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Acta neuropathologica1979; 48(2); 145-148; doi: 10.1007/BF00691156

Optic neuropathy in a horse.

Abstract: A 10-month-old thoroughbred colt developed sudden complete blindness; no other neurological abnormality was detected. At necropsy 3.5 months later lesions were confined to both optic pathways in which there was extensive degeneration of axons and myelin and gliosis. The cause of the optic lesion was not determined but the lesion may be a toxic neuropathy.
Publication Date: 1979-11-01 PubMed ID: 506696DOI: 10.1007/BF00691156Google Scholar: Lookup
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Summary

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The study presents and discusses the case of a young thoroughbred horse that unexpectedly lost its vision completely, with further diagnostics failing to detect any other neurological issues. Upon post-mortem examination several months later, the only identified pathology was extensive damage to the optic pathways, including significant degeneration of nerve fibers and supporting cells, whose cause remains unknown but speculatively attributed to toxic exposure.

Objective

The main objective of the study was to understand the sudden onset of blindness in a young thoroughbred horse. The paper aimed to provide a detailed description of the clinical condition, neuropathological changes, and brainstorm potential causative factors despite the inability to determine the exact etiological agent.

Case Presentation and Results

  • The subject of this study was a 10-month-old thoroughbred colt that suddenly developed complete blindness. Apart from vision loss, no other neurological abnormalities were found during the initial examination, which added to the bafflement about the cause.
  • Three and a half months post the onset of the condition, the horse underwent a necropsy (an autopsy for animals). During this procedure, lesions were found in both optic pathways of the horse – the networks responsible for conducting visual information from the retina to the brain. These lesions were characterized by a significant loss of axons and myelin – the integral components of nerve cells responsible for transmitting signals – and gliosis, a reactive change of the glial cells in response to damage to the central nervous system.
  • Despite these findings, the team could not pinpoint the exact cause of such extensive optic damage. However, they speculated that it might be a case of toxic neuropathy, suggesting the horse could have been exposed to some form of noxious substance leading to the optic lesion. Still, without a definitive cause or additional supporting evidence, this remains a theory.

Conclusion

Ultimately, this research presents an interesting case of sudden blindness in a young horse, pointing to the significance of further studies into equine optic neuropathies. Given the extensive damage to the optic pathways and the lack of other neurological signs, the condition hinted at a case of a possible toxic neuropathy. Conclusive research would require additional investigations, such as screening for potential toxins or the examination of similar cases.

Cite This Article

APA
Kelly DF, Pinsent PJ. (1979). Optic neuropathy in a horse. Acta Neuropathol, 48(2), 145-148. https://doi.org/10.1007/BF00691156

Publication

ISSN: 0001-6322
NlmUniqueID: 0412041
Country: Germany
Language: English
Volume: 48
Issue: 2
Pages: 145-148

Researcher Affiliations

Kelly, D F
    Pinsent, P J

      MeSH Terms

      • Animals
      • Axons
      • Gliosis / pathology
      • Horse Diseases / pathology
      • Horses
      • Male
      • Optic Neuritis / pathology
      • Optic Neuritis / veterinary

      References

      This article includes 3 references
      1. Little PB, Lwin US, Fretz P. Verminous encephalitis of horses: experimental induction with Strongylus vulgaris larvae.. Am J Vet Res 1974 Dec;35(12):1501-10.
        pubmed: 4433067
      2. Little PB. Cerebrospinal nematodiasis of Equidae.. J Am Vet Med Assoc 1972 May 15;160(10):1407-13.
        pubmed: 5023157
      3. O'Brien JJ. Toxicological aspects of some modern anthelmintics.. Aust Vet J 1970 Jul;46(7):297-300.

      Citations

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