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دسته بندی: آنکولوژی ویرایش: نویسندگان: Supriya Mallick, Prashanth Giridhar, Goura K. Rath سری: ISBN (شابک) : 9811626588, 9789811626586 ناشر: Springer سال نشر: 2021 تعداد صفحات: 423 زبان: English فرمت فایل : PDF (درصورت درخواست کاربر به PDF، EPUB یا AZW3 تبدیل می شود) حجم فایل: 13 مگابایت
در صورت تبدیل فایل کتاب Evidence based practice in Neuro-oncology به فرمت های PDF، EPUB، AZW3، MOBI و یا DJVU می توانید به پشتیبان اطلاع دهید تا فایل مورد نظر را تبدیل نمایند.
توجه داشته باشید کتاب تمرین مبتنی بر شواهد در نوروآنکولوژی نسخه زبان اصلی می باشد و کتاب ترجمه شده به فارسی نمی باشد. وبسایت اینترنشنال لایبرری ارائه دهنده کتاب های زبان اصلی می باشد و هیچ گونه کتاب ترجمه شده یا نوشته شده به فارسی را ارائه نمی دهد.
Foreword Contents About the Editors Part I: Epidemiology, Neuro-Anatomy and Neuro-Pathology for a Neuro-Oncologist 1: Epidemiology and Demography of Brain Tumors 1.1 Introduction 1.2 Risk Factors 1.3 Risk Factors Common for Brain Tumors 1.4 Pediatric Brain Tumors 1.5 Genetic Syndromes Associated with Pediatric Brain Tumors 1.6 Brain Tumor in Adults 1.7 Survival Outcomes References 2: Neuro-Anatomy for Oncologist 2.1 Introduction 2.2 The ‘Environments’ of the Brain 2.2.1 The Bony Framework 2.2.1.1 Oncological Significance 2.2.2 Cranial Nerves 2.2.2.1 Oncological Significance 2.2.3 The Meninges 2.2.3.1 Dura Mater Around the Brain and Dural Folds Oncological Significance 2.2.3.2 The Pia, Arachnoid and Subarachnoid Space 2.3 Spinal Cord 2.3.1 Oncological Significance 2.4 Brainstem 2.4.1 Oncologic Significance 2.5 Cerebellum 2.5.1 Oncological Significance 2.6 Diencephalon: The Thalamus, Hypothalamus and Epithalamus 2.6.1 Thalamus 2.6.1.1 Oncological Significance 2.6.2 Epithalamus 2.6.2.1 Oncological Significance 2.6.3 Hypothalamus 2.6.3.1 Oncological Significance 2.7 Pituitary Gland 2.8 Cerebrum: Sulci, Gyri, Functional Areas 2.8.1 Oncological Significance 2.9 White Matter of Cerebrum 2.10 Basal Ganglia 2.10.1 Oncological Significance 2.11 Ventricles of the Brain 2.11.1 Oncological Significance References 3: Pathology, Molecular Biology and Classification of Gliomas 3.1 Evolving Concept of Classification of Glioma and Integrated Diagnosis 3.2 Diffuse Gliomas 3.2.1 Diffuse Astrocytomas (DA), IDH Mutant (WHO Grade II) and Anaplastic Astrocytoma (AA), IDH Mutant (WHO Grade III) 3.2.1.1 Microscopy 3.2.1.2 Molecular Profile 3.2.2 Diffuse Astrocytoma, IDH Wild Type (WHO Grade II) and Anaplastic Astrocytoma, IDH Wild Type (WHO Grade III) 3.2.2.1 Histology 3.2.2.2 Molecular Profile 3.2.3 Glioblastoma, IDH Wild Type, WHO Grade IV 3.2.3.1 Microscopy 3.2.3.2 Molecular Profile 3.2.4 Glioblastoma, IDH Mutant Type 3.2.4.1 Molecular Profile 3.2.5 Diffuse Midline Glioma (DMG), H3K27M Mutant 3.2.5.1 Microscopy 3.2.5.2 Molecular Profile 3.2.6 Diffuse glioma H3.3 G34 – Mutant 3.2.6.1 Microscopy 3.2.6.2 Molecular profile 3.2.7 Pediatric-Type Low-Grade Diffuse Glioma 3.2.7.1 Microscopy 3.2.7.2 Molecular Profile 3.2.8 