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Glioma
This document discusses gliomas, which are central nervous system tumors derived from glial cell lineages. It covers the classification of gliomas into low grade gliomas and high grade gliomas. Low grade gliomas are further classified based on the specific glial cell type involved, such as astrocytes or oligodendrocytes. High grade gliomas include malignant astrocytoma, glioblastoma multiforme, and gliosarcoma. The document discusses the epidemiology, clinical presentation, histopathology, neuroimaging, management, outcomes, and future directions of research for gliomas.
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Glioma
- 2.
- 3. Road Map • Introduction •Classification • Epidemiology • Clinical Presentation • Neuroimaging • Prognostic Factors & Outcome • Treatment Options • Emerging Modalities • Conclusion
- 4.
- 5. • Central NervousSystems’ neoplasms derived from neuroepithelial cell lineages, hence intra-axial • Differentiation/classification by particular glial cell types i.e. astrocytes, oligodendrocytes, ependymocytes etc. • 30% of total CNS tumours & >70% of brain tumours • Divided into two major categories based upon their clinical & biological characteristics; • Low Grade Glioma (LGG) • High Grade Glioma (HGG)
- 6. Glioma Astrocytes Astrocytomas Fibrillary Gemistocytic Protoplasmic Mixed Anaplastic astrocytoma Glioblastoma multiforme Giant cell Glioblastoma Gliosarcoma More circumscribed lesions Pleomorphic xanthoastrocytoma Pilocytic astrocytoma Subependymalgiant cell astrocytoma Oligodendrocytes Oligodendroglioma Mixed Glioma Oligoastrocytoma
- 11.
- 12. • The term‘low grade glioma’ refers to a series of primary brain tumours characterized by; • Benign histology (low proliferation, low neoangiogenesis) • Aggressive behavior • Slowly invade the normal parenchyma • Majority of these tumours are classified as Grade II by WHO classification (although Grade I could also be included)
- 13. LGGs WHO Grade IIinfiltrating astrocytoma Oligodendroglioma Oligoastrocytomas Gangliocytomas Juvenile Pilocytic Astrocytoma Pleomorphic xanthoastrocytoma Dysembryoplastic neuroepithelial tumours
- 14. Astrocytomas by celltype Ordinary Astrocytomas •Fibrillary •Gemistocytic •Protoplasmic Special Astrocytomas •Pilocytic •Microcystic cerebellar •Subependymal giant cell
- 15. Type 1: Solid tumours without infiltration Type3: Infiltrating without solid component Low Grade Gliomas Type 2: Solid tumours with infiltration
- 17. Grading systems forastrocytomas • Bailey & Cushing’s • Kernohan’s System • World health organization • St. Anne’s/Mayo system
- 18. Kernohan’s system • Dividesastrocytomas into 4 grades on basis of; • Anaplasia • Nuclear pleomorphism • Number of mitoses • Grade I/II are grouped together as low grade • Grade III/IV are grouped together as high grade • Grade IV is termed as Glioblastoma multiforme • Less commonly used today
- 19. Equivalence of Kernohan’sto WHO system Kernohan Grade WHO Designation (I) Special tumours: e.g., Pilocytic astrocytoma I II (II) Astrocytoma {low grade} III (III) Anaplastic astrocytoma Malignant astrocytoma IV (IV) Glioblastoma multiforme
- 20. St. Anne/Mayo Criteria& Grading St. Anne/Mayo Criteria • Nuclear atypia: Hyperchromasia & obvious variation in size & shape • Mitoses: Normal or abnormal configuration • Endothelial proliferation: Vascular lumina are surrounded by piled up endothelial cells. Does not include hypervascularity • Necrosis: Only when obviously present. Does not include pseudopalisading when seen alone Grade No. of criteria 1 0 2 1 3 2 4 3 or 4
- 22.
- 23. • 15% ofall brain tumours in adults • 25% of all brain tumours in children • No epidemiologic evidence about increased prevalence in specific ethnic group or nation • Slight male predominance (1.5:1) • Biphasic age distribution (6-12 years and 3rd – 4th decade) • Median age of presentation is 35 years in adults
- 24. 15% 85% Percentage of LGGsamong other CNS tumours LGGs Other CNS tumours
- 25.
