ongoing, with interim results showing that radiotherapy combined with 12 cycles of temozolomide chemotherapy significantly improves patient survival in the absence of 1p/19q combination deletion92 Patients with IDH wild type with or without TERT promoter region mutations have the worst clinical prognosis and should be treated with increased intensity of radiotherapy, also in grade 2 gliomas 93. span style=”font-size:16pt”>.

Radiation therapy for grade 3 glioma should be individualized according to the patient’s specific situation, including general status, molecular pathology, and treatment needs. The treatment options include radiotherapy combined with PCV regimen/temozolomide and participation in clinical trials.

The indications, optimal timing, and dose of postoperative radiotherapy for low-grade gliomas are controversial, and treatment strategies are usually based on the patient’s prognostic risk.

• Risk factors: age ≥40 years, incomplete tumor resection, large tumor size, preoperative neurological function large volume, preoperative neurological deficits, and IDH wild type are poor prognostic factors 94, 95. Aggressive early treatment is recommended for patients whose tumors are not completely resected or who are ≥40 years of age. Patients aged <40 years with fully resected tumors may be selected for close observation.
  

  96, but the decision should be made carefully after taking into account the patient’s condition and molecular pathology.
  

  style=”margin-left: 72pt”>
  • Radiotherapy dose: The recommended total radiotherapy dose for low-grade glioma is 45 to
    

54 Gy in fractionated doses of 1.8-2.0 Gy (level 1 evidence )97. For IDH wild-type low-grade gliomas (grade 4 astrocytomas as defined by the 2021 WHO classification), a dose increase to 59.4-60 Gy is required. With the widespread use of conformal intensity-modulated radiotherapy and molecular staging in the clinic, a modest increase in radiotherapy dose (54-59.4 Gy) can help prolong patient survival, especially for astrocytomas defined by molecular pathology or MGMT promoter non-methylation. Patients 98, 99. Split doses above 2 Gy increase the risk of distant cognitive impairment (level 2 evidence)100.

The total dose can be increased to 60 Gy if the tumor is located below the cone.

Whole brain and whole spinal cord radiation therapy: whole brain including the area within the dura mater, whole spinal cord from the first cervical medulla down to the caudal dural sac, whole brain and whole spinal cord irradiation The total dose was 36 Gy, 1.8-2.0 Gy each time, with additional doses to 54-59.4 Gy for subsequent intracranial lesions and 45 Gy for spinal lesions.

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• Recurrent glioma
  

The location and size of the tumor should be fully considered when evaluating the safety of recurrent glioma recourse radiotherapy. For smaller recurrent lesions, most retrospective studies have used stereotactic radiosurgery or hypofractionated stereotactic radiotherapy techniques104, 105, while conventional fractionated radiotherapy studies have traditionally focused on relatively large recurrent lesions. mostly focused on relatively large volume recurrent

The conventional fractionated radiotherapy studies are mostly focused on relatively large recurrent lesions, and the superimposed doses may cause severe brain tissue damage. The risk of brain tissue tolerance and radiation necrosis should be fully considered106. Studies have shown that radiotherapy combined with bevacizumab and temozolomide prolonged progression-free survival and overall survival in some patients 107, 108.

Brain tissue damage from radiotherapy is classified into three different types depending on the time of onset and clinical presentation: acute (during or within 6 weeks after radiotherapy), subacute (within 6 weeks after radiotherapy), and subacute (within 6 weeks after radiotherapy).

(6 weeks to 6 months after radiotherapy) and advanced (months to years after radiotherapy).

• Acute and subacute radiation injury: Acute and subacute radiation injury may be due to vasodilation, blood-brain barrier acute and subacute radiation injury: acute and subacute radiation injury may be caused by vasodilation, blood-brain barrier damage and edema. Acute injuries are characterized by signs of cranial hypertension, such as nausea, vomiting, headache, and drowsiness. It is usually transient and reversible, and can be relieved by corticosteroids, sometimes on MRI.
  

The subacute radiation brain injury presents with drowsiness and fatigue and usually resolves spontaneously within a few weeks, with corticosteroids administered as necessary to control symptoms.

Other drugs used in glioma treatment are carmustine, irinotecan

(2) Chemotherapy for grade 3 glioma: There is no standard regimen for chemotherapy for grade 3 glioma, and radiotherapy combined with PCV/timozolomide is recommended under molecular pathology guidance. PCV/temozolomide in multiple chemotherapy regimens (level 2 evidence)113, or to participate in clinical trials.