Oligodendroglioma (OG), IDH Mutant, and 1p/19q Co-Deleted 3.2.8.1 Anaplastic Oligodendroglioma (AO), IDH Mutant, and 1p/19q Co-Deleted 3.2.8.2 Microscopy 3.2.8.3 Molecular Profile 3.2.9 Oligoastrocytoma 3.3 Diffuse Glioma: Approach to Diagnosis 3.4 Other Astrocytic Tumors 3.4.1 Pilocytic Astrocytoma (PA), WHO Grade1 3.4.1.1 Microscopy 3.4.1.2 Molecular Profile 3.4.1.3 Pilocytic Astrocytoma with Anaplasia 3.5 Not Otherwise Specified (NOS) and Not Elsewhere Classified (NEC) Categories 3.5.1 Not Otherwise Specified (NOS) 3.5.2 Not Elsewhere Classified (NEC) References 4: Pathology and Molecular Pathology of Ependymoma 4.1 Introduction 4.2 Pathology 4.2.1 Subependymoma 4.2.2 Myxopapillary Ependymoma 4.2.3 Ependymoma and Anaplastic Ependymoma 4.2.4 Ependymoma, RELA Fusion Positive 4.3 Molecular Pathology 4.3.1 PFA Molecular Subgroup (Pediatric Type) 4.3.2 Spinal Ependymoma, NMYC Amplified 4.4 Future Perspectives References 5: Pathology and Molecular Pathology of Meningioma 5.1 Introduction 5.2 Pathology 5.2.1 Gross Pathology 5.2.2 Histopathology and WHO Grade 5.2.3 Immunophenotype 5.2.4 Molecular Pathology 5.2.4.1 NF2 Meningiomas 5.2.4.2 Non-NF2 Meningiomas 5.2.4.3 Familial Syndromes 5.2.4.4 TERT Promotor Mutations 5.2.4.5 DMD Mutations 5.2.4.6 Epigenetics 5.3 Prognosis and Outcome 5.4 Future Perspectives References 6: Pathology and Molecular Biology of Medulloblastoma 6.1 Introduction 6.2 Clinical Profile 6.3 Integrated Diagnosis 6.4 Medulloblastomas, Histologically Defined 6.4.1 Classic Medulloblastoma (Fig. 6.1a) 6.4.2 Desmoplastic/Nodular (D/N) Medulloblastoma (Fig. 6.1b, c) 6.4.3 Medulloblastoma with Extensive Nodularity (MBEN) 6.4.4 Large Cell/Anaplastic (LC/a) Medulloblastoma (Fig. 6.1d) 6.4.5 Patterns 6.5 Medulloblastomas, Molecularly Defined 6.5.1 Medulloblastoma, WNT-Activated 6.5.2 Medulloblastoma, SHH-Activated 6.5.3 Medulloblastoma, Non-WNT/Non-SHH 6.6 Risk Stratification 6.6.1 Clinical Risk Stratification: Chang Staging System 6.6.2 Refined Risk Stratification [17] 6.6.2.1 According to WHO 2016 Classification [1] 6.6.3 Benefits of Risk Stratification 6.7 Management 6.8 Approach to Diagnosis 6.9 Future Perspectives References Part II: Clinical Examination, Neuro-Imaging and Basics of Radiotherapy in Neuro-Oncology 7: Radiology in Modern Neuro-Oncology Practice 7.1 Plain Radiography 7.2 Computed Tomography (CT) 7.2.1 Physical Principles 7.3 Basic Cross-Sectional Neuroanatomy 7.4 Role of CT in Neuro-Oncologic Imaging 7.5 Magnetic Resonance Imaging 7.6 Basic MRI Sequences 7.6.1 T1 Weighted Image 7.6.2 T2 Weighted Image 7.6.3 FLAIR 7.6.4 SWI 7.6.5 DWI 7.6.6 STIR 7.6.7 Post Contrast-Enhanced MRI 7.7 Conventional/Structural MRI Evaluation in Brain Tumors 7.8 Advanced Cross-Sectional Imaging Techniques in Neuro-Oncology 7.8.1 CT Perfusion 7.8.1.1 Technique 7.8.2 Advanced MRI Techniques 7.8.3 MRS 7.8.3.1 Clinical Applications in Brain Tumor Imaging 7.8.4 MR Perfusion 7.8.4.1 DSC Perfusion 7.8.4.2 DCE Perfusion 7.8.4.3 ASL Perfusion 7.8.4.4 