- 26. • Exposure toionizing radiations is the only definite risk factor • No significant hereditary role although they are common in; • NF type I (15 – 20% develop LGGs) • Li-Fraumeni syndrome • Environmental exposure to Nitrites/Nitrates • Allergies/IgE levels association • p53 gene mutation (a consistent finding) • 1p/19q mutations in tumours transforming to high grade
- 27.
- 31. Clinical • Seizures arethe most frequent presenting symptom (50 – 80% of patients) • Other signs symptoms depend upon tumour size & location • Raised ICP associated symptoms/signs; • Headache, Vomiting, lethargy, papilloedema, ataxia • Focal neurologic deficits, frontal lobe signs
- 32.
- 33. Computed Tomography (CT): •A discrete or diffuse hypodense to isodense mass lesion • Minimal or no enhancement (except in 15 – 30% patients) • Calcifications (Oligodendrogliomas/Oligoastrocytomas) • Cystic changes (any histologic type)
- 35. Magnetic Resonance Imaging(MRI): • Hypo- to Iso-intense on T1WI • Hyperintense on T2WI • Minimal- to NO gadolinium enhancement • (25 – 50% oligodendrogliomas are somewhat enhanced) • No significant mass effect • Tendency to invade & reside in white matter • Oligodendrogliomas expands along gyri • Calcifications (20% lesions)
- 38. MRI (contnd) • Differentials& the imaging characteristics of a lesion • T1-weighted MRI with contrast may underestimate the extent of an LGG • The true extent is shown on the T2-weighted sequences, • Diffusion tensor MRI used as a marker of glioma infiltration • Rarely, gliomatosis cerebri
- 44.
- 46. • Diversity ofopinion & research for prognosis/outcome • Age the most important defining factor for prognosis/outcome (more or < 40 y) • LGG preoperative prognostic scoring system • Location of tumour (eloquent/non-eloquent) • KP score (70-80 limit) • Age (40 years limit) • Maximum diameter (4 cm limit) • Grades 1 to 4 • Low risk LGGs => Grades 0 & 1 • High risk LGGS => Grade 4
- 47. • Median survivalfor Oligodendrogliomas 15 years • Median survival for astrocytomas is 10 years • Large tumours & those crossing midline are more aggressive • Increased proliferative indices (Ki 67, MIB-1) & contrast enhanced tumours also have poor prognosis
- 48. • Bauman etal’, four classes of LGG patients • Younger age (18-40 y) with good KPS has median survival of 10 y • Younger age with low KPS or older age & good KPS with NO contrast enhancement has median survival of ≥ 7 y • Older age with good KPS & contrast enhancement has median survival of ≤ 4 y • Older age with low KPS has a survival of only 12 months
- 49. • EORTC’s prognosticmodel: • Age > 40 y • Astrocytic tumour • Tumour > 6 cm in diameter • Tumour crossing midline • Neurologic deficit • Presence of 2 factors median survival of 7.7 y • Presence of 3 to 5 factors survival of 3.2 y
- 50.
- 51.
- 53. 1. Observation withserial neuro exams & imaging 2. Radiation 3. Chemotherapy 4. Radiation with Chemotherapy 5. Surgery
- 54. • Factors promptingtreatment: • Extremely young patients or patients > 50 y • Large tumours that enhance • Short clinical history • Evidence of progression on imaging studies
- 55. Extent of Resection: •Recent evidence favouring early extensive resection • Good life expectancy • Influencing malignant transformation • Progression free survival & overall survival both improves
- 56. Malignant Transformation: • LGGtransformation ranges from 17% to 73% in clinical studies • Risk of progression increases with tumour burden • growth rate of ≥ 8 mm per year Median survival of 5.16 years • growth rate ≤ 8 mm/year median survival of ≥ 15 years • Residual tumour after surgery is an important determinant
- 57. Transformation rates forLGGs Patients diagnosed at age < 45 y Patients diagnosed at age > 45 y Mean time to transformation 44.2 ± 17 months 7.5 ± 5.7 months Time to death 58 months 14 months
- 59. Observation: • Advantages: • Nosurgical morbidity • Lesser cost of follow up treatment • Disadvantages: • Loss of histological diagnosis • Loss to follow up (quite frequent than reported) • Risk of increased malignant transformation • Risk of increasing tumour burden/neurodeficits
