Diffusion Weighted MR Imaging of the Brain, Head and Neck, and Spine

Preface to the 3rd edition
Acknowledgements
Contents
Contributors
Part I: Principles of DW Imaging
	1: Basics of Diffusion Measurements by MRI
		1.1	 Diffusion: A Probabilistic Process
		1.2	 Diffusion Imaging in MR
		1.3	 Diffusion Imaging of the Brain
		1.4	 Principles of Magnetic Resonance Diffusion Imaging
		1.5	 Apparent Diffusion Coefficient
		1.6	 Diffusion Represents a Molecular Event
		1.7	 Requirements in Clinical Diffusion Imaging
		1.8	 Setting the b Value in Clinical DW Imaging
		1.9	 Future Trends in Clinical Diffusion Imaging
		References
	2: Diffusion-Weighted and Tensor Imaging of the Normal Brain
		2.1	 Introduction
		2.2	 Adult Brain
			2.2.1	 Low Signal in Basal Ganglia
			2.2.2	 Diffusion-Weighted Imaging of Gray and White Matter
			2.2.3	 Choroid Plexus
		2.3	 Pediatric Brain
			2.3.1	 Diffusion-Weighted Imaging and ADC of the Pediatric Brain
		2.4	 Diffusion Tensor Imaging and White Matter Anatomy
			2.4.1	 Association Fibers
			2.4.2	 Projection Fibers
			2.4.3	 Commissural Fibers
			2.4.4	 Fibers of the Brain Stem and Cerebellum
			2.4.5	 Clinical Importance of White Matter Fiber Anatomy
		2.5	 Conclusion
		References
	3: Pitfalls and Artifacts of Diffusion-Weighted Imaging
		3.1	 Introduction
		3.2	 Influence of ADC and T2 on the DW Appearance
			3.2.1	 Concepts
			3.2.2	 Apparent Diffusion Coefficient Maps
			3.2.3	 Exponential Images
		3.3	 Clinical Conditions
			3.3.1	 T2 Shine-Through
			3.3.2	 T2 Washout
			3.3.3	 T2 Blackout
		3.4	 Artifacts
			3.4.1	 Eddy Current Artifacts
			3.4.2	 Susceptibility Artifacts
			3.4.3	 N/2 Ghosting Artifact (Nyquist Ghost)
			3.4.4	 Chemical Shift
			3.4.5	 Motion Artifacts
		3.5	 Conclusion
		References
	4: Diffusion Tensor and Kurtosis
		4.1	 Preface
			4.1.1	 Theoretical Considerations for Diffusion Tensor and Diffusion Kurtosis Imaging
				4.1.1.1	 Diffusion-Weighted Imaging
				4.1.1.2	 Diffusion Tensor Imaging Based on a Gaussian Distribution
				4.1.1.3	 Non-Gaussian Diffusion and Diffusion Kurtosis Imaging
			4.1.2	 Studies Using Diffusion Kurtosis Imaging for Central Nervous System Diseases
				4.1.2.1	 Cerebrovascular Diseases
				4.1.2.2	 Brain Tumors
				4.1.2.3	 Demyelinating Diseases
				4.1.2.4	 Neurodegenerative Diseases
				4.1.2.5	 Development and Developmental Abnormalities
			4.1.3	 Glymphatic System and Diffusion Imaging
		4.2	 Conclusion
		References
	5: Intravoxel Incoherent Motion Imaging
		5.1	 Intravoxel Incoherent Motion Concept
		5.2	 IVIM Imaging
		5.3	 Methods of IVIM Analysis
		5.4	 Neuroimaging Applications of IVIM Imaging
			5.4.1	 Physiological Applications
			5.4.2	 IVIM Imaging of Brain Tumors
			5.4.3	 IVIM Imaging of Gliomas
			5.4.4	 Other Brain Tumors
			5.4.5	 Stroke and Brain Ischemia
			5.4.6	 Head and Neck Lesions
		5.5	 Pitfalls and Technical Limitations
		References
	6: Functional MRI and Diffusion Tensor Imaging
		6.1	 Introduction
		6.2	 Functional MRI
		6.3	 HRF and BOLD Imaging
		6.4	 Regional Organization of Brain Systems
			6.4.1	 Primary Sensorimotor Cortex
			6.4.2	 Primary Language Areas
			6.4.3	 Primary Visual and Association Cortex
			6.4.4	 Supplementary Motor Areas
		6.5	 Paradigms and Design
		6.6	 Functional Mapping in Brain Tumor Surgery
		6.7	 Pearls and Pitfalls of Interpretation
		6.8	 Diffusion Tensor Imaging
		6.9	 White Matter Tracts
			6.9.1	 Projection Fibers
			6.9.2	 Association Fibers
			6.9.3	 Commissural Fibers
			6.9.4	 Fibers of Brainstem and Cerebellum
		6.10	 Diffusion Fiber Tracking
		6.11	 Presurgical Brain Mapping with DTI
		References
	7: Physics of Advanced Diffusion Imaging
		7.1	 Pitfalls of the Diffusion Tensor Model
		7.2	 Diffusion Signal of Crossing Fibers
		7.3	 Modifications to the Single Exponential Decay Assumption
		7.4	 Biophysical Compartment Models
		7.5	 Q-Space Imaging Approaches