Technique 7.8.4.5 Clinical Applications 7.8.5 Functional MRI (fMRI) 7.8.5.1 Technique 7.8.5.2 Clinical Applications 7.8.6 DTI References 8: PET in Brain Tumors 8.1 Introduction 8.2 Significance of the Blood–Brain Barrier 8.3 Advantages of PET in Brain Tumor Imaging 8.4 Role of PET 8.4.1 Tumor Detection, Delineation of Tumor, and Differential Diagnosis of Brain Tumors 8.4.2 Tumor Grading 8.4.3 Disease Prognosis 8.4.4 Diagnosis of Recurrent Brain Tumors and Differentiating between Post-therapy Radiation Necrosis from Residual/Recurrent Brain Tumor 8.4.5 Planning Stereotactic Biopsy 8.5 PET Tracers 8.5.1 Glucose Metabolism 8.5.2 Amino Acid Transport 8.5.3 Cellular Proliferation 8.5.4 Hypoxia Imaging 8.5.5 Theragnostic Agent 8.5.6 18F-FDG 8.6 Amino Acid Tracers 8.7 Other Radiopharmaceuticals 8.7.1 18F-Fluorothymidine (18F-FLT) 8.7.2 18F-FMISO 8.7.3 11C-Choline (CHO) and 18F-Fluorocholine (FCHO) 8.7.4 SSTR Ligands (68Ga DOTA-TOC and DOTA-NOC) 8.7.5 68Ga-PSMA 8.8 PET-MRI 8.9 Conclusion References 9: Fundamentals of Radiation for Neuro-Oncology 9.1 Introduction 9.1.1 Important Events 9.1.2 Mechanism of Radiation Action 9.1.3 Evolution of Radiation Delivery 9.1.4 Process of Radiation Treatment Planning 9.2 Treatment Target Volumes and Organ at Risk 9.3 Radiation Induced Brain Injury 9.3.1 Pathophysiology 9.4 Necrosis of Brain 9.5 Reirradiation 9.5.1 Target Volume Delineation 9.5.2 Dose in Reirradiation 9.6 Threshold of Radiation Necrosis 9.7 OAR Delineation References Suggested Reading 10: Stereotactic Radiosurgery: Planning and Evaluation 10.1 Introduction 10.2 Plan Evaluation of SRS 10.2.1 Technique and Target Selection 10.2.2 Dose Calculation Grid 10.2.3 Isodose Prescription 10.2.4 Dose to Brain and Critical OARs 10.2.5 Qualitative Assessment: Spatial Dose Distribution 10.2.6 Quantitative Assessment: DVH and Derived Indices 10.2.6.1 Dose-Volume Histogram (DVH) 10.2.6.2 Dose Variation at Edge of Target: Conformity Index 10.2.6.3 Dose Variation Outside Target: Gradient Index 10.2.6.4 Dose Variation Inside Target: Homogeneity Index 10.2.6.5 Clinical Significance of DVH Indices 10.3 Approval of SRS Plan 10.4 Reporting of SRS 10.5 Conclusion References 11: Radiation Induced Brain Injury 11.1 Necrosis of Brain References Part III: Management of Brain Tumours 12: Grade 1 Gliomas 12.1 Introduction 12.2 Epidemiology 12.3 Pathology 12.4 Clinical Presentation 12.4.1 Other Astrocytic Tumors 12.4.1.1 Pilocytic Astrocytoma (WHO Grade I) 12.4.1.2 Subependymal Giant Cell Astrocytomas 12.4.2 Other Gliomas 12.4.2.1 Angiocentric Glioma 12.4.3 Neuronal and Mixed Neuronal-Glial Tumors 12.4.3.1 Dysembryoplastic Neuroepithelial Tumor (WHO Grade I) 12.4.3.2 Ganglioglioma (WHO Grade I) 12.4.3.3 Gangliocytoma 12.4.3.4 Dysplastic Gangliocytoma of the Cerebellum 12.4.3.5 Desmoplastic Infantile Astrocytoma and Ganglioglioma 12.4.3.6 Papillary Glioneuronal Tumor 12.4.3.7 Rosette-Forming Glioneuronal Tumor References 13: Grade 2 Gliomas 13.1 Introduction 13.2 Epidemiology 13.3 