- 60. Surgical intervention: • Openresection • Open/stereotactic biopsy • Guided by patient’s clinical status, location of tumour & surgeon’s preference • Goals of surgery: • Establishing a diagnosis • Symptoms alleviation • Decompression • Tumour cytoreduction
- 62. Biopsy: • Open/Image guidedor stereotactic (if available) • Indicated in high risk patients or when open surgery is declined/deferred • Advantages: • Minimally invasive • Early identification of histologic type • Disadvantages: • Morbidity/mortality with open biopsy • Image guided biopsy may sample wrong site • Stereotactic biopsy may be too small for a diagnosis
- 63. Surgical Resection: • Itis the principle mode of treatment in the following; • Pilocytic astrocytoma • Threat of herniation • CSF flow obstruction • Seizure control • Delaying adjuvant therapy for smaller children/elderly • Smaller tumours are less aggressive & better surgical candidates
- 64. • Surgery haslimited role in the following; • Disseminated tumours • Multifocal tumours • Eloquent location
- 65. Radiation: • No definitiveproof of survival benefit • Radiation for Pilocytic astrocytoma after surgery may be reserved until recurrence or deep lesions • Fractionated radiation of up to 45 Gy (more focussed, more good) • Malignant transformation may be treated with radiation
- 66. Chemotherapy: • No clearbenefit in terms of survival • PCV (Procarbazine, Lomustine, Vincristine) may have a role in stabilising tumour growth • Temozolomide may have a role for progressive astrocytoma
- 69. Emerging modalities oftreatment
- 70. • Recent researchpoints towards more aggressive treatment strategies • Increasing role of MR modalities such as MR spectroscopy, MR tractography, DWI, DTI, CBV estimation and fMRI • Role of PET and SPECT in metabolic profiling • Neuronavigation assisted resection of deep/eloquent tumours • Awake brain surgery, language & motor task mapping • Intraop MRI, EEG, ECoG and MEG showing promise in reducing surgical morbidity & lesser residual tumours
- 72.
- 74. • Clinical courseis by no means benign as is manifested by histology & radiologic appearance • Aggressive early resection advised but NOT on the expense of patient’s quality of life • Diagnosis purely on the basis of radiology has a failure rate of up to 50% • Early histologic evidence of the diagnosis is paramount both for the surgeon & the patient • Chemo-radiotherapy can be delayed until recurrence or progression
- 75.
- 77.
- 78. Road Map • Introduction •Classification • Epidemiology • Clinical Presentation • Histopathology • Neuroimaging • Management • Outcome & Survival • Future Directions • Conclusion
- 79.
- 80. • Central NervousSystems’ neoplasms derived from neuroepithelial cell lineages, hence intra-axial • Differentiation/classification by particular glial cell types i.e. astrocytes, oligodendrocytes, ependymocytes etc. • 30% of total CNS tumours & >70% of brain tumours • Divided into two major categories based upon their clinical & biological characteristics; • Low Grade Glioma (LGG) • High Grade Glioma (HGG)
- 81. Glioma Astrocytes Astrocytomas Fibrillary Gemistocytic Protoplasmic Mixed Anaplastic astrocytoma Glioblastoma multiforme Giant cell Glioblastoma Gliosarcoma More circumscribed lesions Pleomorphic xanthoastrocytoma Pilocytic astrocytoma Subependymalgiant cell astrocytoma Oligodendrocytes Oligodendroglioma Mixed Glioma Oligoastrocytoma
- 86.
- 87. • Three mostcommon malignant CNS tumours • Malignant or Anaplastic astrocytoma • Glioblastoma Multiforme • Gliosarcoma • Highly malignant with low survival rates • Invasive & infiltrative in nature precluding complete resection • Walter Dandy’s description of recurrence in 1930 • Conflicts & lack of evidence regarding extent of resection • Primary treatment is still surgery in some form
- 88. • The adultnervous system has been discovered to harbour neural stem cells that are capable of self-renewal, proliferation, and differentiation into distinctive mature cell types. • There is now increasing evidence that these neural stem cells, or related progenitor cells, can be transformed into brain tumour stem cells and give rise to malignant gliomas by escaping the mechanisms that control proliferation, programmed differentiation, and apoptosis
- 89.