		7.6	 Summary of Advanced Diffusion Protocols
		7.7	 Future Development of Advanced Diffusion Studies
		References
Part II: Clinical Applications of DW Imaging
	8: Brain Edema
		8.1	 Characterization and Classification of Brain Edema
		8.2	 Cytotoxic or Cellular Edema
		8.3	 Pathophysiology of Cytotoxic Edema
			8.3.1	 Energy Failure
			8.3.2	 Excitotoxic Brain Injury
			8.3.3	 Cytokinopathy/Cytokine Storm and Excitotoxic Mechanisms (Fig. 8.14)
		8.4	 Diffusion-Weighted Imaging and Cytotoxic Edema
			8.4.1	 Conditions that Cause Cytotoxic Edema, and Reversibility
				8.4.1.1	 Cytotoxic Edema of Neurons and Glial Cells
				8.4.1.2	 Cytotoxic Edema and Cortical Spreading Depolarization/Depression
				8.4.1.3	 Axonal Swelling
				8.4.1.4	 Intramyelinic Edema
		8.5	 Vasogenic or Interstitial Edema
			8.5.1	 Conditions that Cause Vasogenic Edema
		8.6	 Diffusion Tensor Imaging and Edema
		8.7	 Conclusion
			8.7.1	 Cytotoxic or Cellular Edema
			8.7.2	 Vasogenic Edema
		8.8	 Brain Edema—Treatment
			8.8.1	 Introduction
			8.8.2	 Types of Cerebral Edema and Diagnosis
			8.8.3	 Mechanisms of Cerebral Edema by Pathology
				8.8.3.1	 Tumor-Associated Edema
				8.8.3.2	 Stroke-Associated Edema
				8.8.3.3	 Intracranial Hemorrhage-Associated Edema
				8.8.3.4	 Traumatic Brain Injury-Related Edema
			8.8.4	 Diagnosis and Clinical Monitoring of Cerebral Edema
			8.8.5	 Medical Management of Cerebral Edema
				8.8.5.1	 General Measures
				8.8.5.2	 Tumor-Related Edema
				8.8.5.3	 Stroke-Related Edema
				8.8.5.4	 Traumatic Brain Injury-Related Edema
			8.8.6	 Surgical Management of Cerebral Edema
				8.8.6.1	 Tumor-Related Edema
				8.8.6.2	 Stroke-Related Edema
				8.8.6.3	 Traumatic Brain Injury-Associated Edema
			8.8.7	 Future of Edema Management
			8.8.8	 Summary of Cerebral Edema Treatment
		References
	9: Infarction
		9.1	 Introduction
			9.1.1	 Diffusion-Weighted Imaging (DWI)
		9.2	 Diffusion-Weighted Imaging and Pathophysiology of Cerebral Infarction
		9.3	 Apparent Diffusion Coefficient (ADC)
			9.3.1	 Explanation for Restricted Diffusion
		9.4	 Time Course of Infarction
			9.4.1	 Hyperacute (<6 h)
			9.4.2	 Acute (6 h to 3 Days)
			9.4.3	 Subacute (3 Days to 3 Weeks)
			9.4.4	 Chronic (3 Weeks to 3 Months)
		9.5	 Diffusion-Weighted Imaging and ADC Characteristics of Gray and White Matter Ischemia
		9.6	 Reversibility and Treatment
		9.7	 Watershed Infarction
		9.8	 Perfusion Versus Diffusion Imaging
		9.9	 Venous Infarction
			9.9.1	 Predisposing Factors
			9.9.2	 Pathophysiology and Imaging
		9.10	 Small Vessel (Lacunar) Infarcts
		9.11	 Brain Stem and Cerebellar Infarcts
		9.12	 Atypical Infarcts
			9.12.1	 Anterior Choroidal Artery
			9.12.2	 Subcallosal Artery
			9.12.3	 Recurrent Artery of Heubner
			9.12.4	 Artery of Percheron
			9.12.5	 Transient Global Amnesia
			9.12.6	 Corpus Callosum Infarcts
		9.13	 Stroke Mimickers
			9.13.1	 Hemiplegic Migraine
			9.13.2	 Stroke-like Migraine Attacks after Radiation Therapy (SMART) Syndrome
		9.14	 Hemorrhagic Infarcts
		9.15	 Diffusion Tensor Imaging
		9.16	 High-b-Value Diffusion-Weighted Imaging
		9.17	 Thin-Section Diffusion-Weighted Imaging
		9.18	 Treatment of Ischemic Stroke
			9.18.1	 Procedural Details and Considerations
		References
	10: Intracranial Hemorrhage
		10.1	 Introduction
		10.2	 lntraparenchymal Hemorrhages: Appearance and Evolution (Fig. 10.1 and Tables 10.1 and 10.2)
			10.2.1 Hyperacute Hematoma
			10.2.2 Acute Hematoma
			10.2.3 Early Subacute Hematoma
			10.2.4 Late Subacute Hematomas
			10.2.5 Chronic Hematomas
			10.2.6 Perihematomal Edema and Injury
		10.3	 Subarachnoid Hemorrhage
		10.4	 Subdural and Epidural Hematoma
		10.5	 Intraventricular Hemorrhage
		10.6	 Intratumoral Hemorrhage
		10.7	 Hemorrhage Related to Vascular Malformation
		10.8	 Hemorrhage Related to Trauma (See Also Chap. 17)
		10.9	 Conclusions