Grade 3 oligodendroglioma with 1p/19q combined deletion, recommended for radiotherapy 102 plus PCV chemotherapy regimen (level 1 evidence)90, 91 size:16pt”>, radiotherapy plus concurrent and/or adjuvant temozolomide chemotherapy (level 2 evidence)90, 91; radiotherapy plus adjuvant temozolomide chemotherapy recommended for those without 1p/19q combination deficiency; radiotherapy plus adjuvant temozolomide chemotherapy recommended for those without 1p/19q combination deficiency Temozolomide chemotherapy 114.

Grade 3 glioma with KPS<60, short course or conventional radiotherapy combined with temozolomide chemotherapy recommended (level 2 evidence) 115.

• GBM chemotherapy (age ≤70 years): KPS ≥60 Patients with MGMT promoter region methylation, conventional radiotherapy plus synchronous and adjuvant temozolomide chemotherapy with or without electric field therapy (level 1 evidence)85, conventional radiotherapy may also be recommended Add synchronous and adjuvant temozolomide combined with lomustine chemotherapy (level 2 evidence) 116 or clinical trials; for MGMT promoter region non-methylation or unclear methylation, recommend Radiotherapy plus concurrent and adjuvant temozolomide chemotherapy with or without electric field therapy (level 1 evidence)85, or clinical trials.
  

  Patients with KPS<60, short course of radiotherapy with or without synchronous and adjuvant temozolomide chemotherapy is recommended (level 2 evidence)115; temozolomide chemotherapy alone is also recommended in the presence of methylation of the MGMT promoter region (level 2 evidence).
  

• Chemotherapy for mesenchymal ventricular meningioma: Chemotherapy is usually administered in the setting of tumor recurrence or whole-brain, whole-spinal cord dissemination, with the following agents: platinum, etoposide, and etoposide.
  

There are many controversies in chemotherapy for low-grade glioma, including the timing of chemotherapy, chemotherapy regimen, and the sequence of chemotherapy and radiotherapy.

According to current evidence-based medicine, radiotherapy combined with chemotherapy should be actively considered for patients with high-risk low-grade glioma . span style=”font-size:8pt”>117, 118. Recommended chemotherapy regimens include: PCV regimen (level 1 evidence)119; temozolomide chemotherapy (level 2 evidence)120; Temozolomide concurrent and/or adjuvant chemotherapy (level 2 evidence)120 size:16pt”>.

Appropriate targeted agents may be recommended for patients with low-grade gliomas with BRAFV600E activating mutations or NTRK fusions.

There is no standard chemotherapy regimen for recurrent glioma after standard treatment. In the case of high-grade recurrent glioma, it is strongly recommended that clinical trials be preferred, and if no appropriate clinical trials are available, the following regimens may be used.

(1) Optional regimens after relapse of low-grade glioma: (1) radiotherapy plus adjuvant PCV chemotherapy; (2) radiotherapy plus adjuvant temozolomide chemotherapy; (3) radiotherapy (2) radiotherapy plus adjuvant temozolomide chemotherapy; (3) radiotherapy with concurrent and adjuvant temozolomide chemotherapy; (4) temozolomide for patients with no prior history of temozolomide treatment 120; (5) lomustine or carmustine; (6) PCV regimen 121; (vii) carboplatin or cisplatin-based chemotherapy regimens 122 ;⑧Targeted agents may be recommended for those with BRAFV600E activating mutations or NTRK fusions.

(2) Optional regimens after relapse of grade 3 glioma: ① Temozolomide 123; ② lomustine or carmustine 124; ③ PCV regimen; ④ bevacizumab 125; ⑤ bevacizumab plus chemotherapy (carmustine/lomustine, temozolomide); ⑥

Etoposide126; (vii) carboplatin- or cisplatin-based chemotherapy regimens; and (viii) appropriate targeted agents can be recommended in the presence of BRAFV600E activating mutations or NTRK fusions.

(3) Options after GBM relapse: ①Bevacizumab 127; (ii) Temozolomide 128; (iii) lomustine or carmustine; ④ PCV regimen; ⑤ regorafenib129; ⑥ bevacizumab plus chemotherapy (carmustine/lomustine, temozolomide); ⑦ etoposide; ⑧ carbostatin or cisplatin-based platinum or cisplatin-based chemotherapy regimens.

