Multiple Sclerosis

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Multiple Sclerosis Human Anatomy and Physiology

You pick up the telephone to call your friend. You dial a number which will, in effect, let the phone know where to send the signals. Except unknown to you, something has worn away the rubber which covers and protects the wires within your phone. Some signals cannot get through, and the ones that do are unclear. As a result your important information does not get conveyed to your friend. This is a circumstance similar to the process that occurs within the body of a person with Multiple Sclerosis. The name itself is revealing: multiple, more than one, and sclerosis, which refers to areas of sclerotic (scarred) tissue. Multiple sclerosis (MS) is a potentially debilitating disease in which your body 's immune system eats away at the protective sheath that covers your nerves. MS is far more common in countries with temperate climates, including Europe, southern Canada, northern United States, New Zealand and southeastern Australia. The risk seems to increase with latitude and affects noticeably more women than men with the onset of clinical symptoms occurring between 15 and 50 years of age. It is the most common demyelization disease of the central nervous system. In the United States alone, there are at least 250,000 cases. Although the exact pathogenesis of the disease is unknown, it is believed that the clinical manifestations of multiple sclerosis are the result of an immune reaction consisting of the penetration of the blood-brain barrier (BBB), entrance into the CNS, and recognition of the myelin basic protein (MBP) and proteolipid (PLP) as foreign. The immune system 's attack on these proteins induces the stripping of the protective coating of myelin and then eventual formation of plaques. These plaques or lesions can be found throughout the central nervous system, but are most prominently found in the white matter, optic nerve, brainstem,



References: Bansil, Shalini et al., "Multiple Sclerosis: Pathogenesis and Treatment," Seminars in Neurology, 1994 June, 14(2):146-153.  Bray, Patrick F., et al., "Antibodies against Epstein-Barr nuclear antigen (EBNA) in multiple sclerosis CSF, and two pentapeptide sequence identities between EBNA and myelin basic protein", Neurology, 1992 September, 42:1798-1804.  Challoner PB et al., "Plaque-associated expression of human herpesvirus 6 in multiple sclerosis." Proceedings of the National Academy of Sciences of the United States of America, 1995 August 1, 92(16):7440-4. Gronning, Marit et al., "Infections in Childhood Adolescence in Multiple Sclerosis", Neuroepidemiology, 1993, 12:61-69.  Lycke, Jan et al., "Acyclovir treatment of relapsing-remitting multiple sclerosis", Journal of Neurology, 1996 243:2140224. Oksenberg, Michael, et al., "Multiple sclerosis: form immunogenics to immunotherapy," Journal of the Neurological Sciences, 1993, 155(Suppl) S29-S37. Panitch, Hillel S., "Influence of Infection on Exacerbations of Multiple Sclerosis", Annals of Neurology, 1994, 36:S25-S28. Poser, Charles H., "The Pathogenesis of Multiple Sclerosis", Journal of the Neurological Sciences", 1993, 115 (suppl):S3-S15. Riise, Trond et al., "Clustering of Residence of Multiple Sclerosis Patients at Age 13 to 20 Years in Hordaland, Norway", American Journal of Epidemiology, 1991 133:932-939. Sola P. et al., "Human herpesvirus 6 and multiple sclerosis: survey of anti-HHV-6 antibodies by immunofluorescence analysis and of viral sequences by polymerase chain reaction." Journal of Neurology, Neurosurgery and Psychiatry, 1993 August, 56(8):917-9. Vaughan, J.H., et al., "An Epstein-Barr virus-related cross reactivity autoimmune response in multiple sclerosis in Norway," Journal of Neuroimmunology, 1996, 69:95-102.

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