- 91. • Most commonprimary brain tumours • 2% of total cancer burden • Disproportionate rate of cancer related morbidity/mortality • At least one third of patients dies within the first year after diagnosis/treatment • Leading cause of death from solid tumours in children • Third leading cause of cancer death between 15-34 y age
- 92. • CNS tumoursincidence is 14.8 per 100000 person-year • Half being malignant • Average age for anaplastic astrocytoma is 40 years • Average age for GBM is 53 years • Peak incidence of GBM between 65 and 74 years • Male to female ratio is 1.5:1 • 2% - 8% of GBMs are gliosarcoma
- 93.
- 95. • Hemispheric occurrenceof GBMs & AAs • Two types of GBMs; • Primary GBM, arising de novo • Secondary GBM, malignant transformation of LGGs • AA has a tendency to progress to GBM • AA tends to recur locally & at resection margins • Three main features presents clinically; • High ICP features • Local/mass effects • Seizures in up to 1/3rd
- 96. • Gliosarcoma occurat temporal, parietal, frontal, occipital lobes in that order • It tend to occur close to leptomeninges • Might have a dural tail/base • Spreads through CSF pathways into ventricles, cranial nerves, spinal cord • Distant (extracranial) metastasis in upto 15% to 30% of gliosarcoma • Signs/symptoms similar to GBM/AA
- 98.
- 100. • Highly invasive/infiltrativetumours • Spread along subarachnoid space • Microsatellite tumour cell nests remain even after curative resection • Walter Dandy demonstrated that GBMs recur even after hemispherectomy • Grading by histologic features, not by TNM status
- 101. • Four featuresfor classifying gliomas (as discussed previously) • Nuclear Atypia • Mitoses • Endothelial proliferation • Necrosis • Combination of these four features results in grading of a particular tumour cell population and a specific WHO grade • Gliosarcoma in addition to the above features have features of mesenchymal origin (multinucleated giant cells, altered fibroblasts)
- 102. St. Anne/Mayo Criteria& Grading St. Anne/Mayo Criteria • Nuclear atypia: Hyperchromasia & obvious variation in size & shape • Mitoses: Normal or abnormal configuration • Endothelial proliferation: Vascular lumina are surrounded by piled up endothelial cells. Does not include hypervascularity • Necrosis: Only when obviously present. Does not include pseudopalisading when seen alone Grade No. of criteria 1 0 2 1 3 2 4 3 or 4
- 104. • MIB-1/Ki-67 indicesare indicators of histological aggressiveness • AA index is usually between 5% to 10%, GBM is 10% to 20% • EGFR amplifications/mutations • Chromosome 10q loss of heterozygosity • Deletion of chromosome p16 • tp53 mutations, PDGFR overexpression, p16 and Rb gene abnormalities
- 105.
- 106. • MRI isthe preferred modality for all brain tumours • CT is usually used in acute setting, for delineating haemorrhages or acute infarctions • CT is particularly useful in identifying haemorrhage or calcification • Once a mass is identified, further characterisation is with the help of MRI
- 109. • HGGs appearirregular hypodense lesion on T1WI • Various degrees of contrast enhancement and oedema • The presence of; • ring-like enhancement • surrounding irregularly shaped areas of presumed necrosis suggests glioblastoma • AAs can appear as nonenhancing tumour • Glioblastomas may present as nonenhancing lesions, especially in older patients
- 111. • Functional MRIcan be used to define the locations of functionally eloquent cortex • in up to 40% of cases, MRI in the first month after radiotherapy may show increased enhancement • the increased enhancement reflects increase in vessel permeability that is a result of radiotherapy, a phenomenon that improves with time and is designated “pseudoprogression” • MRI has poor specificity in identifying viable recurrent tumours in brain treated with surgery/radiotherapy/chemotherapy
- 113. • MR Spectroscopymay be used to differentiate tumours from stroke, old trauma, radionecrosis, infection and MS • FDG-PET effectively demonstrate hypermetabolism in high- grade tumours • FDG uptake also has prognostic value • High FDG uptake in previously low grade tumours means malignant transformation
- 115. • Gliosarcoma onCT is similar to infiltrating glioblastoma • well-demarcated hyperdense mass with heterogeneous or irregular ring enhancement • Majority of gliosarcomas are superficial with a dural base • Vasogenic oedema in almost all cases of gliosarcoma, irrespective of tumour size • Central hypodensity, as a result of necrosis, is less common in gliosarcomas • Osteosarcomatous differentiation often demonstrate calcification, which appears intensely hyperdense
- 116. Left top, Contrast-enhanced,T1-weighted image. Kato T et al. AJNR Am J Neuroradiol 2008;29:1176-1182 ©2008 by American Society of Neuroradiology
- 117. • T1WI+C MRIof gliosarcomas shows diffuse, inhomogeneous enhancement or irregular ring-like enhancement • Gliosarcomas is well-defined lesions with either an inhomogeneous or cystic appearance and surrounding vasogenic oedema • T2WI these tumours are of intermediate intensity with surrounding oedema • gliosarcoma should be included in the differentials of any tumour that appears to be intra-axial but abutting a dural surface and is much less hypointense on T2-weighted images than other glial neoplasms
- 120.