Pathology and Molecular Characteristics 13.4 Imaging in LGGs 13.4.1 Computed Tomography (CT) Scan 13.4.2 Multiparametric Magnetic Resonance Imaging (MRI) 13.4.3 Positron Emission Tomography (PET)-CT Scans 13.5 Treatment 13.5.1 Surgery 13.5.2 Adjuvant Radiotherapy and Chemotherapy 13.5.2.1 Timing of Radiotherapy 13.5.2.2 Dose of Radiotherapy 13.5.2.3 Radiotherapy Target Volume and Technique 13.5.2.4 Addition of Chemotherapy Following Adjuvant RT 13.5.2.5 Radiotherapy Versus Chemotherapy 13.5.2.6 Choice of Adjuvant Chemotherapy: PCV Versus TMZ 13.5.3 Which Patients with LGG may Do Well with Observation Only 13.5.4 Prognostic Factors 13.5.5 Reirradiation/Salvage 13.6 “Other” Astrocytic Tumors 13.6.1 Pleomorphic Xanthoastrocytoma Grade 2 13.7 Other Gliomas 13.7.1 Chordoid Glioma of Third Ventricle 13.8 Mixed Neuronal and Neuronal-Glial Tumors 13.8.1 Central Neurocytoma 13.8.2 Extraventricular Neurocytoma 13.8.3 Cerebellar Liponeurocytoma 13.9 Response to Treatment 13.10 Treatment-Related Morbidity 13.10.1 Early/Acute Effects 13.10.2 Delayed Effects: Hearing, Neurocognition, and Neuroendocrine Dysfunction 13.10.3 Pseudoprogression and Radiation Necrosis 13.11 Current Status and Future Directions References 14: Oligodendroglioma 14.1 Introduction 14.2 Epidemiology 14.2.1 Risk Factors 14.3 Diagnostic Workup 14.3.1 Radiology 14.3.1.1 CT 14.3.1.2 MRI 14.3.2 Pathology 14.4 Prognostic Factors (Favorable) [1] 14.5 Surgery 14.6 Radiation 14.6.1 Radiation for ODG Grade II 14.6.1.1 Optimum Timing 14.6.1.2 Dose 14.6.1.3 Target Volume 14.6.2 Radiation Technique 14.6.3 Supportive Treatment During Radiation 14.6.4 Radiation Alone Vs Radiation with Chemotherapy Vs Chemotherapy Alone for Grade II ODG 14.7 Radiation Alone Vs Radiation with Chemotherapy Vs Chemotherapy Alone for Anaplastic Oligodendroglioma 14.8 Evolving Approaches 14.8.1 Proton Therapy References 15: Anaplastic Astrocytoma 15.1 Introduction and Epidemiology 15.2 Anatomy 15.3 Risk Factors 15.4 Clinical Presentation 15.5 Evaluation 15.6 Treatment 15.7 Radiotherapy Technical Details 15.8 Toxicity 15.9 Follow-up 15.10 Treatment of Recurrence References 16: Mixed Gliomas or Oligoastrocytoma 16.1 Introduction 16.2 Clinical Presentation 16.3 Management 16.4 Surgery 16.5 Adjuvant Therapy 16.6 Follow-up References 17: Glioblastoma 17.1 Introduction 17.2 Epidemiology 17.2.1 Risk Factors 17.3 Diagnostic Workup 17.4 Prognostic Factors (Good) 17.5 Surgery 17.6 Adjuvant Therapy 17.6.1 Radiotherapy 17.6.2 Optimum Timing 17.6.3 Dose 17.6.4 Target Volume 17.6.5 Radiation Technique 17.6.6 Supportive Treatment During Radiation 17.7 Chemotherapy 17.7.1 Temozolomide Forms the Backbone of Chemotherapy in GBM and Is Given Concurrently with RT Followed by Maintenance Phase 17.7.2 Bevacizumab Has Been Extensively Evaluated in GBM. It Is a Humanized Monoclonal Antibody Targeted Against Vascular Endothelial Growth Factor (VEGF-A) 17.7.3 Novel Anti-Angiogenic Therapy 17.7.3.1 Integrins 17.7.3.2 Anti-EGFR Monoclonal Antibody 