Brain Advance Access originally published online on March 17, 2005
Brain 2005 128(5):979-987; doi:10.1093/brain/awh457
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Tissue preconditioning may explain concentric lesions in Baló's type of multiple sclerosis
1 Brain Research Center, Medical University of Vienna, Vienna, Austria, 2 Department of Neuropathology, University of Goettingen, Goettingen, Germany, 3 Department of Neuropathology, Queen's University, Kingston, Ontario, Canada, 4 National Institute for Longevity Sciences, NCGG, Aichi, Japan, 5 Department of Neurology, Municipal Hospital, Szekesfehervar 6 Department of Neuropathology, Municipal Hospital, Esztergom, Hungary, 7 Department of Neurology, Mayo Clinic, Rochester, MN, USA and 8 Department of Neuropsychiatry, Santo Tomas University, Manila, Philippines
Correspondence to: Prof. Dr Hans Lassmann, Brain Research Center, Medical University of Vienna, Spitalgasse 4, A-1090 Wien, Austria. E-mail: hans.lassmann{at}univie.ac.at
Lesions of Baló's concentric sclerosis are characterized by alternating layers of myelinated and demyelinated tissue. The reason for concentric demyelination in this variant of multiple sclerosis is unclear. In the present study we investigated the immunopathology in autopsy tissue of 14 patients with acute multiple sclerosis or fulminant exacerbations of chronic multiple sclerosis with Baló-type lesions in the CNS, focusing on the patterns of tissue injury in actively demyelinating lesions. We found that all active concentric lesions followed a pattern of demyelination that bears resemblances to hypoxia-like tissue injury. This was associated with high expression of inducible nitric oxide synthase in macrophages and microglia. At the edge of active lesions and, less consistently, in the outermost layer of preserved myelin, proteins involved in tissue preconditioning, such as hypoxia-inducible factor 1
and heat-shock protein 70, were expressed mainly in oligodendrocytes and to a lesser degree also in astrocytes and macrophages. Due to their neuroprotective effects, the rim of periplaque tissue, where these proteins are expressed, may be resistant to further damage in an expanding lesion and may therefore remain as a layer of preserved myelinated tissue.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  D. Mahad, I. Ziabreva, H. Lassmann, and D. Turnbull Mitochondrial defects in acute multiple sclerosis lesions Brain, July 1, 2008; 131(7): 1722 - 1735. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Li, C. A. Ghiani, J. Y. Kim, A. Liu, J. Sandoval, J. DeVellis, and P. Casaccia-Bonnefil Inhibition of p53 Transcriptional Activity: A Potential Target for Future Development of Therapeutic Strategies for Primary Demyelination J. Neurosci., June 11, 2008; 28(24): 6118 - 6127. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Chaodong Wang, K.-N. Zhang, X.-M. Wu, Gang Huang, X.-F. Xie, X.-H. Qu, and Y.-Q. Xiong Balo's disease showing benign clinical course and co-existence with multiple sclerosis-like lesions in Chinese Multiple Sclerosis, April 1, 2008; 14(3): 418 - 424. [Abstract] [PDF]
|
|
|
|
|
|
R. Hoftberger, F. Garzuly, H.P. Dienes, J. Grubits, B. Rohonyi, G. Fischer, Z. Hanzely, H. Lassmann, and H. Budka Fulminant central nervous system demyelination associated with interferon-{alpha} therapy and hepatitis C virus infection Multiple Sclerosis, November 1, 2007; 13(9): 1100 - 1106. [Abstract] [PDF]
|
|
|
|
|
|
C. Marik, P. A. Felts, J. Bauer, H. Lassmann, and K. J. Smith Lesion genesis in a subset of patients with multiple sclerosis: a role for innate immunity? Brain, November 1, 2007; 130(11): 2800 - 2815. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Lindquist, N. Bodammer, J. Kaufmann, F. Konig, H.-J. Heinze, W. Bruck, and M. Sailer Histopathology and serial, multimodal magnetic resonance imaging in a multiple sclerosis variant Multiple Sclerosis, May 1, 2007; 13(4): 471 - 482. [Abstract] [PDF]
|
|
|
|
 |
|
 J. M. Ness, D. Chabas, A. D. Sadovnick, D. Pohl, B. Banwell, B. Weinstock-Guttman, and for the International Pediatric MS Study Group Clinical features of children and adolescents with multiple sclerosis Neurology, April 17, 2007; 68(16_suppl_2): S37 - S45. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S Love Demyelinating diseases. J. Clin. Pathol., November 1, 2006; 59(11): 1151 - 1159. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Merkler, T. Ernsting, M. Kerschensteiner, W. Bruck, and C. Stadelmann A new focal EAE model of cortical demyelination: multiple sclerosis-like lesions with rapid resolution of inflammation and extensive remyelination Brain, August 1, 2006; 129(8): 1972 - 1983. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M H Barnett, A P. Henderson, and J W Prineas The macrophage in MS: just a scavenger after all? Pathology and pathogenesis of the acute MS lesion Multiple Sclerosis, April 1, 2006; 12(2): 121 - 132. [Abstract] [PDF]
|
|