Advertisement

Acta Neuropathologica

, Volume 69, Issue 3–4, pp 234–243 | Cite as

Similarities between the Forssman carotid syndrome and experimental allergic encephalomyelitis

  • N. Tsukada
  • S. Ansar Ahmed
  • W. M. H. Behan
  • P. O. Behan
Original Works

Summary

The Forssman carotid syndrome was induced in guinea pigs to study the mechanism of demyelination-like lesions in this animal model and to compare it with experimental allergic encephalomyelitis (EAE). Acute lesions were studied at 1–3 days after intracarotid injection of rabbit anti-Forssman antibody and chronic lesions at 7–21 days post injection, using routine histological, immunofluorescent, and electron-microscopic techniques. The results were compared to those in a group of guinea pigs with acute or chronic lesions of EAE. The picture was remarkably similar in the two conditions, in regard to localization in the central nervous system (CNS), composition of cellular infiltrates, diameter of lesions produced, myelin loss and axonal degeneration, together with gamma globulin deposition in small vessels in affected areas. The differences were that in the Forssman carotid syndrome, in contrast to EAE, there were no mononuclear cell infiltrates in the acute phase, and no evidence of macrophages invading myelin sheaths was detected. Perivascular lesions consisted of demyelination within infiltrates of mononuclear cell in chronic relapsing EAE, but not in the Forssman carotid syndrome. It is suggested that investigation of the distinction between the two models of the CNS may be of benefit in the pathogenetic study of demyelinating disease.

Key words

Forssman carotid syndrome Experimental allergic encephalomyelitis (EAE) Vasculopathy 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Åström KE, Waksman BH (1962) The passive transfer of experimental allergic encephalomyelitis and neuritis with living lymphoid cells. J Pathol Bacteriol 83:89–109Google Scholar
  2. Avrameas S (1969) Coupling of enzymes to protein with glutaraldehyde. Use of the conjugates for the detection of antigens and antibodies. Immunochemistry 6:43–52Google Scholar
  3. Behan PO, Kies M, Lisak W, Sheremata W, Lamarache JB (1973) Immunologic mechanisms in experimental allergic encephalomyelitis in non-human primates. Arch Neurol 29:4–9Google Scholar
  4. Bornstein MB, Raine CS (1976) The initial structural lesion in serum-induced demyelination in vitro. Lab Invest 35:391–401Google Scholar
  5. Field EJ, Raine CS (1966) Experimental allergic encephalomyelitis. An electron-microscopic study. Am J Pathol 49:537–553Google Scholar
  6. Hart MN, Debault LE, Sadewasser KL, Cancilla PA, Henriquez EM (1981) Morphologic effects of antibody to mouse brain endothelium in vivo. J Neuropathol Exp Neurol 40:84–91Google Scholar
  7. Jervis GA (1943) Forssman's “carotid syndrome”, a contribution to the study of anaphylactic changes in the nervous system from the standpoint of pathology. Arch Pathol 35:560–570Google Scholar
  8. Koh C-S, Tsukada N, Yanagisawa N, Kunishita T, Uemura K, Taketomi T (1981) Mild encephalitogenic activity of basic protein-acid lipid complex from myelin and detection of immune complexes in experimental allergic encephalomyelitis. J Neuroimmunol 1:69–80Google Scholar
  9. Kristensson K, Wisniewski HM (1977) Chronic relapsing experimental allergic encephalomyelitis. Studies in vascular permeability changes. Acta Neuropathol (Berl) 39:189–194Google Scholar
  10. Leibowitz S, Morgan RS, Berkinshwa-Smith EMI, Wright GP (1961) Cerebral vascular damage in guinea-pigs induced by various heterophil antisera injected by the Forssman intracarotid technique. Br J Pathol 42:455–463Google Scholar
  11. Oldstone MB, Dixon FJ (1968) Early events in allergic encephalomyelitis. Trans Am Neurol Assoc 93:257–259Google Scholar
  12. Paterson PY (1960) Transfer of allergic encephalomyelitis in rats by means of lymph node cells. J Exp Med 111:119–153Google Scholar
  13. Paterson PY (1977) Autoimmune neurologic disease — experimental animal systems and implications for multiple sclerosis. In: Talal N (ed) Autoimmunity, genetics, immunologic, virologic, and clinical aspects. Academic Press, New York, pp 633–692Google Scholar
  14. Pette E, Mannweiler K, Placios O, Mutze B (1965) Phenomena of the cell membrane and their possible significance for the pathogenesis of so-called autoimmune diseases of the nervous system. Ann NY Acad Sci 122:417–428Google Scholar
  15. Poser CM, Behan PO (1982) Late onset of Guillain-Barré syndrome. J Neuroimmunol 3:27–42Google Scholar
  16. Raine CS, Stone (1977) Animal model for multiple sclerosis —chronic experimental allergic encephalomyetitis in inbred guinea pigs. NY State J Med 77:1693–1696Google Scholar
  17. Raine CS, Bornstein MB (1970) Experimental allergic encephalomyelitis — an ultrastructural study of experimental demyelination in vitro. J Neuropath Exp Neurol 29:177–191Google Scholar
  18. Spear GS (1962) Forssman antigen in the guinea pig: a histologic study. Bull Johns Hopkins Hosp 111:252–265Google Scholar
  19. Tanaka N, Ledue EH (1956) A study of the cellular distribution of Forssman antigen in various species. J Immunol 77:198–212Google Scholar
  20. Vulpe M, Hawkins A, Rozdilsky B (1960) Permeability of cerebral blood vessels in experimental allergic encephalomyelitis studied by radioactive iodinated bovine albumin. Neurology (Minneap) 10:171–197Google Scholar

Copyright information

© Springer-Verlag 1986

Authors and Affiliations

  • N. Tsukada
    • 1
  • S. Ansar Ahmed
    • 1
  • W. M. H. Behan
    • 1
  • P. O. Behan
    • 2
  1. 1.Dept. of Neurology and PathologyGlasgow UniversityGlasgowScotland
  2. 2.Dept. of Medicine (Neurology), School of MedicineShinshu UniversityMatsumotoJapan

Personalised recommendations