E-Book, Englisch, 540 Seiten
ISBN: 978-0-12-384914-4
Verlag: Elsevier Science & Techn.
Format: EPUB
Kopierschutz: 6 - ePub Watermark
Autoren/Hrsg.
Weitere Infos & Material
1;Front Cover;1
2;Neuroinflammation;4
3;Copyright Page;5
4;Contents;6
5;Preface;14
6;Contributors;16
7;Chapter 1. Multiple Sclerosis: Pathophysiology, Clinical Features, Diagnosis, and Management;22
7.1;Introduction;22
7.2;Epidemiology;23
7.3;Pathophysiology;24
7.4;Clinical Manifestations;27
7.5;Neuroimaging: A Concise Review;29
7.6;Diagnosis;36
7.7;Variants of MS;36
7.8;Differential Diagnosis;36
7.9;Management;37
7.10;Treatment of Acute Relapses;37
7.11;Disease-Modifying Agents;38
7.12;Prognosis;41
7.13;Conclusion;41
8;Chapter 2. Epstein–Barr Virus and Multiple Sclerosis: Wrong Place, Wrong Time?;46
8.1;Epstein–Barr Virus;46
8.2;EBV and Diseases;47
8.3;Multiple Sclerosis;48
8.4;Epidemiologic Evidence Linking EBV to MS;48
8.5;EBV Serology and MS;48
8.6;Is there a specific EBV Strain causing MS?;50
8.7;Control of EBV Infection by Host Immune Responses;50
8.8;Control of EBV Infection by Virus-Specific CD8+ T Cells;51
8.9;Control of EBV Infection by Virus-Specific CD4+ T Cells;52
8.10;Is EBV a characteristic feature of the MS Brain?;52
8.11;Conclusion;54
9;Chapter 3. Neutralizing Antibodies and Multiple Sclerosis;60
9.1;Immunogenicity of Beta-Interferons;60
9.2;Interferon Antibody Assays;62
9.3;Prevalence of NAbs to Beta-Interferons;65
9.4;Interferon Antibody Positivity and Persistence;67
9.5;Clinical Implications of Interferon NAbs;68
9.6;Antibodies to GA;70
9.7;Antibodies to Natalizumab;70
9.8;Conclusion;71
10;Chapter 4. Animal Models of Multiple Sclerosis;76
10.1;Etiology, Clinical Course, and Pathology;76
10.2;Immunology of MS, EAE, and TMEV Infection;80
10.3;Conclusions;87
11;Chapter 5. Neuroimaging of Multiple Sclerosis: An Update;102
11.1;Conventional Magnetic Resonance Imaging;102
11.2;Advanced Sequences, New Contrast Agents, High-Field MRI, Quantitative and Nonconventional MRI Techniques;107
11.3;Conclusions;119
12;Chapter 6. Role of IL-12/IL-23 in the Pathogenesis of Multiple Sclerosis;128
12.1;Introduction;128
12.2;IL-12 p40 Family;128
12.3;T-Helper-Cell Lineages and Immune Deviation;129
12.4;IL-12 and Th-1 Differentiation Pathways;130
12.5;IL-12 and T-Cell Encephalitogenicity;132
12.6;Myelin-Specific Th-1 Cells in MS;133
12.7;IFN-? in MS/EAE;133
12.8;Genetically Deficient Mice of the p40 Family;134
12.9;The Discovery of IL-23;135
12.10;Critical Role of IL-23 in EAE;136
12.11;IL-23 Expression in CNS;137
12.12;Th-17 Differentiation Pathways;137
12.13;Molecular Mechanisms Regulating Th-17 Pathway;139
12.14;The Plasticity of Th-17 Cells;141
12.15;In Vitro Differentiation of Encephalitogenic Th-17 Cells;141
12.16;Human Th-17 Cells;142
12.17;Distinct Type of Inflammation Induced by Th-1 or Th-17 Cells;144
12.18;Anti-p40 Therapy;144
12.19;T-bet: A Potential Prognostic Marker and Therapeutic Target in MS;146
13;Chapter 7. Spinal Cord Injury and its Relationship to the Development or Worsening of Clinical Multiple Sclerosis;158
13.1;Introduction;158
13.2;Historical Review;159
13.3;Relationships of Plaques to Blood Vessels;161
13.4;Breakdown of the BBB in Plaque Formation;161
13.5;Inflammatory Cell Infiltrates;163
