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| == Pathophysiology == | | == Pathophysiology == |
| {{Main|Pathophysiology of multiple sclerosis}}
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| Although much is known about how multiple sclerosis causes damage, the reasons why multiple sclerosis occurs are not known.
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| Multiple sclerosis is a disease in which the [[myelin]] (a [[lipid|fatty]] substance which covers the [[axon]]s of [[neuron|nerve cells]]) degenerates. According to the view of most researchers, a special subset of [[lymphocyte]]s, called [[T cell]]s, plays a key role in the development of MS.
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| According to a strictly immunological explanation of MS, the inflammatory process is triggered by the T cells. T cells gain entry into the brain via the [[blood-brain barrier]] (a capillary system that should prevent entrance of T-cells into the nervous system). The blood brain barrier is normally not permeable to these types of cells, unless triggered by either infection or a virus, where the integrity of the [[tight junction]]s forming the blood-brain barrier is decreased. When the blood brain barrier regains its integrity (usually after infection or virus has cleared) the T cells are trapped inside the brain. These [[lymphocyte]]s recognize myelin as foreign and attack it as if it were an invading virus. That triggers [[inflammation|inflammatory]] processes, stimulating other immune cells and soluble factors like [[cytokine]]s and [[antibody|antibodies]]. Leaks form in the [[blood-brain barrier]]. These leaks, in turn, cause a number of other damaging effects such as [[edema|swelling]], activation of [[macrophages]], and more activation of cytokines and other destructive [[protein]]s such as [[matrix metalloproteinase]]s. A deficiency of [[uric acid]] has been implicated in this process.<ref>{{cite journal |author=Rentzos M, Nikolaou C, Anagnostouli M, Rombos A, Tsakanikas K, Economou M, Dimitrakopoulos A, Karouli M, Vassilopoulos D |title=Serum uric acid and multiple sclerosis |journal=Clinical neurology and neurosurgery |volume=108 |issue=6 |pages=527-31 |year=2006 |pmid=16202511}}</ref>
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| It is known that a repair process, called remyelination, takes place in early phases of the disease, but the [[oligodendrocyte]]s that originally formed a [[myelin sheath]] cannot completely rebuild a destroyed myelin sheath. The newly-formed myelin sheaths are thinner and often not as effective as the original ones. Repeated attacks lead to successively fewer effective remyelinations, until a scar-like plaque is built up around the damaged axons, according to [[pathophysiology of multiple sclerosis#Demyelination patterns|four different damage patterns]].<ref>Lucchinetti, C. Bruck, W. Parisi, J. Scherhauer, B. Rodriguez, M. Lassmann, H.''Heterogeneity of multiple sclerosis lesions: implications for the pathogenesis of demyelination'' Ann Neurol, 2000; 47(6):707-17. PMID 10852536</ref> The central nervous system should be able to recruit oligodendrocyte [[stem cell]]s capable of turning into mature myelinating oligodendrocytes, but it is suspected that something inhibits stem cells in affected areas.
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| The [[axon]]s themselves can also be damaged by the attacks.<ref>{{cite journal |author=Pascual AM, Martínez-Bisbal MC, Boscá I,''et al'' |title=Axonal loss is progressive and partly dissociated from lesion load in early multiple sclerosis |journal=Neurology|volume=69 |issue=1 |pages=63-7 |year=2007 |pmid=17606882 |doi=10.1212/01.wnl.0000265054.08610.12}}</ref> Often, the brain is able to compensate for some of this damage, due to an ability called [[neuroplasticity]]. MS symptoms develop as the cumulative result of multiple [[lesion]]s in the brain and [[spinal cord]]. This is why symptoms can vary greatly between different individuals, depending on where their lesions occur.
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| <gallery perRow="2">
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| Image:MS Demyelinisation KB 10x.jpg|Demyelinization in MS. On Klüver-Barrera myelin staining, decoloration in the area of the lesion can be appreciated (Original scale 1:100)
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| Image:Carswell-Multiple Sclerosis2.jpg|Detail of drawing from Carswell book depicting multiple sclerosis lesions in the [[brain stem]]and [[spinal cord]] (1838)
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| </gallery>
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| {{Neuron map|Myelin sheath of a healthy neuron}}
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| ==References== | | ==References== |