		10.10	 Treatment of Intracranial Hemorrhage
			10.10.1 Introduction
			10.10.2 Extra-axial Hemorrhage (Epidural and Subdural Hematoma)
				10.10.2.1	 Epidemiology
				10.10.2.2	 Pathophysiology
				10.10.2.3	 Clinical Presentation
				10.10.2.4	 Diagnosis
				10.10.2.5	 Imaging
				10.10.2.6	 Acute Management
				10.10.2.7	 Surgical Management
				10.10.2.8	 Medical Management
				10.10.2.9	 Prognosis
			10.10.3 Subarachnoid Hemorrhage
				10.10.3.1	 Epidemiology
				10.10.3.2	 Pathophysiology
				10.10.3.3	 Clinical Presentation
				10.10.3.4	 Diagnosis
				10.10.3.5	 Imaging
				10.10.3.6	 Acute Management
				10.10.3.7	 Surgical Management
				10.10.3.8	 Medical Management
				10.10.3.9	 Prognosis
			10.10.4 Intraparenchymal Hemorrhage
				10.10.4.1	 Epidemiology/Pathophysiology
				10.10.4.2	 Clinical Presentation/Diagnosis/Imaging
				10.10.4.3	 Surgical Management
				10.10.4.4	 Medical Management
				10.10.4.5	 Prognosis
			10.10.5 Summary
		References
	11: Vasculopathy and Vasculitis
		11.1	 Definition
		11.2	 Clinical Presentation
		11.3	 Role of Imaging
		11.4	 Treatment
		11.5	 Vasculitis of the CNS
			11.5.1 Primary Angiitis of the Central Nervous System
			11.5.2 Giant Cell (Temporal) Arteritis
			11.5.3 Takayasu’s Arteritis (Aortitis Syndrome)
			11.5.4 Polyarteritis Nodosa
			11.5.5 Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss Syndrome)
			11.5.6 Other Small Vessel Vasculitis
			11.5.7 Variable Vessel Vasculitis
				11.5.7.1	 Bechet’s Disease
				11.5.7.2	 Cogan Syndrome
			11.5.8 Infectious Vasculitis
			11.5.9 Drug-Induced Vasculitis, Including Illicit Drugs
			11.5.10 Vasculitis Associated with Systemic Diseases
		11.6	 Vasculopathy of the CNS
			11.6.1 Moyamoya Disease
			11.6.2 Sickle Cell Disease (SCD)
		11.7	 Posterior Reversible Encephalopathy Syndrome
			11.7.1 Reversible Cerebral Vasoconstriction Syndrome (RCVS)
			11.7.2 CADASIL and CARASIL
			11.7.3 Susac Syndrome
			11.7.4 Uremic Encephalopathy and Uremic Hemolytic Syndrome
			11.7.5 Thrombotic Thrombocytopenic Purpura
				11.7.5.1	 Cerebral Amyloid Angiopathy
				11.7.5.2	 Amyloid Beta-Related Angiitis (ABRA)
			11.7.6 Hypereosinophilic Syndrome
			11.7.7 Radiation-Induced Vasculopathy
			11.7.8 Miscellaneous Vasculopathies
		11.8	 Conclusion
		11.9	 Treatment of CNS Vasculitis and Vasculopathy
			11.9.1 Primary Angiitis of the Central Nervous System
			11.9.2 Giant Cell (Temporal) Arteritis
			11.9.3 Takayasu Arteritis (Aortitis Syndrome)
			11.9.4 Polyarteritis Nodosa and Churg-Strauss Disease
			11.9.5 Henoch-Schonlein Purpura
			11.9.6 Microscopic Polyangiitis
			11.9.7 Cryoglobulinemia
			11.9.8 Hypersensitivity (Leukocytoclastic) Vasculitis
			11.9.9 Behcet’s Disease
				11.9.9.1	 General Management
				11.9.9.2	 Corticosteroids
			11.9.10 Scleroderma
			11.9.11 Rheumatoid Arthritis
			11.9.12 Infectious Vasculitides
				11.9.12.1	 Viral-Related Vasculitides
				11.9.12.2	 Bacterial-Related Vasculitides
				11.9.12.3	 Fungal-Related Vasculitides
			11.9.13 Drug-Induced Vasculitis/Vasculopathy, Including Illicit Drugs
		11.10	 Vasculopathy
			11.10.1 Systemic Lupus Erythematosus
			11.10.2 Moyamoya Disease
				11.10.2.1	 Antiplatelets
				11.10.2.2	 Calcium Channel Blockers
				11.10.2.3	 Revascularization Surgery
			11.10.3 Sickle Cell Disease
				11.10.3.1	 Transcranial Doppler Screening
				11.10.3.2	 Exchange Transfusions
				11.10.3.3	 Hydroxyurea
			11.10.4 Neurosarcoidosis
				11.10.4.1	 General
				11.10.4.2	 Immunosuppression
				11.10.4.3	 Radiation Therapy
				11.10.4.4	 Surgical Intervention
			11.10.5 Posterior Reversible Encephalopathy Syndrome/Hypertensive Encephalopathy
				11.10.5.1	 General Management
				11.10.5.2	 Blood Pressure Management
			11.10.6 Reversible Cerebral Vasoconstriction Syndrome (RCVS)
				11.10.6.1	 General Management
				11.10.6.2	 Immunosuppressants
				11.10.6.3	 Calcium Channel Blockers
