Acute disseminated encephalomyelitis pathophysiology
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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. Although typically observed in white matter, gray matter involvement is also seen in basal ganglia, thalamus and cerebral cortex[2].
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.
- ↑ VAN BOGAERT L (1950). "Post-infectious encephalomyelitis and multiple sclerosis; the significance of perivenous encephalomyelitis". J Neuropathol Exp Neurol. 9 (3): 219–49. doi:10.1097/00005072-195007000-00001. PMID 15437201.