17.7.3.3 Non-Conventional Therapy (Novo TTF) 17.8 Outcome 17.9 Evolving Approaches in Adjuvant Radiotherapy 17.10 Recurrence 17.10.1 Diagnosis Is a Challenge as Progression and Radionecrosis Closely Resemble (Fig. 17.2) 17.10.2 Management of Recurrent GBM [18] 17.11 Special Variants 17.11.1 Pediatric GBM 17.11.2 Elderly GBM 17.11.3 Spinal GBM 17.11.4 Gliosarcoma 17.11.5 GBM-PNET 17.11.6 Other Variants of GBM References 18: Management of Gliomatosis Cerebri 18.1 Introduction 18.2 Symptoms and Signs 18.3 Diagnosis 18.4 Histopathology and Molecular Classification: [13] 18.5 Differential Diagnosis: [7, 16] 18.6 Future Trials 18.7 Conclusion References 19: Pleomorphic Xanthoastrocytoma 19.1 Introduction [1–4] 19.2 Classification 19.3 Investigation 19.3.1 Appearance on CT Scan 19.3.2 MRI 19.4 Pathology 19.5 Treatment 19.5.1 Surgical Excision [5] 19.5.2 Radiation [2, 3, 6–10] 19.5.2.1 Indications for Adjuvant RT 19.5.2.2 Target Volume 19.5.2.3 Dose 19.5.3 Chemotherapy 19.6 Results [2, 3] 19.6.1 Prognostic Factors (Favorable) 19.7 Follow-up 19.8 Treatment Algorithm References 20: Astroblastoma 20.1 Introduction 20.2 Clinical Presentation 20.3 Radiology 20.4 Surgery 20.5 Pathology 20.6 Adjuvant Therapy 20.6.1 Radiation 20.6.2 Chemotherapy 20.6.3 Survival Outcome 20.6.4 Prognostic Factors for Survival 20.7 Follow-up 20.8 Treatment Algorithm [69] Suggested Reading 21: Nervous System Hemangioblastoma 21.1 Introduction and Epidemiology 21.2 Site of Origin 21.3 Clinical Manifestation 21.4 Pathology 21.5 Imaging 21.6 Treatment References 22: Rare/Uncommon Brain Tumors 22.1 Ganglioglioma 22.1.1 Introduction [1, 2] 22.1.2 Classification 22.1.3 Investigation 22.1.4 Pathology 22.1.5 Treatment 22.1.5.1 Surgical Excision 22.1.5.2 Radiation Indications for Adjuvant RT Target Volume Dose 22.1.5.3 Chemotherapy 22.1.6 Results 22.1.6.1 Prognostic Factors (Favorable for AGG) 22.1.7 Follow-up 22.1.8 Treatment Algorithm [1] 22.2 Plasmacytoma 22.2.1 Introduction 22.2.2 Investigation 22.2.3 Treatment 22.2.3.1 Surgical Excision 22.2.3.2 Radiation Indications for Adjuvant RT Target Volume Dose 22.2.4 Chemotherapy 22.2.5 Follow-up 22.3 Rosette Forming Glioneuronal Tumors 22.4 Embryonal Tumors with Multilayered Rosettes (ETMR) 22.4.1 Introduction 22.4.2 Pathology [7, 8] 22.4.3 Radiographic Features 22.4.4 Treatment 22.4.4.1 Surgery 22.4.4.2 Radiation 22.4.4.3 Chemotherapy 22.4.5 Survival Outcome [7, 8] 22.4.6 Follow-up 22.5 Supratentorial PNET: WHO 2016 Has Dropped This Terminology 22.5.1 Introduction 22.5.2 Investigation 22.5.3 Pathology 22.5.4 Treatment 22.5.4.1 Surgical Excision 22.5.4.2 Radiation 22.5.4.3 Chemotherapy 22.5.5 Results 22.5.5.1 Prognostic Factors 22.5.6 Follow-up 22.6 ATRT 22.6.1 Introduction 22.6.2 Pathology [10] 22.6.3 Radiographic Features 22.6.4 Treatment 22.6.4.1 Surgery 22.6.4.2 Radiation [11–13] 22.6.4.3 Chemotherapy 22.6.5 Survival Outcome 22.6.6 Follow-up 22.7 Neurocytoma 22.7.1 Introduction [14] 22.7.2 Pathology 22.7.3 Radiographic Features 22.7.4 