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Relationship of spontaneous fibrillation potentials to muscle fibre segmentation in human muscular dystrophy

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Abstract

DENERVATED skeletal muscle fibres have long been known to show spontaneous fibrillation potentials, this being one of the features resulting from the removal of the trophic influence of the motor nerve1. Electromyography (EMG) has shown spontaneous fibrillations in human myopathies such as myositis or muscular dystrophy2–6, but their true incidence and mechanism is still obscure. We propose that myopathic fibrillations result from segmental necrosis of muscle fibres so that a distal fibre segment is separated from the part carrying the motor endplate. We show here, first, that after experimental myotomy in the baboon biceps muscle, the nerve-free segments develop fibrillation after a consistent delay and second, that by comparing different clinical types of human myopathies a correlation can be found between the incidence of focal necrosis and spontaneous fibrillation potentials. Our findings are consistent with our previous report of collateral innervation of newly formed nuscle fibres in Duchenne muscular dystrophy7.

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References

  1. Thesleff, S., and Ward, M. R., J. Physiol. Lond., 244, 313–323 (1975).

    Article  CAS  Google Scholar 

  2. Norris, F. H., and Chatfield, P. O., Electroenceph. clin. Neurophysiol., 7, 391–397 (1955).

    Article  Google Scholar 

  3. Eaton, L. M., and Lambert, E. H., J. Am. med. Ass., 163, 1117–1124 (1957).

    Article  CAS  Google Scholar 

  4. Smith, H. L., Amick, L. D., and Johnson, W. W., J. Pediat., 69, 67–79 (1966).

    Article  CAS  Google Scholar 

  5. Buchthal, F., and Rosenfalck, P., Electroenceph. clin. Neurophysiol., 20, 321–336 (1966).

    Article  CAS  Google Scholar 

  6. Desmedt, J. E., and Emeryk, B., Am. J. Med., 45, 853–872 (1968).

    Article  CAS  Google Scholar 

  7. Desmedt, J. E., and Borenstein, S., Nature, 246, 500–501 (1973).

    Article  ADS  CAS  Google Scholar 

  8. Buchthal, F., Guld, C., and Rosenfalck, P., Acta physiol., scand., 35, 174–190 (1955).

    Article  CAS  Google Scholar 

  9. Desmedt, J. E., Acta Neurol. Belg., 58, 977–1017 (1958).

    CAS  Google Scholar 

  10. Gilliatt, R. W., and Hjorth, R. J., J. Neurol. Neurosurg. Psychiat., 35, 335–341 (1972).

    Article  CAS  Google Scholar 

  11. Harris, J. B., and Thesleff, S., Nature new biol., 236, 60–61 (1972).

    Article  CAS  Google Scholar 

  12. Belmar, J., and Eyzaguirre, C., J. Neurophysiol., 29, 425–441 (1966).

    Article  CAS  Google Scholar 

  13. Katz, B., and Miledi, R., J. Physiol., 170, 389–396 (1964).

    Article  CAS  Google Scholar 

  14. Miledi, R., Nature, 193, 281–282 (1962).

    Article  ADS  CAS  Google Scholar 

  15. Desmedt, J. E., and Borenstein, S., Archs Neurol., Chicago (in the press).

  16. Pearce, G. W., and Walton, J. N., J. path. Bact. 83, 535–550 (1962).

    Article  CAS  Google Scholar 

  17. Adams, R. D., in Clinical Studies in Myology, part 2 (edit. by Kakulas, B. A.), 695–711 (Excerpta Medica, Amsterdam, 1973).

    Google Scholar 

  18. Adams, R. D., in The Striated Muscle (edit. by Pearson, C. M., and Mostofi, F. K.), 292–300 (Williams and Wilkins, Baltimore, 1973).

    Google Scholar 

  19. Desmedt, J. E., and Borenstein, S., in Exploratory Concepts in Muscular Dystrophy, part 2, (edit. by Milhorat, A. T.), 555–559 (Excerpta Medica, Amsterdam, 1974).

    Google Scholar 

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DESMEDT, J., BORENSTEIN, S. Relationship of spontaneous fibrillation potentials to muscle fibre segmentation in human muscular dystrophy. Nature 258, 531–534 (1975). https://doi.org/10.1038/258531a0

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  • DOI: https://doi.org/10.1038/258531a0

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