Letter | Published:

Conduction block in the peripheral nervous system in experimental allergic encephalomyelitis

Nature volume 296, pages 860862 (29 April 1982) | Download Citation

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Abstract

Experimental allergic encephalomyelitis (EAE) has been widely studied as a model of multiple sclerosis, a central nervous system (CNS) disease of unknown aetiology. The clinical features of both EAE and multiple sclerosis provide the only guide to the progress and severity of these diseases, and are used to assess the response to treatment. In such comparisons the clinical features of EAE are assumed to be due to lesions in the CNS, but in this disease there is also histological evidence of damage to the peripheral nervous system1–8. However, the functional consequences of such peripheral lesions have been entirely ignored. To examine this we have studied nerve conduction in rabbits with EAE. We report here that most of the large diameter afferent fibres are blocked in the region of the dorsal root ganglion and at the dorsal root entry zone, thus accounting for the loss of tendon jerks and also, through the severe loss of proprioceptive information, the ataxia of these animals. We conclude that whenever clinical comparisons are made between EAE and multiple sclerosis, the pathophysiology associated with the histological damage of the peripheral nervous system must be taken into account.

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References

  1. 1.

    , & J. Immun. 57, 179–194 (1947).

  2. 2.

    & J. Neuropath. exp. Neurol. 13, 60–89 (1954).

  3. 3.

    & J. exp. Med. 102, 213–236 (1955).

  4. 4.

    , & Lab. Invest. 21, 105–118 (1969).

  5. 5.

    & J. Neuropath. exp. Neurol. 15, 293–333 (1956).

  6. 6.

    , & Lab. Invest. 21, 316–327 (1969).

  7. 7.

    & J. Neurocytol. 7, 265–282 (1978).

  8. 8.

    , & in Search For the Cause of Multiple Sclerosis and Other Chronic Diseases of the Central Nervous System (ed. Boese, A.) 96–104 (Verlag Chemie, Weinheim, 1980).

  9. 9.

    Archs Neurol. Psychiat., Chicago 58, 391–416 (1947).

  10. 10.

    & J. exp. Med. 61, 689–702 (1935).

  11. 11.

    & Ann. Neurol. 1, 144–148 (1977).

  12. 12.

    in Progress in Neuropathology Vol. 3 (ed. Zimmerman, H. M.) 225–251 (Grune & Stratton, New York, 1976).

  13. 13.

    , , & Ann. N.Y. Acad. Sci. 122, 333–345 (1965).

  14. 14.

    & in The Suppression of Experimental Allergic Encephalomyelitis and Multiple Sclerosis (eds Davison, A. N. & Cuzner, M. L.) 199–209 (Academic, London, 1980).

  15. 15.

    Archs Neurol. 28, 287–292 (1973).

  16. 16.

    , & J. Physiol., Lond. 313, 301–315 (1981).

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Affiliations

  1. Sobell Department of Neurophysiology, Institute of Neurology, University of London, Queen Square, London WC1N 3BG, UK

    • M. P. Pender
    •  & T. A. Sears

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DOI

https://doi.org/10.1038/296860a0

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