Treatment 22.7.4.1 Surgery 22.7.4.2 Radiation [15–17] 22.7.4.3 Chemotherapy 22.7.5 Survival Outcome 22.7.5.1 Central Neurocytoma 22.7.6 Follow-up 22.7.7 Treatment Algorithm [15–17] References 23: Medulloblastoma and Other Embryonal Brain Tumors 23.1 Epidemiology 23.2 Pathology and Classification 23.3 Clinical Presentation 23.3.1 Workup 23.4 Imaging 23.4.1 Staging and Risk Stratification 23.4.2 Treatment Approach 23.4.2.1 Average-Risk Medulloblastoma 23.4.2.2 High-Risk Medulloblastoma 23.4.2.3 Medulloblastoma in Infants 23.4.3 Radiotherapy Technique 23.4.4 Target Volumes in CSI Treatment 23.4.5 Monitoring During Radiotherapy 23.4.6 Chemotherapy 23.4.7 Side Effects and Long-Term Issues 23.5 Ongoing Trials and Future Direction 23.6 Other Embryonal Tumors References 24: Ependymoma 24.1 Introduction 24.2 Workup 24.3 Management of Ependymoma 24.4 Volumes to Be Included for Post-operative Radiotherapy 24.5 Future Directions References 25: Intracranial Germ Cell Tumour 25.1 Introduction 25.2 Histological Subtypes 25.3 Workup: (Both Germinoma and NGGCT) 25.4 Management 25.5 Radiotherapy Dose Prescription 25.6 Volumes to Be Included in Craniospinal Irradiation 25.7 Volumes to Be Included in Whole Ventricular Radiotherapy References 26: Management of Pineal Region Tumors 26.1 Introduction 26.2 Pathological Classification of Pineal Region Tumors: [6] 26.3 Epidemiology 26.4 Clinical Presentation: [8, 9] 26.5 Endoscopy 26.6 Imaging: [13] 26.7 Overview of the Management of Various Pineal Region Tumors 26.8 Future Prospects 26.9 Conclusion References 27: Skull Base Chordoma and Chondrosarcoma 27.1 Introduction 27.2 Origin and Histology of Chordoma and Chondrosarcoma 27.3 Clinical Presentation 27.4 Imaging Findings 27.5 Management 27.6 Surgery 27.7 Radiation Therapy 27.8 Role of Systemic Treatment References 28: Intracranial Hemangiopericytoma 28.1 Introduction 28.2 Pathology 28.3 MGS Grading System for I-HPC 28.4 Imaging 28.4.1 CT Scan 28.4.2 MRI 28.5 Surgery 28.6 Radiation 28.6.1 Indications for Adjuvant RT 28.6.2 Target Volume 28.6.3 Dose 28.7 Chemotherapy 28.8 Follow-up References 29: Management of Choroid Plexus Carcinoma 29.1 Introduction 29.2 Epidemiology 29.3 Clinical Presentation 29.4 Genetic Mutations and Pathogenesis in CPC 29.5 Imaging 29.6 Histopathology: [16] 29.7 Differential Diagnosis 29.8 Treatment of CPCs 29.8.1 Surgery 29.8.2 Adjuvant Therapy 29.8.3 Radiation Therapy 29.8.4 Chemotherapy 29.9 Conclusion 29.10 Management Protocol for Choroid Plexus Carcinoma References 30: Meningioma 30.1 Introduction and Epidemiology 30.2 Etiology and Risk Factors 30.3 Pathology 30.3.1 WHO Classification 30.4 Molecular Pathology 30.5 Clinical Features and Evaluation 30.6 Neuro-Radiology 30.6.1 High Grade Features Include 30.6.2 Radiological Differentials 30.7 Management 30.7.1 Surgery 30.8 Post-operative Radiotherapy 30.8.1 Grade 1 Meningioma 30.8.2 Dose of RT 30.8.3 Grade 2 (Atypical) and Grade 3(Anaplastic) Meningiomas 30.8.4 Spinal Meningiomas 30.8.5 Recurrent