Acta Neuropathologica

, Volume 73, Issue 3, pp 275–280 | Cite as

Feline dysautonomia: an ultrastructural study of neurones in the XII nucleus

  • M. M. Pollin
  • I. R. Griffiths
Regular Papers

Summary

A feline dysautonomia of unknown aetiology has been reported in numerous cats in the United Kingdom since 1981. The consistent histological lesion is a chromatolytic-type change within the neurones of the autonomic nervous system, which is also found less frequently in non-autonomic regions, such as the XII nucleus. This study describes the ultrastructural changes in the XII nucleus within the first 2 weeks of clinical disease. In the abnormal neurones there is a dispersion of the Nissl substance, progressing to dilation of individual cisternae by an electron-dense floccular material. Such cisternae have lost the majority of their ribosomes. Normal Golgi complexes can be seen in neurones where there is only slight dispersion of the Nissl substance, but no Golgi complexes, either normal or abnormal, can be identified in any cell in which the Nissl substance is markedly disrupted. There is proliferation of smooth endoplasmic reticulum in several neurones, and there may also be an increased number of morphologically normal mitochondria. The nuclei of affected neurones are eccentric with crenations of the nuclear envelope, and in some cases nucleolar changes are also observed. Autophagic vacuoles are present in small numbers. Other organelles appear normal. These findings compare closely to those for the autonomic neurones, suggesting that the primary effect of the causal agent(s) is on the protein synthetic pathway of specific neurones.

Key words

Dysautonomia Protein biosynthesis Rough endoplasmic reticulum Golgi apparatus 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Aldskogius H (1978) Fine structural changes in nerve cell bodies of the adult rabbit dorsal motor vagal nucleus during axon reaction. Neuropathol Appl Neurobiol 4:323–341Google Scholar
  2. Barlow RM (1959) Neuropathological observations in grass sickness of horses. J Comp Pathol 79:407–411Google Scholar
  3. Barron KD, Chiang TY, Daniels AC, Doolin PF (1971) Subcellular accompaniments of axon reaction in cervical motorneurones of the cat. Prog Neuropathol 1:225–280Google Scholar
  4. Bernhard W, Granboulan N (1968) Electron microscopy of the nucleolus in vertebrate cells. In: Dalton AJ, Haguenau F (eds) Ultrastructure in biological systems, vol 3, The nucleus. Academic Press, New York, pp 81–149Google Scholar
  5. Gaskell CJ, Edney ATB (1985) Feline dysautonomia distribution. Vet Rec 117:395Google Scholar
  6. Gilmour JS, Mould DL (1977) Experimental studies of neurotoxic activity in blood fractions from acute cases of grass sickness. Res Vet Sci 22:1–4Google Scholar
  7. Griffiths IR, Nash AS, Sharp NJH (1982) The Key-Gaskell syndrome. The current situation. Vet Rec 111:532–533Google Scholar
  8. Griffiths IR, Sharp NJH, McCulloch MC (1985) Feline dysautonomia (the Key-Gaskell syndrome): an ultrastructural study of autonomic ganglia and nerves. Neuropathol Appl Neurobiol 11:17–29Google Scholar
  9. Inamdar S, Easton LB, Lester G (1982) Acquired postganglionic cholinergic dysautonomia. A case report and review of the literature. Pediatrics 70:976–978Google Scholar
  10. Jacobs JM, Miller RH, Whittle A, Cavanagh JB (1979) Studies on the early changes in acute isoniazid neuropathy in the rat. Acta Neuropathol (Berl) 47:85–92Google Scholar
  11. Jones HB, Cavanagh JB (1981) Comparisons between the early changes in isoniazid intoxication and the chromatolytic response to nerve ligation in spinal ganglion cells of the rat. Neuropathol Appl Neurobiol 7:489–501Google Scholar
  12. Key TSA, Gaskell CJ (1982) Puzzling syndrome in cats associated with pupillary dilatation. Vet Rec 110:160Google Scholar
  13. Lieberman AR (1971) The axon reaction: a review of the principal features of perikaryon responses to axon injury. Int Rev Neurobiol 14:49–124Google Scholar
  14. Mahaffey LW (1959) Ganglionic lesions in grass sickness of horses. Vet Rec 71:170–171Google Scholar
  15. Obel A-L (1955) Studies in grass disease. The morphological picture with special reference to the vegetative nervous system. J Comp Pathol 65:334–346Google Scholar
  16. Pollin MM (1985) Feline dysautonomia: the Key-Gaskell syndrome. A clinical pharmacological and pathological study. M.V.M. Thesis, University of GlasgowGoogle Scholar
  17. Pollin MM, Sullivan M (1986) A canine dysautonomia resembling the Key-Gaskell syndrome. Vet Rec 118:402–403Google Scholar
  18. Prineas J (1969) The pathogenesis of dying-back polyneuropathies. Part II: An ultrastructural study of experimental acrylamide intoxication in the cat. J Neuropathol Exp Neurol 28:598–621Google Scholar
  19. Rochlitz I, Bennett AM (1982) Key-Gaskell syndrome in a bitch. Vet Rec 112:614Google Scholar
  20. Sharp NJH, Nash AS, Griffiths IR (1984) Feline dysautonomia (the Key-Gaskell syndrome). A clinical and pathological study of 40 cases. J Small Anim Pract 25:599–615Google Scholar
  21. Sterman AB (1983) Altered sensory ganglia in acrylamide neuropathy. Quantitative evidence of neuronal reorganisation. J Neuropathol Exp Neurol 42:166–176Google Scholar
  22. Torvik A (1976) Central chromatolysis and the axon reaction: a re-appraisal. Neuropathol Appl Neurobiol 2:423–432Google Scholar
  23. Wiley RG, Donohue-Rolfe A, Keusch GT (1985) Axonally transportedShigella cytotoxin is neuronotoxic. J Neuropathol Exp Neurol 44:496–506Google Scholar

Copyright information

© Springer-Verlag 1987

Authors and Affiliations

  • M. M. Pollin
    • 1
  • I. R. Griffiths
    • 1
  1. 1.Department of Surgery/ReproductionUniversity of Glasgow Veterinary SchoolGlasgowUK

Personalised recommendations