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Multiple Sclerosis and Allergic Encephalomyelitis

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Pathological Neurochemistry
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Abstract

During the past 40 years, research in multiple sclerosis gained worldwide interest since this progressively crippling disease of the central nervous system is not localized in any particular area of the world. Multiple sclerosis is a human disorder with varying clinical manifestations resulting from interference in neuronal conduction. The multiplicity of clinical symptoms of the disease and the unpredictable prognosis of individual cases suggested multiple forms caused by a number of agents rather than a single clue to a single cause. Pathological studies of tissues from MS patients revealed destruction of nerve fiber myelin and axis cylinders leading to the formation of “sclerotic plaque,” generally distributed around vessels. Although many exceptions to the general distribution of these lesions have been reported,1–3 it is clear that myelin degeneration resulting in impaired conductivity remains a general finding in multiple sclerosis. In the acute stage of the disease, the vessels become dilated with lymphocytes and plasma cells infiltrating into the perivascular spaces, suggesting cellular involvement and cell-mediated immunity in this disorder. Although a number of theories regarding the etiology and pathogenesis of multiple sclerosis have been proposed, the negative evidence against environmental factors,4 inherited factors,5,6 malnutrition,2,7 infections,8 trauma,9 vaccination against smallpox,10 and viruses11,12 outweigh the positive.

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Hashim, G.A. (1985). Multiple Sclerosis and Allergic Encephalomyelitis. In: Lajtha, A. (eds) Pathological Neurochemistry. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-0797-7_11

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