			11.10.7 Preeclampsia/Eclampsia
				11.10.7.1	 General Management and Monitoring
				11.10.7.2	 Blood Pressure Management
				11.10.7.3	 Antiplatelets
				11.10.7.4	 Magnesium
			11.10.8 Hemolytic Uremic Syndrome
			11.10.9 Cerebral Amyloid Angiopathy
				11.10.9.1	 Anticoagulation and Antiplatelets
				11.10.9.2	 Blood Pressure Control
				11.10.9.3	 Immunosuppression
			11.10.10 Susac Syndrome
				11.10.10.1	 Immunosuppressants
				11.10.10.2	 Anticoagulation and Antiplatelets
			11.10.11 Hypereosinophilic Syndrome
				11.10.11.1	 Imatinib
				11.10.11.2	 Corticosteroids
				11.10.11.3	 Steroid-Sparing Agents
		References
	12: Epilepsy
		12.1	 Definition
		12.2	 Classification
		12.3	 Mechanisms and Pathophysiology of Seizures
		12.4	 Anatomy of the Limbic Lobe on MRI
		12.5	 Hippocampal Malrotation (HIMAL)
		12.6	 MR Imaging of Epilepsy Substrates
			12.6.1 Hippocampal Sclerosis (HS)
			12.6.2 Amygdala Enlargement (AE)
			12.6.3 Malformations of Cortical Development (MCD)
			12.6.4 Brain Tumors Associated with Epilepsy
		12.7	 MR Imaging of Seizure Activity
			12.7.1 Ictal Stage to Peri-ictal Stage
		12.8	 Status Epilepticus (SE)
			12.8.1 Cytotoxic Edema in Status Epilepticus
		12.9	 Acute Encephalopathy with Biphasic Seizures and Late Reduced Diffusion (AESD)
		12.10	 Hemiconvulsion-Hemiplegia Epilepsy Syndrome and Rasmussen Encephalitis
		12.11	 Limbic Encephalitis
		12.12	 Focal Reversible Lesion of the Splenium of the Corpus Callosum
		12.13	 Conclusion
		12.14	 Treatment of Epilepsy
			12.14.1 Treatment
			12.14.2 Diet
			12.14.3 Immunotherapy
			12.14.4 Surgery
				12.14.4.1	 Medial Temporal Lobe Epilepsy
			12.14.5 Electrical Stimulation
		References
	13: Demyelinating Diseases
		13.1	 Demyelinating Diseases
			13.1.1 Multiple Sclerosis (MS)
			13.1.2 Clinically Isolated Syndrome (CIS) and Radiologically Isolated Syndrome (RIS)
			13.1.3 Baló’s Concentric Sclerosis
			13.1.4 Myelinoclastic Diffuse Sclerosis (Schilder’s Disease)
			13.1.5 MS Mimics
			13.1.6 Neuromyelitis Optica Spectrum Disorder (NMOSD)
			13.1.7 Anti-myelin Oligodendrocyte Glycoprotein Antibody (MOG)-Related Demyelination
			13.1.8 Tumefactive Demyelination (TD)
			13.1.9 Acute Disseminated Encephalomyelitis
			13.1.10 Acute Hemorrhagic Leukoencephalitis
		13.2	 Systemic Lupus Erythematosus (SLE)
		13.3	 Steroid-Responsive Encephalopathy Associated with Autoimmune Thyroiditis (Hashimoto’s Encephalopathy)
		13.4	 Chronic Lymphocytic Inflammation with Pontine Perivascular Enhancement Responsive to Steroids (CLIPPERS)
		13.5	 Miscellaneous Conditions
			13.5.1 Erdheim Chester Disease (ECD)
			13.5.2 Hemophagocytic Lymphohistiocytosis (HLH)
		13.6	 Progressive Multifocal Leukoencephalopathy
		13.7	 Conclusion
		13.8	 Treatment of Demyelinating Diseases Section
			13.8.1 Multiple Sclerosis Treatment
				13.8.1.1 Acute Treatment of Multiple Sclerosis Relapses
				13.8.1.2 Multiple Sclerosis Disease-Modifying Therapy
					Relapsing Remitting Multiple Sclerosis Disease-Modifying Therapy
					Progressive Multiple Sclerosis Disease-Modifying Therapy
			13.8.1.3 Pediatric Multiple Sclerosis Treatment
				13.8.2 Acute Disseminated Encephalomyelitis (ADEM) Treatment
			13.8.3 Neuromyelitis Optica Spectrum Disorders (NMOSD) Treatment
				13.8.3.1 Treatment of NMOSD Relapses
				13.8.3.2 NMOSD Maintenance Treatment
			13.8.4 Progressive Multifocal Leukoencephalopathy (PML) Treatment
		References
	14: Degenerative Diseases of the CNS
		14.1	 Alzheimer’s Disease (AD)
			14.1.1 DWI in AD
			14.1.2 Atypical AD Variants
			14.1.3 Other Tauopathies
				14.1.3.1	 Corticobasal Degeneration (CBD)
				14.1.3.2	 Progressive Supranuclear Palsy (PSP)
		14.2	 Dementia with Lewy Body Disease (LBD)
			14.2.1 Imaging
			14.2.2 DTI
		14.3	 Parkinson’s Disease (PD)
			14.3.1 Imaging
			14.3.2 DWI in PD
		14.4	 Multiple System Atrophy (MSA)