13.6;Astrocytic and Other Cellular Changes;164
13.7;Effect of Trauma on the BBB;164
13.8;Studies of Stress on the BBB;166
13.9;Studies Showing that the Site of the BBB Breakdown is related to the Formation of New Demyelinating Plaques;169
13.10;Effect of Electrical Injuries in the Precipitation or Worsening of MS;174
13.11;Therapeutic Trials of Breaking Down the BBB in Patients with MS;176
13.12;Effects of Radiation on the BBB;178
13.13;Bee and Wasp Sting Encephalopathy Reactions with Breakdown of the BBB;179
13.14;Congophilic Amyloid Encephalopathy with Breakdown of the BBB;180
13.15;Neurologic Disorders that may be Precipitated by Trauma;180
13.16;Conclusions;181
14;Chapter 8. Clinical Development and Benefit–Risk Profile of Natalizumab;188
14.1;Introduction;188
14.2;Mechanism of Action;188
14.3;Pharmacokinetics and Pharmacodynamics;189
14.4;Clinical Development;190
14.5;Efficacy;191
14.6;Subgroup Analysis Data;193
14.7;Novel Measures of Efficacy;197
14.8;Post hoc Analyses;201
14.9;Safety;204
14.10;Summary;208
15;Chapter 9. Remyelination in Multiple Sclerosis;214
15.1;Introduction;214
15.2;Remyelination in MS;214
15.3;The Role of Animal Models for the Study of Remyelination;216
15.4;Growth Factors in CNS Remyelination;218
15.5;Transcription Factors in Remyelination;223
15.6;Epigenetic Control of Oligodendrocytes;225
15.7;Clinical Trials for Remyelination in MS;227
15.8;Imaging of Remyelination in Clinical Trials;230
15.9;Obstacles for Regenerative Treatments in MS;231
16;Chapter 10. Transverse Myelitis;246
16.1;Introduction;246
16.2;Clinical Manifestations;247
16.3;Epidemiology;248
16.4;Pathogenesis;248
16.5;Neuropathology;249
16.6;Diagnosis;249
16.7;Differential Diagnosis;252
16.8;Course and Prognosis;253
17;Chapter 11. Neuromyelitis Optica;258
17.1;Definition and Epidemiology;258
17.2;Pathophysiology;258
17.3;Clinical Manifestations;259
17.4;Diagnostic Criteria;261
17.5;Differential Diagnosis;263
17.6;Treatment;264
18;Chapter 12. Optic Neuritis: Pathophysiology, Clinical Features, and Management;274
18.1;Introduction;274
18.2;Definition;275
18.3;Pathophysiology;275
18.4;Clinical Features;279
18.5;Assessment of the Optic Nerve;282
18.6;Prognosis;285
18.7;Management;287
18.8;Conclusion;291
19;Chapter 13. Ischemic Demyelination;298
19.1;Introduction;298
19.2;Manifestations of Hypertensive Microangiopathy;299
19.3;CADASIL;300
19.4;Binswanger’s Disease;304
19.5;White Matter Disease and Cerebral Hemorrhage;306
19.6;Migraine;306
19.7;Pathogenic Models of Ischemic Demyelination;307
19.8;Ischemic Demyelination and Ischemic Stroke Risk;309
20;Chapter 14. Inflammatory Mechanisms in Ischemic Cerebrovascular Disease;314
20.1;Inflammatory Cell Recruitment in Ischemic Stroke;314
20.2;Inflammatory Mechanisms in Cerebrovascular Thrombosis;328
20.3;Conclusions;338
21;Chapter 15. Protection Against Neuroinflammation by Promoting Co-activation of G Protein–Growth Factor Signaling and Metabolic Flexibility in the Brain;346
21.1;The Challenge of Neuroinflammation;346
21.2;MS: Neuroinflammation, Ionic Imbalance, and Energy Depletion;348
21.3;Metabolic Flexibility: Regulation of Energy Substrate Usage in the Brain;351
21.4;Co-activation of Trophic Factor Receptors in the Brain;352
