Tropical spastic paraparesis pathophysiology

Please help WikiDoc by adding content here. It’s easy! Click here to learn about editing.

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.

References

↑ Machigashira N, Yoshida Y, Wang S, Osame M (2001). “HTLV-1-associated myelopathy/tropical spastic paraparesis with pseudohypoparathyroidism”. Neurology. 56 (1): 104–6. PMID 11148245. Retrieved 2012-12-10. Unknown parameter |month= ignored (help)

Template:WH Template:WS

[pmid11148245-1] Machigashira N, Yoshida Y, Wang S, Osame M (2001). “HTLV-1-associated myelopathy/tropical spastic paraparesis with pseudohypoparathyroidism”. Neurology. 56 (1): 104–6. PMID 11148245. Retrieved 2012-12-10. Unknown parameter |month= ignored (help)

[1]