Tumors 30.9 Summary of Adjuvant Treatment 30.10 Late Effects of Radiotherapy 30.11 Techniques of Radiotherapy 30.12 Recent Advances References 31: Pituitary Tumors: Diagnosis and Management 31.1 Introduction 31.2 Pituitary Anatomy and Physiology 31.3 Classification of Pituitary Adenoma 31.4 Etiology and Pathogenesis 31.5 Clinical Presentation 31.6 Evaluation 31.7 Classification 31.8 Treatment 31.9 Follow-up 31.10 Conclusions References 32: Craniopharyngioma 32.1 Introduction 32.2 Epidemiology 32.3 Clinical Presentation [8] 32.4 Radiology 32.4.1 Appearance on CT 32.4.2 Appearance on MRI 32.5 Management 32.6 Pathology 32.7 Adjuvant Therapy [8] 32.7.1 Radiation 32.7.1.1 Management of Recurrence 32.7.2 Long-Term Sequelae 32.7.2.1 Pituitary Dysfunction 32.7.2.2 Hypothalamic Dysfunction References 33: Acoustic Neuroma 33.1 Introduction 33.2 Symptoms 33.3 Investigation 33.4 Grading System 33.5 Histopathology 33.6 Management 33.6.1 Conservative/Observation 33.6.1.1 Predicting Factors for Rapid Growth 33.6.1.2 Limitation 33.6.2 Surgery 33.6.2.1 Indication 33.6.2.2 The Surgical Approaches are Mainly Three Types (Table 33.3) 33.6.3 Radiotherapy 33.6.3.1 Indications 33.6.3.2 Radiation Techniques (Table 33.4) 33.6.3.3 Specific Highlights of Radiation 33.6.3.4 Proton Therapy 33.6.4 Systemic Therapy 33.6.5 Quality of Life 33.7 Treatment Summary in Flowchart References 34: Spinal Cord Tumors 34.1 Introduction 34.2 Clinical Symptoms 34.3 Management (Table 34.1) 34.4 Intramedullary Tumors 34.5 Intradural–Extramedullary Tumors 34.6 Extradural Tumors 34.7 Chemotherapy 34.8 Radiation References 35: Brain Metastases 35.1 Introduction 35.2 Clinical Features 35.3 Diagnosis 35.4 Biopsy Is Indicated if Primary Cancer Is Unknown and Patient Presents with Brain Metastases on Imaging 35.4.1 Standard Management 35.5 Radiotherapy Management Protocols 35.5.1 Stereotactic Radiosurgery 35.6 Dose Prescription in Multiple Metastases and Post-op SRS 35.7 Volumes for Contouring 35.8 Premedication 35.9 Dose Coverage and Constraints 35.10 Medical Management in Brain Metastases 35.11 Blood–Brain Barrier 35.12 Molecular Targets of Metastases Involved in BBB Disruption and Their Function [7] 35.13 Genetic Alterations as per Tumour Type 35.14 Targeted Therapy Showing Benefit in Brain Metastases (List Includes Only Drugs with Proven Evidence) References 36: Paediatric CNS Tumours 36.1 What Will This Chapter Cover? 36.2 Introduction 36.3 Management of Various Paediatric CNS Tumours 36.3.1 Low-Grade Glioma 36.3.2 Investigations 36.3.3 Treatment 36.3.3.1 At Initial Diagnosis 36.3.3.2 Inoperable Sites 36.3.4 Radiation Therapy 36.3.4.1 Indications 36.3.5 High-Grade Glioma 36.3.6 Investigations 36.3.7 Treatment 36.3.7.1 At Initial Diagnosis 36.3.7.2 Adjuvant Treatment 36.3.7.3 Inoperable Disease (Diffuse Intrinsic Pontine Glioma; Thalamic Glioma) 36.3.7.4 Progressive Disease 36.3.8 Medulloblastoma 36.3.9 Treatment 36.3.10 Work Up: (After Surgery) 36.3.11 Risk Stratification for Adjuvant