			14.4.1 DWI in MSA
		14.5	 Frontotemporal Lobar Degeneration
			14.5.1 Introduction
				14.5.1.1	 Imaging
				14.5.1.2	 DTI
		14.6	 Vascular Dementia
		14.7	 Fragile X Syndrome (FXS)
		14.8	 Creutzfeldt-Jakob Disease (CJD)
		14.9	 Neuronal Intranuclear Inclusion Disease (NIID)
		14.10	 Hereditary Diffuse Leukoencephalopathy with Axonal Spheroids (HDLS)
		14.11	 Amyotrophic Lateral Sclerosis (ALS)
		14.12	 Huntington Disease (HD)
		14.13	 Secondary Neuronal Degeneration (Wallerian, Transneuronal, and Retrograde Degeneration)
		14.14	 Treatment Section: Treatment of Dementia
			14.14.1 Alzheimer’s Disease (AD)
			14.14.2 Vascular Dementia (VaD)
			14.14.3 Dementia with Lewy Bodies (DLB)
			14.14.4 Symptomatic Treatment Options for DLB
			14.14.5 Parkinson’s Disease (PD)
		References
	15: Toxic and Metabolic Diseases
		15.1	 Toxic Disease
			15.1.1 Chemotherapy-Induced Leukoencephalopathy
			15.1.2 Carbon Monoxide Intoxication
			15.1.3 Cocaine, Phencyclidine Hydrochloride, Amphetamines, and Related Catecholaminergics
			15.1.4 Opiods (Morphine, Methadone, Oxycodone, Heroin)
			15.1.5 Metronidazole Induced Encephalopathy
			15.1.6 Marchiafava–Bignami Disease
		15.2	 Metabolic Diseases
			15.2.1 Hypoxic–Ischemic Encephalopathy
			15.2.2 Delayed Postanoxic Encephalopathy
			15.2.3 Brain Death
			15.2.4 Hypoglycemia and Hyperglycemia
			15.2.5 Osmotic Demyelination (OD)
			15.2.6 Wernicke’s Encephalopathy
			15.2.7 Hyperammonemic Encephalopathy
			15.2.8 Wilson’s Disease (WD)
			15.2.9 Mitochondrial Encephalopathies
			15.2.10 SMART Syndrome
		15.3	 Treatment of Toxic and Metabolic Diseases 1
			15.3.1 Chemotherapy-Induced Leukoencephalopathy
			15.3.2 Heroin-Induced Spongiform Leukoencephalopathy
			15.3.3 Cocaine, Phencyclidine Hydrochloride, Amphetamines, and Related Catecholaminergics
			15.3.4 Hypoxic–Ischemic Encephalopathy
			15.3.5 Hypoglycemia and Hyperglycemia
			15.3.6 Carbon Monoxide Intoxication
			15.3.7 Delayed Postanoxic Encephalopathy
			15.3.8 Osmotic Demyelination
			15.3.9 Wernicke Encephalopathy
			15.3.10 Marchiafava–Bignami Disease
			15.3.11 Steroid-Responsive Encephalopathy Associated with Autoimmune Thyroiditis (Hashimoto’s Encephalopathy)
		15.4	 Treatment of Toxic and Metabolic Disease 2
			15.4.1 Brain Death Management
				15.4.1.1	 History of Brain Death Concept
				15.4.1.2	 Diagnostic Criteria for Brain Death
				15.4.1.3	 Neuropathology
				15.4.1.4	 Brain Death Causes
				15.4.1.5	 Brain Death Mimickers
				15.4.1.6	 Determination of Brain Death
				15.4.1.7	 Future Directions
		References
	16: Infectious Diseases
		16.1	 Overview of Brain Infections
		16.2	 Bacterial Infection
			16.2.1	 Brain Abscess and Cerebritis
			16.2.2	 Septic Emboli
			16.2.3	 Brain Abscess Caused by Unusual Bacteria
				16.2.3.1	 Differential Diagnosis
			16.2.4	 Bacterial Abscess in the Extra-Axial Space
				16.2.4.1	 Differential Diagnosis
			16.2.5	 Bacterial Vasculitis
			16.2.6	 Whipple Disease
		16.3	 Parasitic Infection
			16.3.1	 Toxoplasmosis
				16.3.1.1	 Differential Diagnosis
			16.3.2	 Neurocysticercosis
			16.3.3	 Cerebral Malaria
		16.4	 Fungal Infection
			16.4.1	 Aspergillosis
			16.4.2	 Mucormycosis
			16.4.3	 Cryptococosis
			16.4.4	 Candidiasis
			16.4.5	 Histoplasmosis
			16.4.6	 Blastomycosis
			16.4.7	 Coccidioidomycosis
		16.5	 Viral Infection
			16.5.1	 Herpes Simplex Encephalitis (HSE) Infection
			16.5.2	 Varicella Zoster Virus (VZV) Infection
			16.5.3	 Epstein-Barr Virus (EBV) Infection
			16.5.4	 Human Herpesvirus-6 (HHV6) Infection
			16.5.5	 Brain Stem Encephalitis
			16.5.6	 West Nile Encephalitis
			16.5.7	 Human Immunodeficiency Virus Infection
			16.5.8	 Progressive Multifocal Leukoencephalopathy (PML)
			16.5.9	 Coronavirus Disease 2019 (COVID-19)
		16.6	 Treatment of Infectious Diseases
			16.6.1	 Brain Abscess and Other Intracranial Suppurative Diseases (Subdural Empyema, Epidural Abscess, Ventriculitis)
