Acute disseminated encephalomyelitis historical perspective: Difference between revisions
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==Historical Perspective== | ==Historical Perspective== | ||
*[[Acute disseminated encephalomyelitis CT|Acute disseminated encephalomyelitis]] has experimental evidence suggests that both primary [[autoimmune]] responses and [[immunological]] responses triggered by infection may play a role in central nervous system inflammation and demyelination. Clinically and | *[[Acute disseminated encephalomyelitis CT|Acute disseminated encephalomyelitis]] has experimental evidence suggests that both primary [[autoimmune]] responses and [[immunological]] responses triggered by infection may play a role in central nervous system inflammation and demyelination. Clinically and [[histopathological]]<nowiki/>ly, two animal models closely resemble.<ref name="Rivers Sprunt Berry pp. 39–53">{{cite journal | last=Rivers | first=Thomas M. | last2=Sprunt | first2=D. H. | last3=Berry | first3=G. P. | title=OBSERVATIONS ON ATTEMPTS TO PRODUCE ACUTE DISSEMINATED ENCEPHALOMYELITIS IN MONKEYS | journal=Journal of Experimental Medicine | publisher=Rockefeller University Press | volume=58 | issue=1 | date=1933-07-01 | issn=1540-9538 | doi=10.1084/jem.58.1.39 | pages=39–53}}</ref><ref name="pmid164412">{{cite journal| author=Lipton HL| title=Theiler's virus infection in mice: an unusual biphasic disease process leading to demyelination. | journal=Infect Immun | year= 1975 | volume= 11 | issue= 5 | pages= 1147-55 | pmid=164412 | doi=10.1128/iai.11.5.1147-1155.1975 | pmc=415190 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=164412 }}</ref> | ||
*To begin, experimental autoimmune encephalomyelitis (EAE) is commonly utilized to investigate the underlying disease processes, after immunization with | *To begin, experimental [[autoimmune]] [[encephalomyelitis]] (EAE) is commonly utilized to investigate the underlying disease processes, after [[immunization]] with [[Central nervous system]] homogenate or encephalitogenic [[myelin]] [[peptides]] emulsified in Freund complete [[adjuvant]]. [[Inflammatory]] [[demyelinating]] [[lesions]] can be seen [[histopathological]]<nowiki/>ly in the [[brain]]<nowiki/>s and [[spinal cord]]<nowiki/>s of affected animals. | ||
*Theiler murine encephalomyelitis, which was first utilized as an animal model in the 1930s, has been used to investigate infectious and parainfectious pathways that may play a role in disease etiology. | *Theiler [[murine]] [[encephalomyelitis]], which was first utilized as an animal model in the 1930s, has been used to investigate [[infectious]] and parainfectious pathways that may play a role in disease etiology. | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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Overview
Historical Perspective
- Acute disseminated encephalomyelitis has experimental evidence suggests that both primary autoimmune responses and immunological responses triggered by infection may play a role in central nervous system inflammation and demyelination. Clinically and histopathologically, two animal models closely resemble.[1][2]
- To begin, experimental autoimmune encephalomyelitis (EAE) is commonly utilized to investigate the underlying disease processes, after immunization with Central nervous system homogenate or encephalitogenic myelin peptides emulsified in Freund complete adjuvant. Inflammatory demyelinating lesions can be seen histopathologically in the brains and spinal cords of affected animals.
- Theiler murine encephalomyelitis, which was first utilized as an animal model in the 1930s, has been used to investigate infectious and parainfectious pathways that may play a role in disease etiology.
References
- ↑ Rivers, Thomas M.; Sprunt, D. H.; Berry, G. P. (1933-07-01). "OBSERVATIONS ON ATTEMPTS TO PRODUCE ACUTE DISSEMINATED ENCEPHALOMYELITIS IN MONKEYS". Journal of Experimental Medicine. Rockefeller University Press. 58 (1): 39–53. doi:10.1084/jem.58.1.39. ISSN 1540-9538.
- ↑ Lipton HL (1975). "Theiler's virus infection in mice: an unusual biphasic disease process leading to demyelination". Infect Immun. 11 (5): 1147–55. doi:10.1128/iai.11.5.1147-1155.1975. PMC 415190. PMID 164412.