¡Oferta! SURGICAL NEUROANGIOGRAPHY VOL.2: CLINICAL AND ENDOVASCULAR TREATMENT ASPECTS IN ADULTS

SURGICAL NEUROANGIOGRAPHY VOL.2: CLINICAL AND ENDOVASCULAR TREATMENT ASPECTS IN ADULTS

Autor(es): BERENSTEIN
Editorial: SPRINGER
Fecha de publicación: marzo 2004
Nº de edición:
Nº de páginas: 1287
Medidas: 21x28x7 cms

9783540416685

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From the reviews:

"Thepresentation of the book is admirable with most chapters beginning withdiscussion of basic pathophysiology and continuing with clinical aspects andpractical advice. The authors are careful not to present simply the latest technologicaladvances, but to underpin the book with clinicopathological aspects of vasculardisease which they regard as fundamental for the successful management of thesedifficult cases. It functions best as a reference text and has an accessibleand easy to use index which helps in this regard." (Justin Cross,Acta Neurochirurgica, 2005)

 

1 Occlusive Vascular Disease

  • 1.1 Introduction

  • 1.2 Arterial Occlusive Disease

  • 1.2.1 Cerebrovascular Physiology

  • 1.2.1.1 The BloodBrain Barrier

  • 1.2.1.2 Cerebral Blood Flow

  • 1.2.1.3 Cerebral Autoregulation

  • 1.2.1.4 Cerebral Blood Volume

  • 1.2.1.5 Blood Viscosity

  • 1.2.1.6 Metabolism in Cerebral Blood Flow

  • 1.2.1.7 Carbon Dioxide Reactivity

  • 1.2.1.8 Oxygen Reactivity

  • 1.2.1.9 Nitrous Oxide in Cerebral Circulation

  • 1.2.1.10 Other Factors

  • 1.2.2 Arterial Ischemic Stroke

  • 1.2.2.1 Definition

  • 1.2.2.2 Neuronal Metabolism and Cerebral Ischemia

  • 1.2.2.3 Selective Neuronal Vulnerability

  • 1.2.2.4 Hemodynamic Effects of Ischemia

  • 1.2.2.5 Nitrous Oxide and Cerebral Ischemia

  • 1.2.2.6 Window of Opportunity

  • 1.2.2.7 Neutrophil

  • 1.2.3 Atherosclerosis

  • 1.2.3.1 Introduction

  • 1.2.3.2 Epidemiology

  • 1.2.3.3 Pathogenesis

  • 1.2.3.4 Mechanisms of Atherogenesis

  • 1.2.3.5 Fatty Streak

  • 1.2.3.6 Fibrous Plaque

  • 1.2.3.7 Unstable Fibrous Plaques

  • 1.2.3.8 Complicated Plaque

  • 1.2.3.9 Carotid Atherosclerosis

  • 1.2.3.10 Conclusion

  • 1.2.3.11 Neuroimaging of Ischemic Stroke

  • 1.2.4 Ischemic Stroke Treatment

  • 1.2.4.1 Medical Treatment of Acute Stroke

  • 1.2.4.2 Thrombolytic Therapy: Introduction

  • 1.2.4.3 Thrombolytics (IV)

  • 1.2.4.4 Recombined Tissue Plasminogen Activator

  • 1.2.4.5 Streptokinase

  • 1.2.4.6 Antiplatelets

  • 1.2.4.7 Coumadin Versus Aspirin

  • 1.2.4.8 Neuroprotective Agents

  • 1.2.4.9 Pharmacological Properties of Neuroprotective Drugs

  • 1.2.4.10 Binding Properties

  • 1.2.4.11 Angiographic Evaluation

  • 1.2.4.12 Middle Cerebral Artery Stroke: Natural History

  • 1.2.4.13 Local Intra-arterial Thrombolysis in the Anterior Circulation

  • 1.2.4.14 Internal Carotid Artery Occlusion

  • 1.2.4.15 Carotid Dissection

  • 1.2.4.16 Central Retinal Artery Occlusion

  • 1.2.4.17 Internal Carotid Artery Stenosis Above the Carotid Bulb

  • 1.2.4.18 General Organization of a Stroke Emergency Team

  • 1.2.4.19 Evolving Treatment Strategies

  • 1.2.5 Extracranial Carotid Artery Stenosis

  • 1.2.5.1 Introduction

  • 1.2.5.2 Natural History

  • 1.2.5.3 Carotid Bruit

  • 1.2.5.4 Imaging

  • 1.2.5.5 Treatment

  • 1.2.5.6 Symptomatic Carotid Stenosis

  • 1.2.5.7 Asymptomatic Carotid Stenosis

  • 1.2.5.8 Restenosis After Carotid Endarterectomy

  • 1.2.6 Carotid Angioplasty and Stenting

  • 1.2.6.1 Introduction

  • 1.2.6.2 Techniques of Carotid Angioplasty and Stenting

  • 1.2.6.3 Intimal Hyperplasia and Restenosis

  • 1.2.6.4 Follow-up Monitoring

  • 1.2.7 Posterior Circulation Stroke (Stroke Prevention)

