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Equine veterinary journal1977; 9(1); 40-42; doi: 10.1111/j.2042-3306.1977.tb03974.x

Ataxia in a Welsh cob filly due to a venous malformation in the thoracic spinal cord.

Abstract: An 8-month old Welsh Cob filly had shown progressive ataxia of the hindquarters since about 3 months of age. Autopsy revealed a venous malformation resulting in malacia in the ninth thoracic segment of the spinal cord. It is proposed that the tissue destruction associated with this congenital lesion gave rise to the ataxia.
Publication Date: 1977-01-01 PubMed ID: 837902DOI: 10.1111/j.2042-3306.1977.tb03974.xGoogle Scholar: Lookup
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  • Journal Article

Summary

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The research paper discusses a rare case of spinal cord malformation in an 8-month old Welsh Cob filly, which caused progressive ataxia or loss of full control of bodily movements. This is due to the malacia in the ninth thoracic segment of the horse’s spinal cord, a condition believed to be a result of the animal’s congenital defect.

Background of the Study

  • This study details the unique case of a Welsh Cob filly that exhibited symptoms of progressive ataxia since it was 3 months old. Ataxia is a neurological disorder that results in a lack of voluntary coordination of muscle movements.
  • The filly in this study belonged to the Welsh Cob breed, which is a type of small horse native to Wales.
  • Despite being a novel case, the researchers included no information on whether such cases were common or rare in Welsh Cob fillies or in horses generally.

Findings of the Autopsy

  • Upon death, an autopsy was performed on the filly. The autopsy revealed a venous malformation, which is an abnormal cluster of veins, in the ninth thoracic segment of the horse’s spinal cord.
  • As a result of the venous malformation, the spinal cord had developed malacia – a condition characterized by the softening of an organ due to the death of tissues or loss of cell structure and function. This malacia was found to be located exactly where the venous malformation was.

Connection between Venous Malformation and Ataxia

  • The researchers propose that the congenital (present at birth) venous malformation led to the tissue destruction that in turn, gave rise to ataxia.
  • It is suggested that the venous malformation could have interrupted the normal functioning of the ninth thoracic segment of the spinal cord, leading to the filly’s progressive ataxia.
  • The manifestation of progressive ataxia from such an early age in the filly supports the proposal that the venous malformation and resulting malacia were congenital and led to the onset of ataxia.

Cite This Article

APA
Gilmour JS, Fraser JA. (1977). Ataxia in a Welsh cob filly due to a venous malformation in the thoracic spinal cord. Equine Vet J, 9(1), 40-42. https://doi.org/10.1111/j.2042-3306.1977.tb03974.x

Publication

ISSN: 0425-1644
NlmUniqueID: 0173320
Country: United States
Language: English
Volume: 9
Issue: 1
Pages: 40-42

Researcher Affiliations

Gilmour, J S
    Fraser, J A

      MeSH Terms

      • Animals
      • Ataxia / etiology
      • Ataxia / pathology
      • Ataxia / veterinary
      • Female
      • Horse Diseases / congenital
      • Horse Diseases / pathology
      • Horses
      • Spinal Cord / blood supply
      • Spinal Cord / pathology
      • Veins / abnormalities

      Citations

      This article has been cited 4 times.
      1. De Freitas MI, Housley D, Caine A, Fauchon E, Baiker K, Corbetta D, Cherubini GB. Myelopathy secondary to an intramedullary arteriovenous malformation in a mature dog. J Vet Intern Med 2021 Mar;35(2):1098-1104.
        doi: 10.1111/jvim.16045pubmed: 33527500google scholar: lookup
      2. Zhang M, Dickinson RM. Equine small intestinal angiomatosis. Can Vet J 2020 Nov;61(11):1159-1161.
        pubmed: 33149352
      3. Nappert G, Vrins A, Breton L, Beauregard M. A retrospective study of nineteen ataxic horses. Can Vet J 1989 Oct;30(10):802-6.
        pubmed: 17423438
      4. McEntee M, Summers BA, de Lahunta A, Cummings J. Meningocerebral hemangiomatosis resembling Sturge-Weber disease in a horse. Acta Neuropathol 1987;74(4):405-10.
        doi: 10.1007/BF00687221pubmed: 3687394google scholar: lookup