@article{cartier2013neuropathological,
  title = {Neuropathological Study of Acute Myelopathy and Encephalopathy Associated to HTLV-I},
  author = {Luis Cartier and Carmen Vergara and Eugenio Ramírez and María Antonieta Valenzuela},
  year = 2013,
  url = {https://ibimapublishing.com/articles/IJCRM/2013/996020/},
  journal = {International Journal of Case Reports in Medicine},
  volume = 2012 (2012),
  pages = 8,
  doi = 10.5171/2012.996020,
  abstract = {Background a chronic and progressive parapares is without remission silent on MRI is the ordinary neurological presentation of HTLV-I, expression of a central axonopathy product of axoplasmic transport alterations. Infrequently acute forms like “T2 hyperintense acute myelopathy on MRI” have been reported. The Purpose of this presentation will be to describe the histopathological expression of this acute form and look for their pathogenesis. Patient and method: A 60 years old woman carrier of refractory anaemia and subjected to multiple transfusions, positive for HTLV-I.  She developed a severe cognitive impairment and paraplegia set up in four weeks. MRI showed T2 hyper intense lesions in white matter of brain hemispheres and in cervico-thoraxic segments of the spinal cord. She died suddenly by myocardial infarction. The neuropathological studies showed white matter necrosis insymmetricfrontal areas, conservation of cortical structures and U fibbers; necrosis in bothlateral tracts of the spinal cord (T2- T4) without gray substance damage; the microvascular walls of these areas immuno-stained with anti-Tax, expressed Tax- protein suggesting HTLV-I infection.Conclusions: This necrotizing leukopathy in absence of a primary inflammation would be the expression of HTLV-I endothelial cells infection in specific white matter areas, changing of the blood-brain barrier permeability.  },
  keywords = {Endothelial HTLV-I infection. HTLV-I acute encephalomyelopathy. Necrotizing-encephalomyelopathy.},
  note = Article ID: 996020
}