Diffusion-weighted MR imaging of the brain /

Diffusion-weighted MR imaging of the brain /

Saved in:
Bibliographic Details
Author / Creator:Moritani, T. (Toshio)
Imprint:Berlin : Springer, 2005.
Description:1 online resource (xiv, 229 p.) : 661 fig. (some col.), 11 tab.
Language:English
Subject:
Brain -- Magnetic resonance imaging.
Diffusion magnetic resonance imaging.
Brain -- Diseases -- Diagnosis.
Brain -- Diseases -- Diagnosis.
Brain -- Magnetic resonance imaging.
Diffusion magnetic resonance imaging.
Brain Diseases -- diagnosis.
Diffusion Magnetic Resonance Imaging.
Brain -- pathology.
Format: E-Resource Book
URL for this record:http://pi.lib.uchicago.edu/1001/cat/bib/8875540
Hidden Bibliographic Details
ISBN:9783540263869
3540263861
6610235031 (electronic bk.)
9786610235032 (electronic bk.)
3540253599
Notes:Includes bibliographical references and index.
Description based on print version record.
Other form:Print version: Moritani, T. (Toshio). Diffusion-weighted MR imaging of the brain. Berlin : Springer, 2005 3540253599 9783540253594
Table of Contents:
  • 1. Basics of Diffusion Measurements by MRI
  • 1.1. Diffusion Imaging in MR
  • 1.2. Diffusion Imaging of the Brain
  • 1.3. Magnetic Resonance Principles of Diffusion Imaging
  • 1.4. Apparent Diffusion Coefficient
  • 1.5. Diffusion Represents a Molecular Event
  • 1.6. Requirements in Clinical Diffusion Imaging
  • 1.7. Setting the b-Value in Clinical DW Imaging
  • 1.8. Future Trends in Clinical DW Imaging
  • References
  • 2. Diffusion-Weighted 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 ofthe Pediatric Brain
  • 2.4. Conclusion
  • References
  • 3. Pitfalls and Artifacts of DW 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. Brain Edema
  • 4.1. Characterization and Classification of Brain Edema
  • 4.2. Definition and Classification of Cytotoxic Edema
  • 4.3. Pathophysiology of Cytotoxic Edema
  • 4.3.1. Energy Failure
  • 4.3.2. Excitotoxic Brain Injury
  • 4.4. Diffusion-Weighted Imaging and Cytotoxic Edema
  • 4.4.1. Conditions that Cause Cytotoxic Edema, and Reversibility
  • 4.5. Vasogenic or Interstitial Edema
  • 4.5.1. Conditions that Cause Vasogenic Edema
  • 4.6. Conclusion
  • 4.6.1. Cytotoxic or Cellular Edema
  • 4.6.2. Vasogenic Edema
  • References
  • 5. Infarction
  • 5.1. Clinical Significance and Therapeutic Considerations for Brain Infarcts
  • 5.1.1. Stroke Mimickers
  • 5.1.2. Diffusion-Weighted Imaging
  • 5.2. Diffusion-Weighted Imaging and Pathophysiology of Cerebral Infarction
  • 5.3. Apparent Diffusion Coefficient
  • 5.3.1. Explanation for Restricted Diffusion
  • 5.4. Time Course of Infarction
  • 5.4.1. Hyperacute (
  • 5.4.2. Acute (6 Hours to 3 Days)
  • 5.4.3. Subacute (3 Days to 3 Weeks)
  • 5.4.4. Chronic (3 Weeks to 3 Months)
  • 5.5. Diffusion-Weighted Imagingand ADC Characteristics of Gray and White Matter Ischemia
  • 5.5.1. Relative ADC
  • 5.6. Reversibility and Treatment
  • 5.7. Watershed Infarction
  • 5.8. Perfusion Versus Diffusion Imaging
  • 5.9. Venous Infarction
  • 5.9.1. Predisposing Factors
  • 5.9.2. Pathophysiology
  • 5.10. Small Vessel Infarcts
  • 5.11. Brain Stem and Cerebellar Infarcts
  • 5.12. Corpus Callosum Infarcts