- 122. General Medical Management: •Most of the signs/symptoms of HGGs require general medical management • it is important to keep in mind most common problems; • peritumoral oedema, seizures, fatigue, • venous thromboembolism & cognitive dysfunction
- 123. • Antiepileptics selectionneed care, keeping in mind drug- drug interactions • Phenytoin & Carbamazepine induce cytochrome p-450 enzymes & may increase metabolism of chemotherapeutics • Drugs such as levetiracetam are favoured • Use of prophylactic AEDs is controversial • The American Academy of Neurology recommend against the use of prophylactic AEDs
- 124. • Peritumoral oedemais treated with corticosteroids • Cushing’s syndrome & corticosteroid myopathy • Increased risk for Pneumocystis jiroveci pneumonitis • Vitamin D, calcium supplements, & bisphosphonates • 20% to 30% cumulative risk of VTE • Anticoagulation is safe, unless known risk of haemorrhage • LMWHs are safer than warfarin
- 125. • Malignant gliomapatients experience severe fatigue • Methylphenidate & modafinil are indicated for it • Donepezil/memantine may help reduce memory dysfunction • Major depression is common & needs proper management Surgery: • Three main goals; i. Tissue diagnosis ii. Reduce mass effect iii. Reduce tumour burden
- 127. • Imaging cannotaccurately diagnose the tumour type or grade • Need for tissue diagnosis in order to • make treatment recommendations • Assessment & formulation of prognosis • Tumour mass reduction results in • Improvement of signs & symptoms • Decrease steroid requirement • Prevent early death resulting from mass effect
- 128. • Effect ofextensive resection on prolonging survival is questionable • Extensive resection of HGGs is difficult because; • They are invasive & infiltrative, and • They are usually located in eloquent areas • The effect of gross total resection (GTR), near total resection (NTR) or subtotal resection is unclear • However, extensive resection may help chemo-/radiotherapy to have their maximal effect by reducing tumour mass
- 131. • Radiation &Chemotherapy: • Carmustine-loaded biodegradable polymers (Gliadel wafers) placement in tumour cavity after resection • Improved survival by 2 to 5 months • Temodar (radiotherapy with Temozolomide chemotherapy) also has improved survival in RCTs
- 132.
- 134. • Overall theprognosis & outcome for patients with HGGs is poor • Median survival of less than 2 years for GBM & 2 to 5 years for AA • Even extensive resection leaves nests of tumour cells behind which acts as havens for recurrence • Currently age & KPS score are the most significant prognostic factors • Gliosarcoma has worse prognosis than Glioblastoma and AA
- 135. Recent Developments &Future Directions
- 136. • Functional mappingfor eloquence has had a tremendous effect upon safe resection without incurring major disabilities • Neuronavigation (CT or MR based) assisted resection • Neuronal stem cells identification & their use as targets/vectors for immunomodulatory/cytotoxic therapy • Advances in molecular/biologic understanding of the glioma development is guiding future therapies for receptor/gene targeted interventions • Recent approval of Gliadel wafers, Temodar regimen & MGMT promoter methylation is improving survival • Development of glioma treatment response criteria for clinical trials such as McDonald & RANO criteria
Editor's Notes