  • 1.2.7.1 Introduction

  • 1.2.7.2 Clinical Presentation

  • 1.2.7.3 Pretherapeutic Evaluation in Cerebral Vascular Insufficiency

  • 1.2.7.4 Management of Posterior Circulation Insufficiency

  • 1.2.7.5 Basilar Thrombosis

  • 1.2.7.6 Takayasus Arteritis

  • 1.2.8 Cerebral Angioplasty

  • 1.2.8.1 Vasospasm

  • 1.3 Venous Occlusive Disease

  • 1.3.1 Etiology

  • 1.3.2 Incidence

  • 1.3.3 Clinical Presentation and Natural History

  • 1.3.4 Imaging

  • 1.3.5 Treatment

  • Appendix

2 Dural and Bony Tumors

  • 2.1 Introduction

  • 2.2 Meningiomas

  • 2.2.1 Epidemiology

  • 2.2.1.1 Origin

  • 2.2.1.2 Incidence

  • 2.2.1.3 Association of Meningiomas with Other Tumors

  • 2.2.1.4 Sex Hormone Receptors in Meningiomas

  • 2.2.1.5 Chromosomal Patterns in Meningiomas

  • 2.2.1.6 Meningiomas in Children

  • 2.2.1.7 Familial Occurrence

  • 2.2.1.8 Meningioma Incidence, Prevalence, and Mortality

  • 2.2.1.9 Etiology of Human Meningiomas

  • 2.2.1.10 Oncogenic Viruses

  • 2.2.2 Pathology

  • 2.2.2.1 Growth and Spread

  • 2.2.2.2 Malignant Meningioma

  • 2.2.2.3 Angioblastic Meningioma and/or Hemangiopericytoma

  • 2.2.2.4 Meningioangiomatosis

  • 2.2.2.5 Meningeal Meningiomatosis

  • 2.2.3 Clinical Presentation

  • 2.2.3.1 Sites

  • 2.2.3.2 Epidural Meningiomas

  • 2.2.3.3 Meningiomas of the Orbit

  • 2.2.3.4 Meningiomas Involving the Cavernous Sinus

  • 2.2.3.5 Meningiomas in Other Unusual Sites

  • 2.2.3.6 Intracranial Vascular Involvement

  • 2.2.3.7 Peritumoral Edema in Meningiomas

  • 2.2.4 Pretherapeutic Evaluation

  • 2.2.4.1 CT Scanning in Meningiomas

  • 2.2.4.2 MRI Scanning

  • 2.2.4.3 Angiographic Investigation

  • 2.2.4.4 Differential Diagnosis

  • 2.2.5 Therapeutic Strategy and Clinical Objectives

  • 2.2.6 Technical Aspects of Embolization

  • 2.2.7 Special Considerations in Meningioma Embolization

  • 2.2.7.1 Extracranial Tumor Extension

  • 2.2.7.2 Recurrent Meningiomas

  • 2.2.7.3 Internal Carotid Supply to Recurrent or Malignant Meningiomas After Radiation Therapy Has Failed