  • 5.13. Hemorrhagic Infarcts
  • References
  • 6. Intracranial Hemorrhage
  • 6.1. Introduction
  • 6.2. Intraparenchymal Hemorrhages: Appearance and Evolution
  • 6.2.1. Hyperacute Hematoma
  • 6.2.2. Acute Hematoma
  • 6.2.3. Early Subacute Hematoma
  • 6.2.4. Late Subacute Hematomas
  • 6.2.5. Chronic Hematomas
  • 6.3. Subarachnoid Hemorrhage
  • 6.4. Subdural and Epidural Hemorrhages
  • 6.5. Intraventricular Hemorrhage
  • 6.6. Intra-tumoral Hemorrhage
  • 6.7. Hemorrhage Related to Vascular Malformation
  • 6.8. Hemorrhage Related to Trauma
  • 6.9. Conclusions
  • References
  • 7. Vasculopathy and Vasculitis
  • 7.1. Definition
  • 7.2. Clinical Presentation
  • 7.3. Treatment
  • 7.4. Vasculitis of the CNS
  • 7.4.1. Characterization of CNS Vasculitis
  • 7.4.2. Primary Angitis of the Central Nervous System
  • 7.4.3. Giant Cell (Temporal) Arteritis
  • 7.4.4. Takayasu's Arteritis (Aortitis Syndrome)
  • 7.4.5. Polyarteritis Nodosa
  • 7.4.6. Churg-Strauss Disease
  • 7.4.7. Other Small Vessel Vasculitis
  • 7.4.8. Collagen Vascular Diseases
  • 7.4.9. Infectious Vasculitis
  • 7.4.10. Drug-Induced Vasculitis, Including Illicit Drugs
  • 7.5. Vasculopathy of the CNS
  • 7.5.1. Systemic Lupus Erythematosus
  • 7.5.2. Moyamoya Disease
  • 7.5.3. Sickle Cell Disease
  • 7.5.4. Posterior Reversible Encephalopathy Syndrome
  • 7.5.5. Hypertensive Encephalopathy
  • 7.5.6. Preeclampsia/Eclampsia
  • 7.5.7. Immunosuppressive Drug-Induced Vasculopathy
  • 7.5.8. Uremic Encephalopathy and Hemolytic Uremic Syndrome
  • 7.5.9. Thrombotic Thrombocytopenic Purpura
  • 7.5.10. Cerebral Amyloid Angiopathy
  • 7.6. Conclusion
  • References
  • 8. Epilepsy
  • 8.1. Definition
  • 8.2. Classification
  • 8.3. Mechanisms and Pathophysiology of Epilepsy
  • 8.4. Magnetic Resonance Imaging of Epilepsy
  • 8.4.1. Diffusion-Weighted Imaging in Epilepsy
  • 8.4.2. Magnetic Resonance Signal Alterations in Epilepsy
  • 8.4.3. Ictal Stage to Periictal Stage
  • 8.4.4. Status Epilepticus
  • 8.4.5. Cytotoxic Edema in Status Epilepticus
  • 8.4.6. Other Imaging Techniques for Epilepsy
  • 8.5. Hemiconvulsion-Hemiplegia Epilepsy Syndrome
  • 8.6. Focal Lesion in the Spleniumof the Corpus Callosum in Epileptic Patients
  • 8.7. Conclusion
  • References
  • 9. Demyelinating and Degenerative Disease
  • 9.1. Demyelinating Disease
  • 9.1.1. Multiple Sclerosis
  • 9.1.2. Acute Disseminated Encephalomyelitis
  • 9.1.3. Progressive Multifocal Leukoencephalopathy
  • 9.2. Degenerative Disease
  • 9.2.1. Wallerian or Transneuronal Degeneration
  • 9.2.2. Creutzfeldt-Jakob Disease
  • 9.2.3. Amyotrophic Lateral Sclerosis
  • 9.3. Conclusion
  • References
  • 10. Toxic and Metabolic Disease
  • 10.1. Toxic Disease
  • 10.1.1. Chemotherapy-Induced Leukoencephalopathy
  • 10.1.2. Heroin-Induced Spongiform Leukoencephalopathy
  • 10.1.3. Cocaine, Phencyclidine Hydrochloride, Amphetamines and Related Catecholaminergics
  • 10.1.4. Central Pontine Myelinolysis and Extrapontine Myelinolysis
  • 10.1.5. Wernicke Encephalopathy
  • 10.1.6. Marchiafava-Bignami Disease
  • 10.2. Metabolic Disease
  • 10.2.1. Mitochondrial Encephalopathy
  • 10.2.2. Phenylketonuria
  • 10.2.3. Other Metabolic Diseases and Leukodystrophies