- #13 The term “low-grade glioma” refers to a series of primary brain tumours characterized by benign histology (low proliferation, low neoangiogenesis phenomena) and aggressive behaviour related to the slowly progressive tendency to invade the normal brain parenchyma. These neoplasms are classified as grade II (out of IV) by the World Health Organization classification of brain tumours and include the following entities: grade II astrocytoma (further divided in fibrillary and protoplasmic), grade II oligoastrocytoma, and grade II oligodendroglioma. Pilocytic astrocytomas, or grade I astrocytomas, are occasionally referred to as low-grade gliomas but due to their peculiar behaviour, require separate considerations. In adults, the term LGG typically refers to the diffuse, infiltrating variety of tumours classified as World Health Organization (WHO) grade II lesions—specifically, low-grade astrocytomas, oligodendrogliomas, or mixed oligoastrocytomas. Low-grade gliomas are slow growing tumours, typically affecting younger individuals (median age 35), and mainly males (male/female ratio 1.5) who clinically present with seizures (often partial seizures). Headache, personality changes, and focal neurologic deficits represent the other most common symptoms. The neurologic symptoms include motor/sensory deficits, dysphasia/aphasia, disinhibition, apathy, and visuospatial disturbances according to tumour location and size. Interestingly, some authors report the tendency of low-grade gliomas to occur in eloquent areas or in their proximity. Overall, the median survival of low-grade gliomas is about 10 years and well-defined negative prognosticators include older age (>40 years), larger size (>5-cm diameter), eloquent location, and reduced Karnofsky performance status. The optimal treatment for low-grade gliomas has yet to be determined. Watchful observation, needle biopsy, and open biopsy, as well as surgical resection have all been advocated by different authors. No evidence of class I or II exists regarding the optimal management of these patients, even if the more modern tendency is to obtain at least some type of tissue diagnosis. The rationale behind the observational or “wait-and-see” policy was the occasionally indolent or very slowly progressive behaviour of these tumours. On the other hand, following the modern oncologic concepts, some authors proposed performing a biopsy to obtain a histopathologic confirmation of the nature of the neoplasm before deciding on further management. Surgical resection of low-grade gliomas is still matter of debate, although recent studies are increasingly sup- porting its role. Surgery can in fact achieve multiple aims: more reliable histologic diagnosis with eventual molecular profile (e.g., 1p/19q loss and MGMT status), symptom relief; beneficial effect on seizure control, and lower rate of recurrence and malignant transformation. Nevertheless, surgery carries unavoidable (albeit low) risks that can potentially and permanently affect the patient’s quality of life. Given this general information on low-grade glioma behaviour and the possibility of treatment, it is clear that a modern surgical approach to these tumours has the goal of maximal resection of the mass and minimizing post- operative morbidity to preserve the patient’s functional integrity. 13,18-20,23 Since the natural history of the tumour can be relatively long (with or without surgery), the conservation of simple and complex neurologic functions of patients is mandatory. To achieve the goal of a satisfactory tumour resection associated with full preservation of the patient’s abilities, a series of neuropsychological, neurophysiologic, neuroradiologic, and intraoperative investigations must be performed. In this chapter, we will describe the rationale, indications, and modality for performing a safe and rewarding surgical removal of low-grade gliomas.
- #16 Type 1: Solid tumours only, without infiltration of brain parenchyma. Most amenable to surgical resection. Most favourable prognosis. Includes gangliogliomas, Pilocytic astrocytomas, pleomorphic xanthoastrocytomas, and some protoplasmic astrocytomas. (No oligodendroglioma in this group) Type 2: Solid tumours associated with surrounding tumour-infiltrated brain parenchyma. Surgical resection may be possible, depending on tumour location. Often low grade astrocytomas Type 3: Infiltrative tumour cells without solid tumour tissue. Risk of neurologic deficit may preclude surgical resection. Usually oligodendrogliomas.