21.5;Neuroprotection: Pharmacologic Approaches;353
21.6;Additional Issues for Neuroprotective Strategies;360
22;Chapter 16. Mesenchymal Stem Cells, Inflammation, and Neurodegenerative Diseases;368
22.1;Introduction;368
22.2;MSCs and Inflammation;371
22.3;MSCs and Dendritic Cells;372
22.4;MSCs and T Lymphocytes;373
22.5;MSCs and B Lymphocytes;374
22.6;MSCs and NK Cells;374
22.7;Immunogenicity of MSCs;375
22.8;MSC Migration into Inflamed Tissues and Tumors;376
22.9;MSCs and Tumors;378
22.10;Migration of Differentiated and Undifferentiated Stem Cells;379
22.11;Anti-Inflammatory Activities of MSCs in Clinical and Experimental Studies;380
22.12;MSCs and Neurodegenerative Diseases;381
22.13;The Routes and Timing of Injection of Stem Cells;387
22.14;Side Effects of Stem Cell Therapy;388
23;Chapter 17. Inflammatory Mediators in Obstructive Sleep Apnea;402
23.1;Introduction to Obstructive Sleep Apnea;402
23.2;Risk Factors and Epidemiology of OSA;403
23.3;Chapter Objectives;403
23.4;OSA and Cardiovascular Risk;405
23.5;OSA and the Metabolic Syndrome;405
23.6;OSA and Daytime Neurocognitive Impairment;406
23.7;The Overlap Between OSA, Obesity, and Asthma;407
23.8;OSA and Oxidative Stress;408
23.9;Systemic Inflammatory Mediators Associated with OSA;409
23.10;Summary;414
24;Chapter 18. The Role of Neuroinflammation in Parkinson’s Disease;424
24.1;Introduction to Parkinson’s Disease;424
24.2;Neuroinflammation in the Pathogenesis of PD;427
24.3;Evidence of Neuroinflammation in PD;429
24.4;Molecular Pathways Involved in Neuroinflammation of PD;431
24.5;Is Anti-Inflammatory Therapy the Answer for PD Prevention?;434
25;Chapter 19. Neuroinflammation and Pediatric Lupus;444
25.1;Introduction;444
25.2;Manifestations of NPSLE;444
25.3;Proposed Etiology of NPSLE Neurobehavioral Syndromes;446
25.4;Diagnosis of NPSLE;449
25.5;Diagnosis of Cognitive Dysfunction Syndromes in Children;451
25.6;Computer-Based Neurocognitive Testing;452
25.7;Imaging for Diagnosing Neurocognitive Dysfunction;453
25.8;Treatment of NPSLE;455
26;Chapter 20. Central Nervous System Vasculitis;460
26.1;Introduction to Vasculitides;460
26.2;The CNS in Primary Vasculitides;461
26.3;Secondary CNS Vasculitides;473
26.4;Conclusions;479
27;Chapter 21. Systemic Lupus Erythematosus—Vasculopathy/Vasculitis, Susac Syndrome, and Myasthenia Gravis;488
27.1;Introduction;488
27.2;Selected Etiologic Factors;490
27.3;Pathophysiology of Vasculopathy and Vasculitis in SLE;490
27.4;Susac Syndrome as an Example of a Rare Autoimmune Vasculopathy;495
27.5;Neurologic Symptoms Related to Vasculopathy and Vasculitis;498
27.6;SLE and Myasthenia Gravis;499
28;Chapter 22. Inflammatory Mechanisms in Guillain–Barré Syndrome;508
29;Chapter 23. Neurologic Manifestations of Herpes Zoster;518
29.1;Introduction;518
29.2;Primary VZV Infection;518
29.3;Herpes Zoster;520
29.4;Postherpetic Neuralgia;520
29.5;VZV Vasculopathy;521
29.6;VZV Meningoencephalitis;523
29.7;VZV Myelopathy;523
29.8;VZV Cerebellitis;523
29.9;VZV Retinal Necrosis;524
29.10;Zoster Sine Herpete;524
29.11;Vaccination;525
29.12;Molecular Aspects of VZV Infection and Latency;526
29.13;Development of Animal Models;529
29.14;Simian Varicella Virus;530
29.15;Conclusion;532