  • 2.2.7.4 Pial Supply

  • 2.2.7.5 Pre- and Postembolization Medical Management

  • 2.2.7.6 Time of Operation

  • 2.2.7.7 Complications of Embolization

  • 2.3 Other Bony and Dural Tumors

  • 2.3.1 Cerebral Tumors

  • 2.3.2 Neurinomas

  • 2.3.3 Esthesioneuroblastomas

3 Nasopharyngeal Tumors

  • 3.1 Juvenile Angiofibromas

  • 3.1.1 Macroscopic Pathology

  • 3.1.2 Microscopic Pathology

  • 3.1.3 Epidemiology

  • 3.1.4 Pathophysiology

  • 3.1.4.1 Juvenile Angiofibromas and Sex Hormones

  • 3.1.4.2 Physiology and the Nasal Mucosa

  • 3.1.4.3 Hormones and the Vascular System

  • 3.1.4.4 Global Hypothesis for the Development of Juvenile Angiofibromas

  • 3.1.5 Clinical Findings

  • 3.1.6 Natural History

  • 3.1.7 Pretherapeutic Evaluation

  • 3.1.7.1 Computed Tomography

  • 3.1.7.2 Magnetic Resonance Imaging

  • 3.1.7.3 Angiography

  • 3.1.8 Therapeutic Goals

  • 3.1.8.1 Radiation Therapy

  • 3.1.9 Technical Aspects of Embolization

  • 3.1.10 Tumor Recurrence

  • 3.2 Other Nasopharyngeal Tumors

  • 3.3 Conclusion

4 Paragangliomas

  • 4.1 Introduction

  • 4.2 Embryology

  • 4.3 Epidemiology

  • 4.4 Pathology

  • 4.4.1 Vascular Architecture

  • 4.5 Natural History

  • 4.6 Clinical Aspects

  • 4.6.1 Tympanic Paragangliomas

  • 4.6.2 Jugular Paragangliomas

  • 4.6.3 Cervical Paragangliomas

  • 4.6.4 Paragangliomas in Other Locations

  • 4.6.5 Secretory Paragangliomas

  • 4.6.6 Associated Lesions

  • 4.7 Differential Diagnosis

  • 4.8 Pretherapeutic Evaluation

  • 4.8.1 Angiographic Protocol

  • 4.8.2 Temporal Paragangliomas: Specific Features

  • 4.8.3 Cervical Paragangliomas: Specific Features

  • 4.9 Therapeutic Strategies

  • 4.10 Technical Aspects of Embolization

  • 4.11 Complications of Embolization of Paragangliomas

5 Other Head and Neck Tumors

  • 5.1 Thyrolaryngeal Tumors

  • 5.2 Craniofacial Tumors

6 Traumatic ArteriovenousFistulae

  • 6.1 Introduction

  • 6.2 Traumatic Carotid Cavernous Fistulae

  • 6.2.1 Etiology and Epidemiology

  • 6.2.2 Clinical Aspects of Traumatic Carotid Cavernous Fistulae

  • 6.2.2.1 Ophthalmological Symptoms

  • 6.2.2.2 Corneal Ulcerations and/or Infections and Secondary Glaucoma

  • 6.2.2.3 Diplopia

  • 6.2.2.4 Cranial Nerve Involvementn in Traumatic Carotid Cavernous Fistulae

  • 6.2.2.5 Bruit

  • 6.2.2.6 Arterial Steal

  • 6.2.2.7 Hemispheric Arterial Insufficiency

  • 6.2.2.8 Associated Traumatic Lesions

  • 6.2.3 Pretherapeutic Evaluation

  • 6.2.3.1 Location of the Fistula

  • 6.2.3.2 Venous Drainage of the Fistula

  • 6.2.4 Therapeutic Objectives and Strategy

  • 6.2.4.1 Embolization

  • 6.2.4.2 Emergency Treatment

  • 6.2.4.3 Surgical Approach to Carotid Cavernous Fistulae

  • 6.2.4.4 Conservative Treatment of Traumatic Carotid Cavernous Fistulae

  • 6.2.5 Technical Aspects of Embolization

  • 6.2.5.1 Balloon Selection

  • 6.2.5.2 Manual Compression

  • 6.2.5.3 The Use of NBCA in the Management of Carotid Cavernous Fistulae

  • 6.2.6 Postembolization Care

  • 6.3 Other Traumatic Arteriovenous Fistulae

  • 6.3.1 Extracavernous Arteriovenous Fistulae

  • 6.3.2 Vertebral Arteriovenous Fistulae

  • 6.3.3 Common Carotid Fistulae

  • 6.3.4 External Carotid Fistulae

  • 6.3.5 Malignant Fistulae

  • 6.3.6 Other Epistaxis

  • 6.3.6.1 Coagulopathy

  • 6.3.6.2 Spontaneous Epistaxis

  • 6.3.6.3 Tumoral Epistaxis

  • 6.3.6.4 Biopsy

  • 6.3.6.5 Traumatic Epistaxis

7 Aneurysmal Vasculopathies

  • 7.1 From Aneurysm to Aneurysmal Vasculopathies

  • 7.1.1 General Perspectives

  • 7.1.1.1 Medical Challenge

  • 7.1.1.2 Decision-Making Challenge in Patients with Unruptured Aneurysms

