Ultrastructural Variability of Demyelinating Lesions in Experimental Allergic Encephalomyelitis and Multiple Sclerosis

  • H. Lassmann
  • K. Kitz
  • H. M. Wisniewski
Part of the Acta Neuropathologica Supplementum book series (NEUROPATHOLOGIC, volume 7)

Abstract

The pathology of chronic relapsing experimental encephalomyelitis (EAE) and multiple sclerosis are similar in several essential aspects. The similarities include the perivenous inflammation, primary segmental demyelination, formation of large, macrosco-pically visible demyelinated plaques, reactive gliosis and variable degree of remyelination (5). Differences, however, were stressed by several authors mainly regarding size of the lesions, growth of actively demyelinating lesions, involvement of inflammatory cells in the demyelinating process with special emphasis on macrophage response, role of local cells in demyelination and removal of debris and vascular (capillary) pathology.

Key words

demyelinating lesions EAE MS ultrastructure 

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References

  1. 1.
    Alvord EC, Shaw CM, Hruby S, Kies MW (1979) Has myelin basic protein received a fair trial in the treatment of multiple sclerosis. Ann Neurol 6:461–468PubMedCrossRefGoogle Scholar
  2. 2.
    Field EC (1979) Multiple sclerosis: recent advances in aetiopathogenesis. In: Recent advances in neuropathology I. Churchill, Livingstone, pp 277–298Google Scholar
  3. 3.
    Guseo A, Jellinger K (1975) The significance of perivascular infiltrations in multiple sclerosis. J Neurol 211:51–60PubMedCrossRefGoogle Scholar
  4. 4.
    Kitz K, Lassmann H, Wisniewski HM (in press) Oligodendroglial and astroglial involvement in myelin degradation in EAE in rats. Brain ResGoogle Scholar
  5. 5.
    Lassmann H, Wisniewski HM (1979) Chronic relapsing experimental allergic encephalomyelitis. Clinicopathological comparison with multiple sclerosis. Arch Neurol 36:490–497PubMedCrossRefGoogle Scholar
  6. 6.
    Lassmann H, Kitz K, Wisniewski HM (1980) Structural variability of demyelinating lesions in different models of subacute and chronic EAE. Acta Neuropathol (Berl)Google Scholar
  7. 7.
    McKeown SR, Allen IV (1978) The cellular origin of lysosomal enzymes in the plaque in multiple sclerosis. Neuropathol Appl Neurobiol 4:471–482PubMedCrossRefGoogle Scholar
  8. 8.
    Marburg O (1906) Die sogenannte „akute multiple Sklerose“. JB Psychiatr 27:211–312Google Scholar
  9. 9.
    Prineas J (1975) Pathology of the early lesion in multiple sclerosis. Hum Pathol 6:531–554PubMedCrossRefGoogle Scholar
  10. 10.
    Prineas J, Raine CS (1976) Electron microscopy and immunperoxidase studies in early multiple sclerosis lesions. Neurology 26/29Google Scholar
  11. 11.
    Prineas J, Wright RG (1978) Macrophages, lymphocytes and plasma cells in the perivascular compartment in chronic multiple sclerosis. Lab Invest 38:409–421PubMedGoogle Scholar
  12. 12.
    Suzuki K, Andrews JM, Waltz JM, Terry RD (1969) Ultrastructural studies of multiple sclerosis. Lab Invest 20:444–454PubMedGoogle Scholar
  13. 13.
    Waksman BH, Adams RD (1962) A histologic study of the early lesions in experimental allergic encephalomyelitis in the guinea pig and rabbit. Am J Pathol 41:135–153PubMedGoogle Scholar
  14. 14.
    Wolfgram F (1979) What if multiple sclerosis isn’t an immunological or a viral disease? The case for a circulating toxin. Neurochem Res 4:1–14PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag 1981

Authors and Affiliations

  • H. Lassmann
    • 1
    • 2
    • 3
  • K. Kitz
    • 1
    • 2
    • 3
  • H. M. Wisniewski
    • 1
    • 2
    • 3
  1. 1.Neurological Institute of University of ViennaViennaAustria
  2. 2.Institute of Micromorphology and Electronmicroscopy of the University of ViennaAustria
  3. 3.N.Y.S. Institute of Basic Research in Mental RetardationUSA

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