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Drawing of sclerotic lesions from Babinski's thesis "Etude anatomique et clinique de la sclérose en plaques", 1885
Multiple sclerosis (MS) can be pathologically defined as the presence of distributed glial scars (scleroses) in the central nervous system that must show dissemination in time (DIT) and in space (DIS) to be considered MS lesions.[1][2]
The scars that give the name to the condition are produced by the astrocyte cells attempting to heal old lesions.[3] These glial scars are the remnants of previous demyelinating inflammatory lesions (encephalomyelitis disseminata) which are produced by the one or more unknown underlying processes that are characteristic of MS.
Apart from the disseminated lesions that define the condition, the CNS white matter normally shows other kinds of damage. At least five characteristics are present in CNS tissues of MS patients: Inflammation beyond classical white matter lesions (NAWM, NAGM), intrathecal Ig production with oligoclonal bands, an environment fostering immune cell persistence, Follicle-like aggregates in the meninges (B-cells mostly infected with EBV[4]) and a disruption of the blood–brain barrier even outside of active lesions.[5]
Confluent subpial cortical lesions are the most specific finding for MS, being exclusively present in MS patients.[6] Though this feature can only be detected during an autopsy[7] there are some subrogate markers under study[8] Damage in MS consists also in areas with hidden damage (normal appearing white and gray matters) and two kinds of cortical lesions: Neuronal loss and cortical demyelinating lesions. The neural loss is the result of neural degeneration from lesions located in the white matter areas and the cortical demyelinating lesions are related to meningeal inflammation.[9][10]
The scars in the white matter are known to appear from confluence of smaller ones[11]
Currently the term "multiple sclerosis" is ambiguous and refers not only to the presence of the scars, but also to the unknown underlying condition that produces these scars. Besides clinical diagnosis uses also the term "multiple sclerosis" for speaking about the related clinical courses. Therefore, when referring to the presence of the scars is better to use the equivalent term astrocytic fibrillary gliosis.[9]
^Lublin FD (2016). Sealfon SC, Motiwala R, Stacy CB (eds.). "Multiple Sclerosis and Other Inflammatory Diseases". Mount Sinai Expert Guides: Neurology. Chichester, UK: John Wiley & Sons, Ltd: 873–874. doi:10.1002/9781118621042.ch23. ISBN 9781118621042.
^Dutta R, Trapp BD (June 30, 2006). "Pathology and definition of multiple sclerosis". Rev Prat. 56 (12): 1293–8. PMID 16948216.
^Brosnan CF, Raine CS (2013). "The astrocyte in multiple sclerosis revisited". Glia. 61 (4): 453–465. doi:10.1002/glia.22443. PMID 23322421. S2CID 43783397.
^Franciotta D, Salvetti M, Lolli F, Serafini B, Aloisi F (Sep 2008). "B cells and multiple sclerosis". Lancet Neurol. 7 (9): 852–8. doi:10.1016/S1474-4422(08)70192-3. PMID 18703007. S2CID 7128448.
^Meinl E, Krumbholz M, Derfuss T, Junker A, Hohlfeld R (November 2008). "Compartmentalization of inflammation in the CNS: A major mechanism driving progressive multiple sclerosis". J Neurol Sci. 274 (1–2): 42–4. doi:10.1016/j.jns.2008.06.032. PMID 18715571. S2CID 34995402.
^Lassmann H (2014). "Multiple sclerosis: Lessons from molecular neuropathology". Experimental Neurology. 262: 2–7. doi:10.1016/j.expneurol.2013.12.003. PMID 24342027. S2CID 25337149.
^Kutzelnigg A, et al. (2007). "Widespread Demyelination in the Cerebellar Cortex in Multiple Sclerosis". Brain Pathology. 17 (1): 38–44. doi:10.1111/j.1750-3639.2006.00041.x. PMC 8095596. PMID 17493036. S2CID 38379112.
^Absinta M, et al. (Apr 2015). "Gadolinium-based MRI characterization of leptomeningeal inflammation in multiple sclerosis". Neurology. 85 (1): 18–28. doi:10.1212/WNL.0000000000001587. PMC 4501940. PMID 25888557.
^ abBogdan F, Popescu GH, et al. (Aug 2013). "", Pathology of Multiple Sclerosis " Where Do We Stand?". Continuum. 19 (4): 901–921. doi:10.1212/01.CON.0000433291.23091.65. PMC 3915566. PMID 23917093.
^Haider L (2016). "The topograpy of demyelination and neurodegeneration in the multiple sclerosis". Brain. 139 (3): 807–15. doi:10.1093/brain/awv398. PMC 4766379. PMID 26912645.
^Young, N. P; Weinshenker, B. G; Parisi, J. E; Scheithauer, B; Giannini, C; Roemer, S. F; Thomsen, K. M; Mandrekar, J. N; Erickson, B. J; Lucchinetti, C. F (2010). "Perivenous demyelination: Association with clinically defined acute disseminated encephalomyelitis and comparison with pathologically confirmed multiple sclerosis". Brain. 133 (2): 333–48. doi:10.1093/brain/awp321. PMC 2822631. PMID 20129932.
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