				16.6.1.1	 Bacterial Brain Abscess
				16.6.1.2	 Fungal Brain Abscess
				16.6.1.3	 Subdural Empyema and Epidural Abscess
				16.6.1.4	 Pyogenic Ventriculitis
			16.6.2	 Meningitis
				16.6.2.1	 Acute Bacterial Meningitis
			16.6.3	 Management of Encephalitis and Viral Infections
				16.6.3.1	 Herpes Simplex Virus (HSV)
				16.6.3.2	 Varicella-Zoster Virus (VZV)
				16.6.3.3	 Human Herpesvirus Types 6 (HHV-6)
				16.6.3.4	 Progressive Multifocal Leukoencephalopathy (PML)
			16.6.4	 HIV
				16.6.4.1	 Opportunistic Infections (Cryptococcal Meningitis)
				16.6.4.2	 Management of Brain Mass Lesions in a HIV-Positive Patient (CNS Toxoplasmosis and CNS Lymphoma)
				16.6.4.3	 HIV-Associated Neurocognitive Disorder (HAND)
		References
	17: Trauma
		17.1	 Introduction
		17.2	 Diffuse Axonal Injury
		17.3	 Grading of DAI and Location
		17.4	 Computed Tomography (CT) and Magnetic Resonance (MR) Imaging
		17.5	 Diffusion-Weighted Imaging (DWI)
		17.6	 Pediatric Patients
		17.7	 Hypoxic Ischemic Injuries
		17.8	 Cerebral Fat Embolism (CFE)
		17.9	 Traumatic Optic Neuropathy (TON)
		17.10	 DWI in Mild Traumatic Brain Injuries (mTBI)
		17.11	 Diffusion Tensor Imaging (DTI) and Fractional Anisotropy (FA)
		17.12	 Diffusion Kurtosis Imaging (DKI)
		17.13	 DWI Thermometry
		17.14	 DWI and Cognition
		17.15	 DWI in Focal Traumatic Lesions
		17.16	 Contusions
		17.17	 Extra-axial Hematoma
		17.18	 Diffusion in Vascular Injuries and Infarcts
		17.19	 Diffusion in Secondary Injuries and Postoperative Complications
		17.20	 Summary
		17.21	 Treatment of Head Injury
			17.21.1	 Space-Occupying Lesion
		References
	18: Brain Neoplasm
		18.1	 Introduction
		18.2	 Tumors of Neuroepithelial Tissue
			18.2.1 Localized Astrocytomas (Other Astrocytomas)
			18.2.2 Diffuse Astrocytic and Oligodendroglial Tumors
			18.2.3 High-Grade Gliomas
			18.2.4 Peritumoral Infiltration
			18.2.5 Gliomatosis Cerebri
			18.2.6 Pseudoprogression and Pseudoresponse
			18.2.7 Gliosarcoma
			18.2.8 Ependymal Tumors
			18.2.9 Other Gliomas
			18.2.10 Choroid Plexus Tumors
		18.3	 Neuronal and Mixed Neuronal-Glial Tumors
			18.3.1 Dysplastic Cerebellar Gangliocytoma (DCG)/Lhermitte-Duclos Disease
			18.3.2 Dysembryoplastic Neuroepithelial Tumor (DNET)
			18.3.3 Ganglioglioma
			18.3.4 Central Neurocytoma
		18.4	 Tumors of Pineal Region
		18.5	 Embryonal Tumors
		18.6	 Tumors of Cranial and Spinal Nerves
		18.7	 Mesenchymal Meningothelial Tumors
			18.7.1 Meningioma and Its Variants
		18.8	 Mesenchymal Non-meningothelial Tumors
			18.8.1 Hemangiopericytoma
			18.8.2 Hemangioblastoma
			18.8.3 Lipoma
		18.9	 Lymphoma and Hematopoietic Neoplasm
			18.9.1 Primary CNS Lymphoma
			18.9.2 Posttransplant Lymphoproliferative Disorder (PTLD)
			18.9.3 Histiocytic Tumors
			18.9.4 CNS Manifestations of Leukemia
		18.10	 Germ Cell Tumor
		18.11	 Epidermoid Cysts and Arachnoid Cysts
			18.11.1 Epidermoid Cyst
			18.11.2 Arachnoid Cyst
		18.12	 Tumors of the Sellar Region
			18.12.1 Craniopharyngioma
			18.12.2 Rathke’s Cleft Cyst
			18.12.3 Germ Cell Tumor
			18.12.4 Pituitary Adenoma
		18.13	 Metastatic Tumors
		18.14	 Radiation Necrosis
		18.15	 Conclusion
		18.16	 Treatment of Brain Neoplasm 1: Medical Management of Primary Brain Tumors in Adult
			18.16.1 Introduction
			18.16.2 Treatment of Infiltrating Gliomas
				18.16.2.1	 Glioblastoma
				18.16.2.2	 Astrocytoma
				18.16.2.3	 Oligodendroglioma
				18.16.2.4	 Diffuse Midline Glioma, H3 K27M Mutant
			18.16.3 Treatment of Primary CNS Lymphoma
			18.16.4 Future Directions
				18.16.4.1	 Targeted Therapy
				18.16.4.2	 Heterogeneity
		18.17	 Treatment of Brain Neoplasm 2: Radiation Therapy for Brain Tumors: Brain Metastases and Malignant Glioma
			18.17.1 Brain Metastases
				18.17.1.1	 Background
				18.17.1.2	 Radiation Treatment Techniques
