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Journal of equine science2016; 27(3); 119-124; doi: 10.1294/jes.27.119

Four cases of equine motor neuron disease in Japan.

Abstract: In this study, fasciculation of the limbs and tongue was observed in four horses kept by a riding club. Neurogenic muscle atrophy was also observed in biopsy of pathological tissues. In addition, in two cases that subjected to autopsy, Bunina-like bodies of inclusion in the cell bodies of neurons in the spinal cord ventral horn were confirmed, leading to a diagnosis of equine motor neuron disease (EMND). Serum vitamin E concentrations varied between 0.3 and 0.4µg/ml, which is significantly lower than the levels in normal horses. Although lack of vitamin E is speculated to be a contributory factor for development of EMND, no significant improvement was observed following administration of vitamin E.
Publication Date: 2016-09-30 PubMed ID: 27703407PubMed Central: PMC5048359DOI: 10.1294/jes.27.119Google Scholar: Lookup
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Summary

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The researchers examined four horses that presented signs of neurodegenerative disease, ultimately concluding that they suffered from Equine Motor Neuron Disease (EMND), a condition possibly linked to vitamin E deficiency.

Objective of the Study

  • This research paper presents a detailed study and diagnosis of four cases of a neurodegenerative disease known as equine motor neuron disease (EMND) in horses in Japan.

Observations Made

  • The research team observed some unusual behaviors in the horses; these included fasciculation of the limbs and tongue (twitching or spasms) and neurogenic muscle atrophy (muscle wasting caused by nerve damage).
  • Two of the horses were autopsied, and the researchers found Bunina-like bodies, which are physical signs of motor neuron degeneration within neurons in the spinal cord ventral horn, which led to the diagnosis of EMND.

Role of Vitamin E

  • The team found that the serum vitamin E concentrations in the horses ranged between 0.3 and 0.4µg/ml, a significantly lower level compared to normal horses.
  • Speculations were made suggesting that this deficiency of vitamin E could have contributed to the development of EMND.

Effect of Vitamin E Administration

  • However, despite the dominant speculation around vitamin E deficiency playing a role in the disease, the researchers observed no significant improvement in the horse’s conditions after administering vitamin E.
  • This suggests that while vitamin E deficiency might be linked to EMND, it is not necessarily a solution or a way to treat the condition.

Conclusion

  • This study represents an exploratory look into the occurrence of EMND in horses, offering some evidence for a possible link to vitamin E deficiency, but also indicating that more research may be needed to fully understand and treat the disease.

Cite This Article

APA
Sasaki N, Imamura Y, Sekiya A, Itoh M, Furuoka H. (2016). Four cases of equine motor neuron disease in Japan. J Equine Sci, 27(3), 119-124. https://doi.org/10.1294/jes.27.119

Publication

ISSN: 1340-3516
NlmUniqueID: 9503751
Country: Japan
Language: English
Volume: 27
Issue: 3
Pages: 119-124

Researcher Affiliations

Sasaki, Naoki
  • Department of Clinical Veterinary Science, Obihiro University of Agriculture and Veterinary Medicine, Hokkaido 080-8555, Japan.
Imamura, Yui
  • Department of Clinical Veterinary Science, Obihiro University of Agriculture and Veterinary Medicine, Hokkaido 080-8555, Japan.
Sekiya, Akio
  • Department of Basic Veterinary Medicine, Obihiro University of Agriculture and Veterinary Medicine, Hokkaido 080-8555, Japan.
Itoh, Megumi
  • Department of Clinical Veterinary Science, Obihiro University of Agriculture and Veterinary Medicine, Hokkaido 080-8555, Japan.
Furuoka, Hidefumi
  • Department of Basic Veterinary Medicine, Obihiro University of Agriculture and Veterinary Medicine, Hokkaido 080-8555, Japan.

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Citations

This article has been cited 1 times.
  1. Cahalan SD, Boehm I, Jones RA, Piercy RJ. Recognising the potential of large animals for modelling neuromuscular junction physiology and disease.. J Anat 2022 Nov;241(5):1120-1132.
    doi: 10.1111/joa.13749pubmed: 36056593google scholar: lookup