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There is now evidence that irreversible brain damage accumulates very early in the course of multiple sclerosis. This book reviews the main neurobiological, magnetic resonance imaging, and clinical aspects of the early phases of the dis ease. Mechanisms ofirreversible axonal damage and the role played by the inter action of glia and the axon are highlighted. In contrast to what was believed for a long time, the sufficient availability of oligodendrocyte precursor cells to promote remyelination in acute lesions has now been demonstrated. For reasons not understood, this remyelination process fails or does not start, particularly in the chronic stages ofthe disease. These findings emphasize the importance of the "milieu" changes induced by an inflammatory process in limiting remyelination. However, first indications are that part of this inflammatory process may have a neuroprotective effect. Pathological studies in multiple sclerosis have now clearly demonstrated that destructive processes may be followed by recovery phases in such a way that myelin may be morphologically and functionally reconstituted. These findings provide the rationale for early treatment and emphasize the importance of clinical trials in early multiple sclerosis. Early treatment is one of the most important aspects in multiple sclerosis today.
Inhaltsverzeichnis
1 - Evidence for an Early Treatment of Multiple Sclerosis.- 2 - Inflammation, Demyelination, and Axonal Degeneraton: Three Aspects of the Pathogenesis of Multiple Sclerosis Revealed by Campath-1 H Treatment.- 3 - Genetic Regulation of Nerve Cell Death/Glial Activation and Protective Effects of Myelin Basic Protein Autoimmune Neurotrophin Production in Mechanically Induced Neurodegeneration.- 4 - Neuroprotective Treatment in Primary Progressive Multiple Sclerosis: A Phase I/II Study with Riluzole.- 5 - Neuropathology and Disease Progression in Multiple Sclerosis.- 6 - Autoimmune Inflammation and Multiple Sclerosis.- 7 - Early Treatment of Progression in Multiple Sclerosis.- 8 - Imaging for Tissue Characterization in Multiple Sclerosis and Other White Matter Diseases.- 9 - Monounsaturated Fatty Acids and Neuroprotection. The Results of a Study of Cognitive Decline in Old Age. Is There a Case for this Treatment in Multiple Sclerosis?.- 10 - Neuroprotection in Acute Ischemic Stroke: Lessons for Early Treatment in Multiple Sclerosis.- 11 - Soluble VCAM-1 Release Indicates Inflammatory Blood-Brain Barrier Pathology and Further Modulates Adhesion.- 12 - Early Treatment in Multiple Sclerosis with Intravenous Immunoglobulin: Rationale and Study Design.- 13 - Serial Magnetic Resonance Imaging in Patients with a First Clinical Episode Suggestive of Multiple Sclerosis: Outline of a Research Protocol.- 14 - T1-Hypointense Lesions (T1 Black Holes) in Mild-to-Moderate Disability Relapsing Multiple Sclerosis.- 15 - Acute Monosymptomatic Optic Neuritis: Potential Clues to Early Therapy in Multiple Sclerosis.- 16 - Antibody Mediated Demyelination.- 17 - Anti-MOG Antibodies as Early Predictors for Conversion to Relapsing-Remitting Disease Course inPatients Suggestive of Multiple Sclerosis.- 18 - Sunlight, Vitamin D, and Multiple Sclerosis.- 19 - The Yin and Yang of Inflammation in Multiple Sclerosis.- 20 - Management of Interferon-ß1b (Betaseron) Failures in Multiple Sclerosis with Interferon-?n3 (Alferon N).
Zusammenfassung
There is now evidence that irreversible brain damage accumulates very early in the course of multiple sclerosis. This book reviews the main neurobiological, magnetic resonance imaging, and clinical aspects of the early phases of the dis ease. Mechanisms ofirreversible axonal damage and the role played by the inter action of glia and the axon are highlighted. In contrast to what was believed for a long time, the sufficient availability of oligodendrocyte precursor cells to promote remyelination in acute lesions has now been demonstrated. For reasons not understood, this remyelination process fails or does not start, particularly in the chronic stages ofthe disease. These findings emphasize the importance of the "milieu" changes induced by an inflammatory process in limiting remyelination. However, first indications are that part of this inflammatory process may have a neuroprotective effect. Pathological studies in multiple sclerosis have now clearly demonstrated that destructive processes may be followed by recovery phases in such a way that myelin may be morphologically and functionally reconstituted. These findings provide the rationale for early treatment and emphasize the importance of clinical trials in early multiple sclerosis. Early treatment is one of the most important aspects in multiple sclerosis today.