  • 7.1.1.3 Ethical Challenge

  • 7.1.1.4 Academic and Nosological Challenges

  • 7.1.2 Physiopathogenesis and Risks

  • 7.1.2.1 Classification

  • 7.1.3 Segmental Vulnerability

  • 7.1.3.1 Embryological Origin

  • 7.1.3.2 Age of Aneurysms

  • 7.2 Extradural Aneurysms

  • 7.2.1 Introduction

  • 7.2.2 Extradural Internal Carotid Artery Aneurysms

  • 7.2.2.1 Cervical Internal Carotid Aneurysms

  • 7.2.2.2 Acute Spontaneous Dissection of the Carotid Artery

  • 7.2.2.3 Petrous Internal Carotid Artery Aneurysms

  • 7.2.2.4 Aneurysms of the Cavernous Segment of the Internal Carotid Artery

  • 7.2.2.5 Cervical Fibromuscular Dysplasia

  • 7.2.3 Internal Carotid Artery Occlusion in Extradural Internal Carotid Artery Aneurysms

  • 7.2.3.1 Tolerance to Carotid Occlusion

  • 7.2.3.2 Postembolization Care

  • 7.2.4 Extradural Vertebral Aneurysms

  • 7.2.5 Aneurysms of the External Carotid Artery

  • 7.3 Intradural Aneurysms

  • 7.3.1 Saccular Arterial Aneurysms and Associated Diseases

  • 7.3.1.1 Polycystic Kidney Disease

  • 7.3.1.2 EhlersDanlos Syndrome

  • 7.3.1.3 Neurofibromatosis Type 1

  • 7.3.1.4 Bourneville Disease

  • 7.3.1.5 Fibromuscular Dysplasia

  • 7.3.2 Saccular Arterial Aneurysms Without Diagnosed Associated Diseases

  • 7.3.2.1 Nonsyndromic Familial Arterial Aneurysms

  • 7.3.2.2 Multiple Saccular Arterial Aneurysms

  • 7.3.2.3 Arterial Anatomy, Single,Mirror, and Twin Saccular Arterial Aneurysms

  • 7.4 Intradural Artery Dissections

  • 7.5 Intradural Giant Saccular and Nonsaccular Arterial Aneurysms

  • 7.5.1 General Remarks

  • 7.5.2 Giant Intracranial Aneurysms with Thrombosis

  • 7.5.3 Nonsaccular Giant Arterial Aneurysms

  • 7.5.3.1 Megadolicho Arteries and Serpentine Arterial Aneurysms

  • 7.5.4 Multiple Giant Arterial Aneurysms and Mirror Giant Arterial Aneurysms

  • 7.6 Infectious, Immune, and Inflammatory Intradural Aneurysms

  • 7.6.1 Infectious Arterial Aneurysms

  • 7.6.2 Intradural Fusiform Aneurysms in Patients with Immune Deficiencies

  • 7.6.3 Inflammatory Diseases and Arterial Aneurysms

  • 7.7 Flow-Related Arterial Aneurysms and Other Aneurysmal Vasculopathies

  • 7.7.1 Intradural Traumatic Arterial Aneurysms

  • 7.7.2 Arterial Aneurysms Associated with Proliferative Diseases

  • 7.7.3 Arterial Aneurysms with Congenital Heart Disorders and Coarctation of the Aorta

  • 7.8 Therapeutic Management

  • 7.8.1 Introduction

  • 7.8.2 Method

  • 7.8.3 Results of the Endovascular Approach

  • 7.8.4 Management of Multiple Arterial Aneurysms

  • 7.8.5 Management of Giant Arterial Aneurysms

8 Dural Arteriovenous Shunts

  • 8.1 Historical Review

  • 8.2 Pathophysiology

  • 8.3 The OsteoduralVenous Complex

  • 8.3.1 Dural Venous Plexus

  • 8.3.2 Transdural Veins

  • 8.4 Classification

  • 8.5 Clinical Presentation of Dural Arteriovenous Shunts

  • 8.5.1 Cranial Nerve Symptoms

  • 8.5.2 Tinnitus and Objective Bruits

  • 8.5.3 Focal Neurological Deficits

  • 8.5.4 Global Neurological Deficits

  • 8.5.5 Intracranial Hemorrhage

  • 8.5.6 Hormonal Influences

  • 8.5.7 Associated Conditions and Multiplicity

  • 8.6 Natural History

  • 8.7 Progression of Symptoms

  • 8.8 Pretherapeutic Evaluation

  • 8.9 Therapeutic Aspects

  • 8.9.1 Indications and Strategy

  • 8.9.2 Topographic Considerations

  • 8.9.3 Technical Aspects

  • 8.9.4 Timing of Embolization

  • 8.9.5 Results of Embolization

  • 8.9.6 Complications of Embolization

  • 8.9.7 Surgery

9 Cerebral Vascular Malformations: Incidence, Classification,Angioarchitecture, and Symptomatology of BrainArteriovenous and Venous Malformations

