Acute disseminated encephalomyelitis pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
Revision as of 06:53, 9 November 2022
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sujaya Chattopadhyay, M.D.[2]
Overview
The exact mechanism of acute disseminated encephalomyelitis is not determined. However, it is usually preceded by an environmental trigger, e.g. an [infection]] or vaccination and affects individuals with a genetic predisposition.
Pathophysiology[1]
- Acute disseminated encephalomyelitis is described as an autoimmune disorder, resulting in central nervous system demyelination.Enviromental stimuli activate cellular and humoral responses which cross-react with myelin autoantigens namely, myelin basic protein, myelin oligoendrocyte protein, proteolipid protein.
- In an alternative mechanism, post-vaccination and post-infective circulating immune complexes in the CNS give rise to an inflammatory reaction, resulting in increased vascular permeability and congestion. This disrupts the blood- brain barrier, allowing infiltration by antigens and mononuclear cells. They cause perivascular edema and hemorrhage which culminate in demyelination, necrosis and gliosis.
References
- ↑ Torisu H, Okada K (2019). "Vaccination-associated acute disseminated encephalomyelitis". Vaccine. 37 (8): 1126–1129. doi:10.1016/j.vaccine.2019.01.021. PMID 30683508.