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دانلود کتاب Evidence based practice in Neuro-oncology

دانلود کتاب تمرین مبتنی بر شواهد در نوروآنکولوژی

Evidence based practice in Neuro-oncology

مشخصات کتاب

Evidence based practice in Neuro-oncology

دسته بندی: آنکولوژی
ویرایش:  
نویسندگان: , ,   
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 

قیمت کتاب (تومان) : 41,000



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توضیحاتی در مورد کتاب تمرین مبتنی بر شواهد در نوروآنکولوژی

این کتاب مدیریت مبتنی بر شواهد در عصب انکولوژی را ارائه می دهد که تمام جنبه ها مانند آسیب شناسی، رادیولوژی، جراحی، پرتو درمانی و شیمی درمانی را پوشش می دهد. تومورها این امر مستلزم یک راهنمای کامل است که باید رویکردی مبتنی بر شواهد و شخصی را برای برخورد با بیماران ارائه دهد.

این کتاب همچنین پیشرفت‌های اخیر در درمان شخصی را پوشش می‌دهد که از طریق پایه مربوط به آناتومی، تصویربرداری، رادیولوژی، جراحی، پرتودرمانی و درمان سیستمیک تومورهای مغز و ستون فقرات شکل گرفته است. علاوه بر این، جنبه های عملی برنامه ریزی چاقوی گاما و سایر جنبه های جراحی رادیویی را نیز پوشش می دهد. این کتاب باید کمک ارزشمندی را به متخصصان مغز و اعصاب انجام دهد تا پزشکی شخصی مبتنی بر شواهد را بهتر انجام دهند.

توضیحاتی درمورد کتاب به خارجی

This book provides evidence-based management in neuro-oncology covering all aspects such as pathology, radiology, surgery, radiation, and chemotherapy.The field of neuro-oncology is rapidly evolving and new evidence is coming out every day towards the optimal management of brain tumors. This necessitates a requirement of a complete guide that shall provide an evidence-based and personalized approach towards dealing with patients.  

This book also covers recent advances in personalized treatment formed through the relevant basis of anatomy, imaging, radiology, surgical, radiation and systemic treatment of brain and spinal tumors. In addition it also covers the , practical aspects of the planning of the Gamma knife and other radio surgical aspects. The book shall provide valuable assistance to practicing neuro-oncologists to practice better evidence-based personalized medicine. 


فهرست مطالب

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




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