9 Targeted agents may be recommended for those with BRAF V600E activating mutations or NTRK fusions.

The principle of electric field for tumor therapy is to continuously influence the arrangement of polar molecules in tumor cells by means of alternating electric field with low field strength at medium frequency, thus interfering with the mitosis of tumor cells and exerting anti-tumor effects. The electric field is used to treat glioma. The electric field therapy system for glioma treatment is a non-invasive, portable device that works by applying an electric field patch to the scalp, which has been shown to be safe and effective130. Recommended for newly diagnosed GBM (level 1 evidence) and recurrent high-grade glioma

(Level 2 evidence). In May 2020, the State Drug Administration approved the marketing application for electric field therapy and approved its use in combination with temozolomide for newly diagnosed GBM (Level 1 evidence). In May 2020, the State Drug Administration approved the marketing application for electric field therapy and approved its use in combination with temozolomide for the treatment of patients with newly diagnosed GBM and as monotherapy for the treatment of patients with relapsed GBM.

There is no uniform definition of old age, and this guideline refers to those aged >70 years. The main molecular genetic features of GBM include ATRX

BRAF, IDH, and TP53 mutation rates are significantly decreased and PTEN mutation rate is significantly increased.

131 , TP53 mutations and EGFR amplification may be associated with patient prognosis 132 . Aging

The main treatment options for GBM patients include surgical resection, radiotherapy, and temozolomide chemotherapy. For older GBM patients with KPS ≥60, the US 2021 NCCN guidelines also recommend electric field therapy (Level 1 evidence).

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• Surgical treatment
  

Surgical resection of tumors provides a definite survival benefit in older GBM patients (level 1 evidence)133, and total tumor resection is more beneficial for postoperative functional recovery (level 2 evidence)134. Surgical resection has a good safety and clinical benefit in those with a good evaluation of the comprehensive geriatric status assessment 135. Therefore, surgery is also recommended as a priority for older patients with glioma, whereas surgery needs to be considered carefully in older patients over 80 years of age and is not recommended for older patients with poor preoperative scores.

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• Radiotherapy and chemotherapy
  

Radiotherapy and chemotherapy can definitively extend the overall survival time of patients. Short-course or conventional radiotherapy combined with temozolomide chemotherapy (level 1 evidence)136is recommended for elderly GBM patients with KPS ≥60; short-course radiotherapy or temozolomide chemotherapy is recommended for those with KPS<60 radiotherapy or temozolomide chemotherapy.

Diffuse midline gliomas are gliomas of the midline structures that occur in the thalamus, brainstem, and spinal cord. There is no definitive epidemiological data in China, but overseas reports suggest that the peak incidence is 6-7 years in children and 20-50 years in adults, with no significant gender differences137, with difficult treatment and very poor prognosis. The 2021 WHO classification of central nervous system tumors designates diffuse midline glioma as grade 4. Clinical and imaging

Patients with suspected diffuse midline glioma It is recommended to test for H3K27M mutations, mainly H3.3 K27 mutations, H3.1/2 K27 mutations, H3 wild with EZHIP overexpression, and EGFR mutations, of which H3K27M mutations are the most common alterations in pediatric diffuse endogenous pontine glioma, and patients with worse prognosis 138, 139.

The tumor is in a critical location and is infiltrative in growth, making complete resection difficult and usually not routinely recommended. In most cases, tumor biopsy is possible and recommended to clarify pathology and molecular pathology and to guide comprehensive treatment.

140.

There are no established radiotherapy and chemotherapy regimens. Radiotherapy may improve the objective tumor response rate in some patients (level 3 evidence)141, which can be referred to the GBM treatment protocol . size:8pt”>142, with appropriate adjustment of radiotherapy dose according to the specific situation. Radiotherapy combined with temozolomide chemotherapy or targeted therapy is also a treatment option 142, 143, and appropriate patients are recommended for clinical trials.

Most patients with glioma have varying degrees of postoperative physical and psychosocial impairments that limit their daily activities and social participation. These impairments limit patients’ daily activities and social participation, and reduce their quality of life. Reasonable and appropriate rehabilitation therapy can effectively reduce the disability rate associated with glioma and is an essential part of the clinical management of glioma. In addition, patients with glioma require comprehensive palliative care throughout the disease process, and appropriate palliative care can effectively reduce the symptom burden of patients with glioma and improve patient outcomes, especially for those with glioma.

for patients with end-stage disease) and caregivers. The clinical management of these two types of treatments also requires the attention of the glioma treatment team.