  • 9.1 Incidence of Cerebral Vascular Malformations

  • 9.2 Principles of Classification

  • 9.3 Classification of Cerebral Vascular Malformations

  • 9.3.1 Brain Arteriovenous Shunts

  • 9.3.1.1 General Appearance of Arteriovenous Shunts

  • 9.3.1.2 Multiple Brain Arteriovenous Malformations

  • 9.3.1.3 Topographic Analysis of Brain Arteriovenous Malformations

  • 9.3.1.4 Angioarchitecture of Brain Arteriovenous Malformations

  • 9.3.1.5 ClinicalAngioarchitectural Correlation in Brain Arteriovenous Malformations

  • 9.3.2 Venous Variations,Malformations, and Mixed Lesions

  • 9.3.2.1 Developmental Venous Anomalies

  • 9.3.2.2 Cavernous Hemangiomas

  • 9.3.2.3 Cerebral Cavernous Malformations

  • 9.3.2.4 Occult and Cryptic Malformations

  • 9.3.2.5 SturgeWeber Syndrome

10 Goals and Objectives in the Management of Brain ArteriovenousMalformations

  • 10.1 Introduction

  • 10.2 Indications for Treatment of Brain Arteriovenous Malformations

  • 10.2.1 Age

  • 10.2.2 Sex

  • 10.2.3 Lifestyle and Occupation

  • 10.2.4 Presenting Symptoms

  • 10.2.4.1 Hemorrhage

  • 10.2.4.2 Seizures

  • 10.2.4.3 Headaches

  • 10.2.4.4 Neurological Deficits

  • 10.2.5 Location, Size, and Deep Venous Drainage

  • 10.2.6 Brain Arteriovenous Malformations and Arterial Aneurysms

  • 10.3 Therapeutic Management Strategy

  • 10.4 Embolization

  • 10.4.1 Partial (Targeted) Embolization

  • 10.4.2 Partial (Palliative) Embolization

  • 10.4.3 Curative Embolization

  • 10.4.4 Preoperative Embolization

  • 10.4.5 Intraoperative Embolization Therapy

  • 10.4.6 Embolization Prior to Radiosurgery

  • 10.4.6.1 Size Reduction

  • 10.4.6.2 Targeted Embolization Prior to Stereotactic Radiosurgery

  • 10.4.7 Staging of Embolization

  • 10.4.8 Emergency Embolization

  • 10.4.9 Contraindications for Endovascular Treatment

  • 10.4.10 Embolization Results

11 Spinal ArteriovenousMalformations

  • 11.1 Parachordal Arteriovenous Fistulae (Extracranial, Vertebro-Vertebral, Paraspinal, Extradural, and Extraspinal Arteriovenous Fistulae)

  • 11.1.1 General Remarks

  • 11.1.2 Cranial (Branchial) Arteriovenous Shunts

  • 11.1.2.1 Maxillary Artery-to-Vein Arteriovenous Fistulae (Stapedial)

  • 11.1.2.2 Ascending Pharyngeal-Internal Jugular Arteriovenous Fistulae (Hypoglossal)

  • 11.1.3 Vertebro-Vertebral Arteriovenous Fistulae (Proatlantal and Intersegmental)