Therapy 36.3.12 Adjuvant Therapy 36.3.13 Dose Prescription 36.3.14 Reduced Dose CSI Regimen 36.3.15 Radiation Therapy Volumes 36.3.16 Adjuvant Chemotherapy 36.3.16.1 Indications 36.3.17 Relapsed Medulloblastoma 36.3.18 Atypical Teratoid Rhabdoid Tumour (ATRT) 36.3.18.1 Management 36.3.18.2 Adjuvant Therapy 36.3.18.3 Radiation Therapy 36.4 Pre-irradiation Induction Therapy 36.5 Chemoradiation Induction Therapy 36.6 Post-radiation Induction Therapy 36.7 Maintenance Therapy 36.8 Continuation Therapy with Doxorubicin (Patients Who Have Received <18 Gy RT to Thoracic Spine/Mediastinum) 36.9 Continuation Therapy without Doxorubicin (Patients Who Have Received >18 Gy RT to Thoracic Spine/Mediastinum) 36.10 Intrathecal Therapy 37: Primary Central Nervous System Lymphoma 37.1 Types 37.2 Presentation 37.3 Workup 37.4 Radiologic Characteristics 37.4.1 CT 37.4.2 MRI 37.5 Differential Diagnosis 37.6 Histology 37.7 Prognostic Factors 37.8 Recurrent PCNSL References Part IV: Miscellaneous 38: Neurocognition in Neurooncology 38.1 What Is Neurocognition? 38.2 Major Neurocognitive Domains 38.2.1 Causes for Neurocognitive Decline in Brain Tumours [2] 38.3 Tumour-Induced Neurocognitive Decline 38.3.1 Depending on Location of Tumour [3] 38.3.2 Depending Also on Rate of Growth of Tumour 38.4 Treatment-Associated Neurocognitive Decline 38.4.1 Impact of Surgery 38.4.2 Impact of Radiotherapy [4–6] 38.4.3 Impact of Chemotherapy/Targeted Therapy [7–13] 38.4.4 Impact of Anti-Epileptics [14] 38.4.5 Impact of Steroids [15] 38.4.6 Impact of Tumour-Treating Fields on Cognition [16] 38.4.7 Management of Neurocognitive Decline References Suggested Reading 39: Syndromes Associated with Brain Tumors 39.1 Introduction 39.1.1 Neurofibromatosis Type 1 39.1.2 Neurofibromatosis Type 2 39.1.3 Tuberous Sclerosis Complex 39.1.4 Von Hippel–Lindau Syndrome 39.1.5 Multiple Hamartoma (Cowden) Syndrome 39.1.6 Brain Tumor Polyposis (Turcot) Syndrome 39.1.7 Nevoid Basal Cell Carcinoma Syndrome (Gorlin Syndrome) 39.1.8 Li–Fraumeni Syndrome References 40: Endocrine Management in Neurooncology 40.1 Introduction 40.2 Hypothalamo-Pituitary Axis Dysfunction 40.2.1 Effect of Sellar Tumours on Hypothalamo–Pituitary Function 40.2.2 Effect of Radiotherapy on Hypothalamo–Pituitary Function 40.2.3 Effect of Drugs on Hypothalamo–Pituitary Function 40.3 Assessment of Pituitary Function 40.3.1 GH Deficiency 40.3.2 Central Precocious Puberty 40.3.3 Adrenocorticotropic Hormone Deficiency 40.3.4 Thyroid-Stimulating Hormone Deficiency 40.3.5 Gonadotropin Deficiency 40.3.6 ADH Deficiency (Vasopressin) 40.4 Pituitary Adenoma and Hypersecretion Syndromes 40.4.1 Prolactinoma [5] 40.4.1.1 Clinical Features 40.4.1.2 Diagnosis 40.4.1.3 Treatment 40.4.2 Growth Hormone-Secreting Pituitary Adenoma [6] 40.4.2.1 Clinical Features 40.4.2.2 Diagnosis 40.4.2.3 Treatment 40.4.3 ACTH-Producing Pituitary Adenoma [7] 40.4.3.1 Clinical Features 40.4.3.2 Diagnosis 40.4.3.3 Treatment [8] 40.4.4 TSH-Producing Pituitary Adenoma References