				18.17.1.3	 Diagnosis and Imaging Assessment
				18.17.1.4	 Surveillance
				18.17.1.5	 Malignant Glioma
		R eferences
	19: Pediatrics
		19.1	 Introduction
		19.2	 Water Content of the Pediatric Brain
		19.3	 Normal Structures
		19.4	 Diffusion Tensor Imaging and Anisotropy
		19.5	 Infarction and Ischemia
			19.5.1 Moyamoya Disease
			19.5.2 Sickle Cell Disease
			19.5.3 Cerebral Venous Sinus Thrombosis
			19.5.4 Vein of Galen Malformations
			19.5.5 Hypoxic Ischemic Encephalopathy
			19.5.6 Hypoglycemic Encephalopathy
		19.6	 Trauma
			19.6.1 Nonaccidental Head Injury
			19.6.2 Diffuse Axonal Injury and Brain Contusion
		19.7	 Infections
			19.7.1 Encephalitis
			19.7.2 Brain Abscess
			19.7.3 Acute Flaccid Myelitis
		19.8	 Tumors
			19.8.1 Brain Tumors
		19.9	 Encephalopathies
			19.9.1 Hypertensive Encephalopathy/Posterior Reversible Encephalopathy Syndrome (PRES)
			19.9.2 Acute Necrotizing Encephalopathy
		19.10	 Demyelinating Diseases
			19.10.1 Acute Disseminated Encephalomyelitis and Multiple Sclerosis
		19.11	 Metabolic and Toxic Diseases
			19.11.1 Charcot-Marie-Tooth
			19.11.2 Central Tegmental Tract Hyperintense Lesions
			19.11.3 Inborn Errors of Metabolism Including Leukodystrophies
			19.11.4 Lysosomal Disorders
			19.11.5 Peroxisome Disorders
			19.11.6 Mitochondrial Disorders
			19.11.7 Metabolic Leukoencephalopathies
		19.12	 Congenital Anomalies
			19.12.1 Sturge–Weber Syndrome
			19.12.2 Hemimegalencephaly
			19.12.3 Polymicrogyria, Focal Cortical Dysplasia, and Tuberous Sclerosis
			19.12.4 Corpus Callosum Agenesis/Dysgenesis
			19.12.5 Other Anomalies
		19.13	 Conclusion
		19.14	 Treatment 1: Leukodystrophy
			19.14.1 Definition
			19.14.2 Presentation
			19.14.3 Diagnostic Evaluation
			19.14.4 Treatment
		19.15	 Treatment 2: Pediatric Brain Tumors
			19.15.1 Neurosurgery
			19.15.2 Radiation Therapy
			19.15.3 Chemotherapy
			19.15.4 Progress in Targeted Therapy and Immunotherapy
		Ref erences
	20: Head and Neck
		20.1	 Introduction
		20.2	 Cholesteatomas
		20.3	 Subcutaneous and Intracranial Epidermoid Cysts
		20.4	 Cholesterol Granuloma
		20.5	 Mucocele
		20.6	 Fibrous Dysplasia, Paget’s Disease, and Bone Marrow Hyperplasia
		20.7	 Other Benign Lesions, Differential Diagnoses, and Artifacts
		20.8	 Infection (Abscess and Pus Collection), Mastoiditis, Malignant Otitis Externa
		20.9	 Orbital Lesions
		20.10	 Salivary Gland Tumors
		20.11	 Bone Metastases
		20.12	 Squamous Cell Carcinoma (SCCA) and Lymphoma in Head and Neck Area
			20.12.1 Lymph Node Metastasis
			20.12.2 Perineural Tumor Spread
		20.13	 Conclusion
		20.14	 Treatment of Head and Neck Cancers
			20.14.1 Staging and Treatment of Oral Cavity Squamous Cell Carcinoma
			20.14.2 Staging and Treatment of Larynx Squamous Cell Carcinoma
			20.14.3 Staging and Treatment of p16-Positive Oropharyngeal Squamous Cell Carcinoma
		References
	21: Spine Infection
		21.1	 Introduction
		21.2	 MRI and Diffusion-Weighted Imaging
		21.3	 Typical Pyogenic Infections
		21.4	 Common Patterns of Spinal Infection and Extension of Pyogenic Abscess
			21.4.1	 Osteomyelitis/Discitis
			21.4.2	 Epidural/Paraspinal Abscess with Osteomyelitis/Discitis
			21.4.3	 Epidural/Paraspinal Abscess with Facet Joint Infection
			21.4.4	 Epidural/Paraspinal Abscess Without Concomitant Osteomyelitis/Discitis or Facet Joint Infection
			21.4.5	 Intradural Abscess (Subdural Abscess, Purulent Meningitis, and Spinal Cord Abscess)
		21.5	 Management of Patients with Spinal and Paraspinal Infections
			21.5.1	 Treatment of Osteomyelitis/Discitis
			21.5.2	 Treatment of Spinal Epidural Abscess
		21.6	 Tuberculosis and Atypical Infections
		21.7	 Mimics of Spinal Infection
			21.7.1	 Degenerative Disc Disease
			21.7.2	 Schmorl’s Nodes
			21.7.3	 Ankylosing Spondylitis
		21.8	 Mimics of Epidural/Paraspinal Abscesses
		21.9	 Limitation and Pitfalls on Diffusion-Weighted Imaging and Apparent Diffusion Coefficient Maps
