By Jürg Kesselring (editor), Jane Smith (translator)
This concise, abundantly illustrated textual content offers an entire review of a number of sclerosis. through together with fresh study findings in genetics, immunology and pathophysiology, the authors offer trustworthy and up to date counsel at the epidemiology, prognosis, diagnosis and therapy of MS. Of specific curiosity to neuroscientists and neurologists would be the experiences of experimental versions of MS, pathology of the demyelinated plaque, HLA institutions and the function of immune mechanisms. members study the environmental and geographical components within the etiology of MS, together with the potential function of infectious brokers. The medical sections of the publication comprise dialogue of neurological, sexual, mental and cognitive disturbances. A overview of diagnostic standards and rehabilitation measures are widespread positive aspects of this hugely useful booklet.
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Additional info for Multiple Sclerosis
Example text
Depending on the questions asked, two different classes of experimental models have proved to be useful for MS research. a. General models of the mechanisms of degeneration and regeneration in the nervous system, and of the mechanisms of demyelination and glial scar formation. Although these models might be quite different from MS itself, they have contributed considerably to our understanding of how myelin can be destroyed, how the brain tissue reacts to myelin destruction, and to what extent remyelination can occur.
DISTRIBUTION OF PLAQUES IN THE NERVOUS SYSTEM A characteristic feature of MS pathology is the disseminated distribution of demyelinated lesions throughout the brain and spinal cord. Although plaques may appear at random in any areas of the CNS, certain predilection sites for plaque formation have been described (Steiner 1931; Hallervorden 1940; Fog 1950; Lumsden 1970; Oppenheimer 1978). In the brain, these sites include the periventricular white matter, especially at the lateral angle of the cerebral ventricles (see Fig.
In some animal species, a disease similar to EAN has been induced by autosensitization with galactocerebroside (Saida et al. 1979) and gangliosides (Nagai et al. 1976). Similar to EAE, peripheral autoimmune neuritis can be induced by the transfer of monospecific T-cell lines directed against P2 or PO proteins (Linington et al. 1984b; 1992b). Contrary to the situation in the CNS, these EAN models are associated with significant demyelination. A possible explanation for the phenomenon may be that Schwann cells can express Class II MHC molecules and can present autoantigen to T-lymphocytes (Wekerle et al.