Tropical spastic paraparesis pathophysiology: Difference between revisions
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{{Tropical spastic paraparesis}} | {{Tropical spastic paraparesis}} | ||
{{CMG}} | {{CMG}} | ||
==Pathophysiology== | ==Pathophysiology== | ||
When infected by [[HTLV-1]]<ref name="pmid11148245">{{cite journal |author=Machigashira N, Yoshida Y, Wang S, Osame M |title=HTLV-1-associated myelopathy/tropical spastic paraparesis with pseudohypoparathyroidism |journal=[[Neurology]] |volume=56 |issue=1 |pages=104–6 |year=2001 |month=January |pmid=11148245 |doi= |url=http://www.neurology.org/cgi/pmidlookup?view=long&pmid=11148245 |accessdate=2012-12-10}}</ref> the host mounts an antigen specific immune response towards the [[HTLV-1]] antigen. [[Cytotoxic T-lymphocytes]] of the host’s immune response release [[cytokines]] in an effort to fight the infection. These [[cytokines]] facilitate the [[endothelium|transendothelial]] migration of [[lymphocytes]] across the blood-brain barrier. Once [[cytokines]] are within the central nervous system demyelination is brought as a result of bystander cell injury. The disease is [[chronic (medicine)|chronic]], progressing slowly, usually causing symptoms 20-30 years after infection. | |||
==References== | ==References== | ||
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Latest revision as of 19:01, 18 September 2017
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Tropical spastic paraparesis Microchapters |
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Differentiating Tropical spastic paraparesis from other Diseases |
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Diagnosis |
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Treatment |
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Case Studies |
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Tropical spastic paraparesis pathophysiology On the Web |
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American Roentgen Ray Society Images of Tropical spastic paraparesis pathophysiology |
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Directions to Hospitals Treating Tropical spastic paraparesis |
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Risk calculators and risk factors for Tropical spastic paraparesis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
When infected by HTLV-1[1] the host mounts an antigen specific immune response towards the HTLV-1 antigen. Cytotoxic T-lymphocytes of the host’s immune response release cytokines in an effort to fight the infection. These cytokines facilitate the transendothelial migration of lymphocytes across the blood-brain barrier. Once cytokines are within the central nervous system demyelination is brought as a result of bystander cell injury. The disease is chronic, progressing slowly, usually causing symptoms 20-30 years after infection.