		21.10	 Conclusions
		References
	22: Primary and Metastatic Spine Tumors
		22.1	 Introduction
		22.2	 DWI of Spinal Tumors
			22.2.1	 Technique
			22.2.2	 DWI Signal and ADC of the Spine
		22.3	 Metastatic Tumors to the Spine
			22.3.1	 Imaging
			22.3.2	 Management
		22.4	 Primary Spine Tumors
		22.5	 Benign Tumors
			22.5.1	 Giant Cell Tumor
				22.5.1.1	 Imaging
				22.5.1.2	 Management
			22.5.2	 Hemangioma
				22.5.2.1	 Imaging
				22.5.2.2	 Management
			22.5.3	 Eosinophilic Granuloma (Langerhans Cell Histiocytosis)
				22.5.3.1	 Imaging
				22.5.3.2	 Management
			22.5.4	 Osteoid Osteoma and Osteoblastoma
				22.5.4.1	 Imaging
				22.5.4.2	 Management
			22.5.5	 Osteochondroma
				22.5.5.1	 Imaging
				22.5.5.2	 Management
			22.5.6	 Aneurysmal Bone Cysts
				22.5.6.1	 Imaging
				22.5.6.2	 Management
		22.6	 Malignant Spinal Tumors
			22.6.1	 Plasma Cell Tumors
				22.6.1.1	 Imaging
				22.6.1.2	 Management
			22.6.2	 Chordoma
				22.6.2.1	 Management
			22.6.3	 Primary Spinal Ewing’s Sarcoma
				22.6.3.1	 Imaging
				22.6.3.2	 Management
			22.6.4	 Osteosarcoma
				22.6.4.1	 Imaging
				22.6.4.2	 Management
			22.6.5	 Chondrosarcoma
				22.6.5.1	 Imaging
				22.6.5.2	 Management
		22.7	 Summary
		References
	23: Spinal Cord Lesions
		23.1	 Introduction
		23.2	 MR Sequences of the Spinal Cord
		23.3	 Vascular Etiologies (Table 23.1)
			23.3.1	 Cord Infarction
			23.3.2	 Arteriovenous Malformations and Foix-Alajouanine Syndrome
		23.4	 Inflammatory Etiologies (Table 23.2)
			23.4.1	 Idiopathic Transverse Myelitis (ITM)
			23.4.2	 Acute Disseminated Encephalomyelitis (ADEM)
			23.4.3	 Multiple Sclerosis
			23.4.4	 Neuromyelitis Optica (NMO)
			23.4.5	 Sarcoidosis
			23.4.6	 Subacute Combined Degeneration (SCD)
		23.5	 Infectious Etiologies (Table 23.3)
			23.5.1	 Infectious Myelitis
			23.5.2	 Intramedullary Abscess
		23.6	 Mechanical Cord Injury (Table 23.3)
			23.6.1	 Compressive Myelopathy
			23.6.2	 Spinal Cord Contusion
			23.6.3	 Syrinx and Pre-syrinx State
		23.7	 Neoplasm
			23.7.1	 Astrocytoma
			23.7.2	 Ependymoma
			23.7.3	 Intramedullary Metastasis
			23.7.4	 Lymphoma
			23.7.5	 Waldenstrom’s Macroglobulinemia and Bing-Neel Syndrome
		23.8	 Conclusion
		23.9	 Treatment of Intramedullary Spinal Cord Tumors
			23.9.1	 Introduction
			23.9.2	 Ependymoma
				23.9.2.1	 Imaging
				23.9.2.2	 Treatment
			23.9.3	 Malignant Astrocytoma
				23.9.3.1	 Imaging
				23.9.3.2	 Treatment
			23.9.4	 Surgical Technique
			23.9.5	 Our Experience
			23.9.6	 Conclusion
		References
Part III: Futures of Diffusion Imaging
	24: Future Directions for Diffusion Imaging of the Brain and Spinal Cord
		24.1	 Introducing the Diffusion-Time
			24.1.1	 b-Value
			24.1.2	 Gaussian or Free Diffusion
			24.1.3	 Restricted Diffusion
				24.1.3.1	 b-Value-Dependent Signal with Constant Diffusion Time
				24.1.3.2	 b-Value-Dependent Signal with Constant q
		24.2	 In Vivo Application of Diffusion-Time-Dependent DWI
			24.2.1	 Shortening the Diffusion-Time
			24.2.2	 Increasing the Diffusion-Time
		24.3	 Extracting Microstructural Information from DWI
			24.3.1	 Basics and Limitations
			24.3.2	 Clinical Applications
			24.3.3	 Summary
		References
	25: Diffusion Imaging of the Head and Neck in the Future
		25.1	 Current State of Diffusion Imaging in the Head and Neck
		25.2	 Techniques: Current and Future
			25.2.1	 EPI Diffusion
			25.2.2	 Non-EPI Diffusion (TSE Diffusion)
			25.2.3	 Intravoxel Incoherent Motion
			25.2.4	 Reproducibility of ADC Values
			25.2.5	 Enhanced Dual-Stage Correlated Diffusion Imaging
		25.3	 Clinical Applications
			25.3.1	 Benign Versus Malignant Lesions
			25.3.2	 Prediction and Monitoring of Treatment Response
			25.3.3	 Recurrence Versus Posttreatment Changes
		25.4	 What the Future Holds
		References
Part IV: How to use this book
	26: How to Use This Book