  • References
  • 11. Infectious Diseases
  • 11.1. Overview of Brain Infections
  • 11.2. Bacterial Brain Abscess
  • 11.3. Septic Emboli
  • 11.4. Brain Abscess Caused by Unusual Bacteria
  • 11.4.1. Differential Diagnosis
  • 11.5. Bacterial Abscess in the Extra-Axial Space
  • 11.5.1. Differential Diagnosis
  • 11.6. Bacterial Vasculitis
  • 11.7. Toxoplasmosis
  • 11.7.1. Differential Diagnosis
  • 11.8. Disseminated Aspergillosis
  • 11.9. Herpes Encephalitis
  • 11.10. Human Immunodeficiency Virus Infection
  • References
  • 12. Trauma
  • 12.1. Introduction
  • 12.2. Diffuse Axonal Injury
  • 12.2.1. Location
  • 12.2.2. Computed Tomography and MR Imaging
  • 12.2.3. Diffusion-Weighted Imaging
  • 12.3. Brain Contusion
  • 12.3.1. Location
  • 12.3.2. Computed Tomography and MR Imaging
  • 12.3.3. Diffusion-Weighted Imaging Findings
  • 12.4. Hemorrhage Related to Trauma
  • 12.4.1. Computed Tomography and MR Imaging
  • 12.4.2. Diffusion-Weighted Imaging
  • 12.5. Vascular Injuries
  • References
  • 13. Brain Neoplasms
  • 13.1. Introduction
  • 13.2. Gliomas
  • 13.2.1. High-Grade Tumors
  • 13.2.2. Peritumoral Infiltration
  • 13.2.3. Treatment Response
  • 13.3. Epidermoid Tumors and Arachnoid Cysts
  • 13.4. Primitive Neuroectodermal Tumors
  • 13.5. Meningiomas
  • 13.6. Malignant Lymphomas
  • 13.7. Craniopharyngiomas
  • 13.8. Metastases
  • 13.9. Conclusion
  • References
  • 14. Pediatrics
  • 14.1. Water Content of the Pediatric Brain
  • 14.2. Normal Structures
  • 14.3. Anisotropy
  • 14.4. Infarction and Ischemia
  • 14.4.1. Moyamoya Disease
  • 14.4.2. Sickle Cell Disease
  • 14.4.3. Hypoxic Ischemic Encephalopathy
  • 14.5. Trauma
  • 14.5.1. Battered Child Syndrome
  • 14.5.2. Diffuse Axonal Injury and Brain Contusion
  • 14.6. Encephalopathies
  • 14.6.1. Mitochondrial Encephalopathy
  • 14.6.2. Acute Necrotizing Encephalopathy
  • 14.6.3. Hypertensive Encephalopathy
  • 14.7. Infections
  • 14.7.1. Encephalitis
  • 14.7.2. Brain Abscess
  • 14.8. Brain Tumor
  • 14.9. Dysmyelination and Demyelination
  • 14.9.1. Pelizaeus-Merzbacher Disease
  • 14.9.2. Vanishing White Matter Disease
  • 14.9.3. Metabolic or Toxic Leukoencephalopathies
  • 14.9.4. Multiple Sclerosis
  • 14.9.5. Osmotic Myelinolysis
  • 14.10. Conclusion
  • References
  • 15. How to Use This Book
  • Table 1. Differential diagnoses for lesions with a high diffusion signal associated with low ADC and iso intense T2 signal
  • Table 2. Differential diagnoses for lesions with a high diffusion signal associated with iso-high ADC and a high intense T2 signal
  • Table 3. Differential diagnoses for lesions with a high diffusion signal associated with a low ADC and high intense T2 signal
  • Table 4. Differential diagnoses for lesions with an iso diffusion signal associated with a high ADC and high intense T2 signal
  • Table 5. Differential diagnoses for lesions with a low diffusion signal associated with a high ADC and high intense T2 signal
  • Table 6. Differential diagnoses for lesions with a low diffusion signal associated with a high ADC and iso intense T2 signal
  • Table 7. Differential diagnoses for lesions with artifacts
  • Subject Index

Similar Items