- #24 Even though LGGs are diffusely distributed along a variety of supratentorial regions, they have a particular predilection for the insula and supplementary motor area In contrast, LGGs rarely involve the cerebellum, brainstem, or spinal cord, as is commonly found in children
- #27 From 15% to 20% of individuals with neurofibromatosis type 1 develop LGGs affecting the optic nerves, optic chiasm, and hypothalamus (optic pathway gliomas) Observations of an association between drinking water and brain tumours suggest that ingestion of an environmental contaminant has an impact, 5-7 perhaps from chlorinated sources like chloroethane, a by-product of sewage treatment, or nitrate/nitrite contamination of drinking water supplies. Recent epidemiological studies have also reported that adults with low- as well as high-grade gliomas are 1.5-to 4-fold less likely than control subjects to have allergies, which ranks the lack of allergies among the most consistent risk factors for glioma reported to date
- #34 The typical computed tomography (CT) appearance is one of an either discrete or diffuse hypodense to isodense mass lesion, showing minimal or no enhancement with intravenous contrast administration In about 15% to 30% of patients, however, tumour enhancement can be discerned Calcifications may also occur, particularly among oligodendrogliomas or mixed oligoastrocytomas
- #36 Vasogenic oedema and mass effect are uncommon because of the slow-growing nature of these tumours Oligodendrogliomas, for example, are frequently located within the frontal lobes, involve the cortex, and display calcifications, in contrast to other LGGs. The epicentres of low-grade astrocytomas are typically within the white matter, whereas oligodendrogliomas can be more superficial and will occasionally expand the adjacent gyrus Calcifications are apparent in 20% of lesions and are characterized by foci of high T1 and low T2 signals
- #39 Differentials could be sought from the imaging characteristics of a lesion The true extent is shown on the T2-weighted sequences, although on these sequences, tumour extent and surrounding oedema are indistinguishable Rarely, large LGGs will involve three or more cerebral lobes (gliomatosis cerebri) For patients with supratentorial mass lesions that exhibit the typical imaging features of LGG, structural MRI has a false positive rate as high as 50% when attempting to predict the histological diagnosis of astrocytoma This risk of anaplasia in MRI non-enhancing lesions increases significantly with patient age Thus, observation of LGGs is not a prudent option, and early tissue diagnosis is essential. These misleading imaging features are likely due to the intrinsic heterogeneity of LGGs.
- #47 Although substantial heterogeneity exists when profiling LGG patient outcome, several clinical factors are known to be predictive An LGG preoperative prognostic scoring system developed at the University of California at San Francisco (UCSF) assigns a prognostic score based upon the sum of points assigned to the presence of each of the four following factors (1 point per factor): (1) location of tumour in presumed eloquent cortex, (2) Karnofsky performance scale (KPS) score 80 or less, (3) age more than 50 years, and (4) maximum diameter more than 4 cm
- #50 The EORTC (European Organization for Research and Treatment of Cancer) developed a prognostic scoring system based on two large, randomized, multicentre trials with more than 600 patients. In their multivariate analysis, Age older than 40 years, Astrocytic tumour type, Tumour size greater than 6 cm, Tumour crossing the midline, and Neurological deficit at diagnosis were retained in the model. A favourable prognostic score was defined as no more than two of these adverse factors and was associated with a median survival of 7.7 years The presence of three to five prognostic factors was associated with a median survival of 3.2 years (95% confidence interval [CI] = 3.0, 4.0).
- #61 The choice depends in part on the patient’s clinical status, the anatomic location of the tumour, and the surgeon’s preference Currently, the only agreed-on surgical standard for adults with suspected or known supratentorial non–optic-pathway LGGs is to obtain a tissue diagnosis before active treatment commences
- #63 One pitfall of relying on stereotactic biopsy for tissue diagnosis is the possibility of misdiagnosis or inaccurate tumour grading owing to tumour heterogeneity and diagnosis bias resulting from limited tumour sampling Including the enhancing regions in the biopsy is necessary This strategy, however, is complicated because higher grade lesions may not always show contrast enhancement in imaging studies
- #114 FDG= Fluorodeoxyglucose
- #117 Left top, Contrast-enhanced, T1-weighted image. Right top, MET PET is superimposed on MR imaging. Left bottom, CHO PET is superimposed on MR imaging. Right bottom, FDG PET is superimposed on MR imaging. A, A 32-year-old woman presented with diffuse astrocytoma. MET T/N ratio = 1.72, CHO T/N ratio = 1.38, and FDG T/N ratio = 0.66. B, A 23-year-old woman presented with oligoastrocytoma. MET T/N ratio = 2.76, CHO T/N ratio = 1.82, and FDG T/N ratio = 0.92. C, A 44-year-old man presented with oligodendroglioma. MET T/N ratio = 3.71, CHO T/N ratio = 2.74, and FDG T/N ratio = 1.07. D, A 62-year-old woman presented with anaplastic astrocytoma. MET T/N ratio = 4.26, CHO T/N ratio = 10.17, and FDG T/N ratio = 1.24. E, A 68-year-old man presented with glioblastoma multiforme. MET T/N ratio = 6.85, CHO T/N ratio = 33.38, and FDG T/N ratio = 2.55.
- #129 A lower tumor load has been shown to increase the efficacy of adjuvant chemotherapy and radiotherapy in killing the remaining cancer cells and increasing survival