Multiple Sclerosis reaction paper Multiple sclerosis is a disease characterized by inflammation and degeneration of the myelin sheath of neurons

in the brain and spinal cord. This leads to a system-wide disruption of synaptic transmission, and causes an extensive range of clinical symptoms. Some of the positive symptoms include increased or abnormal sensation caused by demyelination such as tingling or numbness, visual problems such as diplopia and vertigo. Negative symptoms include fatigue, spasms, tremors, and emotional changes such as depression. MS is typically diagnosed with and M !, examination of evo"ed potentials in response to sensory input, and finally a spinal tap of the #S$. This is especially important to rule out other possible diseases such as encephalitis, syphilis, and panencephalitis. There are four general categories of MS that patients can fall under based on the progression of symptoms. The most common type to mention is "nown as relapse remitting, in which early onset of MS begins with periods of relapse and remission, but no apparent worsening of symptoms until about %& years later. This is common for '&( of MS patients. There appears to be a genetic component to the pathogenesis of MS as well, and it interestingly occurs most commonly among #aucasians of Scandinavian and Scottish descent. Some environmental causes are thought to include a lac" of vitamin ), especially given the prevalence in populations far from the e*uator, as well as the assault from the +pstein-,arr virus. -hile there is no definitive mechanism to date, the most popular hypothesis for the pathogenesis of MS is that some genetic disposition such as tight .unction abnormalities, in con.unction with environmental factors, ultimately leads to an overactive glial response. This response is characterized by excessive inflammation and release of factors such as cyto"ines and T-cells. /n overactive inflammatory response often leads to the production of toxic byproducts, and it is also thought that T-cells also target myelin of oligodendrocytes as well. )emyelination of oligodendrocytes has severe conse*uences, namely the loss of axons to maintain action potentials down the axons. This ultimately leads to a brea"down of the entire neuron, and produces the clinical symptoms mentioned above. The aspect about multiple sclerosis that ! found most interesting was the contribution of the +pstein barr virus to the onset of the disorder. 0&( of Northern +uropean MS cases have patients with the antibodies for +,1, and a ma.ority of the world2s population possesses the antibodies for +,1 in general, particularly among developing countries 34ucas, %5667. There is also a stronger association with later infection of +,1 and MS development, and it is also worth mentioning that pediatric instances of MS, which consist of about &( of all instances, have a rate of about '5( of patients having the +,1 antibodies. 8ne hypothesis is that +,1 may induce MS pathogenesis by upregulating the expression of a protein "nown as 9,-crystallin, which initiates the #): T cell response leading to the degradation of myelin in oligodendrocytes 34ucas, %5667. -hile there is a growing body of evidence supporting the role of +,1 in MS cases, still further investigation is re*uired in order to generate more consistent findings, and larger sample sizes for better accuracy 34ucas, %5667. ;erhaps a next step in con.unction with understanding the pathogenesis of MS would be to further investigate

how +,1 wor"s in the human body, and develop vaccines for prevention of both MS and +,1 related pathology. Source<

Lucas, RM, A M Hughes, M-L J Lay, et al. "Epsteine-Barr Virus and Multiple Sclerosis." J Neurol Neurosurg Psychiatry. !."# $!#""%& ""'!""' .