  • 11.1.3.1 Vertebro-Vertebral Arteriovenous Fistulae

  • 11.1.3.2 Clinical Findings

  • 11.1.4 Paraspinal Arteriovenous Fistulae

  • 11.2 Spinal Cord Vascular Lesions

  • 11.3 Spinal Cord Arteriovenous Malformations

  • 11.3.1 Classification of Spinal Cord Arteriovenous Malformations

  • 11.3.2 Angioarchitecture

  • 11.3.2.1 Arterial Features

  • 11.3.2.2 Direct Arteriovenous Fistulae

  • 11.3.2.3 High-Flow Angiopathy

  • 11.3.2.4 Arterial Aneurysms in Spinal Cord Arteriovenous Malformations

  • 11.3.2.5 Dural Supply

  • 11.3.2.6 Nidus

  • 11.3.2.7 Veins

  • 11.3.3 Pretherapeutic Evaluation

  • 11.3.3.1 Clinical Assessment

  • 11.3.3.2 Noninvasive Imaging Modalities

  • 11.3.3.3 Angiography

  • 11.4 Spinal Cord Hemodynamics

  • 11.4.1 Particular Forms of Spinal Cord Arteriovenous Malformations

  • 11.4.1.1 Spinal Cord Intradural Arteriovenous Fistulae

  • 11.4.1.2 Spinal Arteriovenous Metameric Syndromes

  • 11.4.1.3 Associated Cerebral and Spinal Arteriovenous Malformations

  • 11.4.2 Clinical Aspects

  • 11.4.2.1 Natural History and Clinical Presentation

  • 11.4.2.2 Prognosis

  • 11.4.2.3 Aggravating Factors

  • 11.5 Treatment of Vascular Lesions

  • 11.5.1 Indications

  • 11.5.2 Results of Spinal Cord Arteriovenous Malformation Embolization

  • 11.5.3 Complications of Embolization

  • 11.5.4 Surgery in the Treatment of Spinal Cord Arteriovenous Malformations

  • 11.5.5 Radiotherapy of Spinal Cord Arteriovenous Malformations

  • 11.5.6 Medical Therapy

12 Spinal Dural ArteriovenousFistulae

  • 12.1 Pathology

  • 12.1.1 Macroscopic Appearance

  • 12.1.2 Microscopic Appearance

  • 12.1.3 Pathological Changes in the Spinal Cord

  • 12.2 Pathophysiology

  • 12.3 Clinical Presentation of Spinal Dural Arteriovenous Fistulae

  • 12.4 Imaging of Spinal Dural Arteriovenous Fistulae

  • 12.5 Treatment of Spinal Dural Arteriovenous Fistulae

  • 12.5.1 Indications

  • 12.5.2 Embolization of Spinal Dural Arteriovenous Fistulae: Techniques

  • 12.5.3 Results of Spinal Dural Arteriovenous Fistula Embolization

  • 12.5.4 Surgery for Spinal Dural Arteriovenous Fistulae

  • 12.5.5 Postoperative Follow-up

13 Tumors of the Spinal Columnand Spinal Cord

  • 13.1 Introduction

  • 13.2 Spinal Angiography

  • 13.3 Angiographic Protocol

  • 13.4 Embolization

  • 13.4.1 Cervical Tumors

  • 13.4.2 Thoracic, Lumbar, and Sacral Tumors

  • 13.4.3 Chemoembolization

  • 13.4.4 Intralesional Embolization

  • 13.5 Benign Tumors

  • 13.5.1 Vertebral Hemangiomas

  • 13.5.1.1 Associated Lesions

  • 13.5.1.2 Pretherapeutic Evaluation

  • 13.5.1.3 Treatment

  • 13.5.1.4 Embolization

  • 13.5.2 Aneurysmal Bone Cysts

  • 13.5.2.1 Clinical Presentation

  • 13.5.2.2 Pretherapeutic Evaluation

  • 13.5.2.3 Angiography

  • 13.5.2.4 Differential Diagnosis

  • 13.5.2.5 Pathogenesis

  • 13.5.3 Other Benign Vascular Tumors

  • 13.5.4 Giant Cell Tumors

  • 13.5.4.1 Pathology

  • 13.5.4.2 Clinical Presentation

  • 13.5.4.3 Radiographic Findings

  • 13.5.4.4 Embolization

  • 13.6 Malignant Tumors

  • 13.6.1 Pretherapeutic Evaluation

  • 13.6.2 Embolization

  • 13.7 Spinal Cord Tumors

  • 13.7.1 Hemangioblastomas

  • 13.7.1.1 Histopathology

  • 13.7.1.2 von Hippel-Lindau Disease

  • 13.7.2 Pretherapeutic Evaluation of Hemangioblastomas

  • 13.7.2.1 Computerized Tomography

  • 13.7.2.2 Magnetic Resonance Imaging

  • 13.7.2.3 Angiography

  • 13.7.3 Feeding Arteries

  • 13.7.4 Draining Veins

  • 13.7.5 Treatment and Embolization

  • 13.8 Other Intradural Vascular Tumors and Spinal Hemorrhage

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