Leukoencephalopathy resolution after atypical mycobacterial treatment: a case report

Carregando...
Imagem de Miniatura
Citações na Scopus
1
Tipo de produção
article
Data de publicação
2015
Título da Revista
ISSN da Revista
Título do Volume
Editora
BIOMED CENTRAL LTD
Citação
BMC NEUROLOGY, v.15, article ID 159, 6p, 2015
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Background: Association of leukoencephalopathy and atypical mycobacteriosis has been rarely reported. We present a case that is relevant for its unusual presentation and because it may shed further light on the pathogenic mechanisms underlying reversible encephalopathies. Case report: We report the case of a Hispanic 64-year-old woman with cognitive decline and extensive leukoencephalopathy. Magnetic resonance imaging revealed white-matter lesions with increased water diffusivity, without blood-brain-barrier disruption. Brain biopsy showed tissue rarefaction with vacuolation, mild inflammation, few reactive astrocytes and decreased aquaporin water-channel expression in the lesions. Six months later, she was diagnosed with atypical mycobacterial pulmonary infection. Brain lesions resolved after antimycobacterial treatment. Conclusion: We hypothesize leukoencephalopathic changes and vasogenic edema were associated with decreased aquaporin expression. Further studies should clarify if reversible leukoencephalopathy has a causal relationship with decreased aquaporin expression and atypical mycobacterial infection, and mechanisms underlying leukoencephalopathy resolution after antimycobacterial treatment. This article may contribute to the understanding of pathogenic mechanisms underlying magnetic resonance imaging subcortical lesions and edema, which remain incompletely understood.
Palavras-chave
Reversible encephalopathy syndrome, PRES, Mycobacteriosis, Leukoencephalopathy, Vasogenic edema, Aquaporin water-channel
Referências
  1. Bartynski WS, 2006, AM J NEURORADIOL, V27, P2179
  2. Char G, 2000, W INDIAN MED J, V49, P70
  3. CHESTER EM, 1978, NEUROLOGY, V28, P928
  4. Chetty KG, 1997, INT J TUBERC LUNG D, V1, P579
  5. Dalhoff A, 2003, LANCET INFECT DIS, V3, P359, DOI 10.1016/S1473-3099(03)00658-3
  6. DASTUR DK, 1966, ACTA NEUROPATHOL, V6, P311
  7. DASTUR DK, 1986, CHILD NERV SYST, V2, P13, DOI 10.1007/BF00274027
  8. Feske SK, 2011, SEMIN NEUROL, V31, P202, DOI 10.1055/s-0031-1277990
  9. Guerriero S, 2012, CASE REP OPHTHALMOL, DOI [10.1155/2012/850176, DOI 10.1155/2012/850176]
  10. HANSSON HA, 1975, ACTA NEUROPATHOL, V32, P187
  11. Hinchey J, 1996, NEW ENGL J MED, V334, P494, DOI 10.1056/NEJM199602223340803
  12. Kim HJ, 2011, EUR NEUROL, V65, P156, DOI 10.1159/000324170
  13. Lammie GA, 2007, ACTA NEUROPATHOL, V113, P227, DOI 10.1007/s00401-006-0172-7
  14. Lee J, 2010, J NEUROIMMUNE PHARM, V5, P210, DOI 10.1007/s11481-010-9199-6
  15. Lee VH, 2008, ARCH NEUROL-CHICAGO, V65, P205, DOI 10.1001/archneurol.2007.46
  16. Magana SM, 2009, NEUROLOGY, V72, P712, DOI 10.1212/01.wnl.0000343001.36493.ae
  17. Mak A, 2008, RHEUMATOLOGY, V47, P256, DOI 10.1093/rheumatology/kem319
  18. Okada H, 2010, INTERNAL MED, V49, P2113, DOI 10.2169/internalmedicine.49.3323
  19. UDANI PM, 1970, J NEUROL SCI, V10, P541, DOI 10.1016/0022-510X(70)90187-5
  20. Viehman J Alexander, 2013, HIV AIDS (Auckl), V5, P61, DOI 10.2147/HIV.S36545
  21. Wolf NA, 2007, J NEUROIMMUNOL, V185, P115, DOI 10.1016/j.jneuroim.2007.02.001
  22. Zorzella-Pezavento SF, 2013, CLIN DEV IMMUNOL, V2013