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Related Experiment Videos

Equine motor neuron disease; a preliminary report.

J F Cummings1, A de Lahunta, C George

  • 1Department of Anatomy, New York State College of Veterinary Medicine, Cornell University, Ithaca 14853.

The Cornell Veterinarian
|October 1, 1990
PubMed
Summary

A novel equine motor neuron disease caused progressive weakness and muscle wasting in horses. Pathological findings in affected horses resemble those seen in human amyotrophic lateral sclerosis (ALS).

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Area of Science:

  • Veterinary Neurology
  • Equine Pathology
  • Neurodegenerative Diseases

Background:

  • A previously unreported motor neuron disease has been identified in horses.
  • The condition affects horses of various ages and breeds, presenting with progressive weakness and muscle wasting.
  • This equine disease shares similarities with human neurodegenerative conditions.

Purpose of the Study:

  • To describe the clinical and pathological features of a newly identified equine motor neuron disease.
  • To investigate the underlying neuropathology of this fatal condition in horses.
  • To compare the observed changes with human neurodegenerative disorders, specifically amyotrophic lateral sclerosis (ALS).

Main Methods:

  • Clinical observations of affected horses, including signs of weakness, fasciculations, atrophy, and weight loss.

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  • Pathological examination of spinal cord, brain stem, and peripheral nerves.
  • Histopathological analysis of motor neurons, including neurofilament accumulation, chromatolysis, neuronophagia, and glial replacement.

    • Main Results:

    • Ten horses from the northeastern United States were diagnosed with this spontaneous motor neuron disease.
    • Progressive signs of generalized weakness, muscle fasciculations, atrophy, and weight loss were observed over months.
    • Pathology revealed degeneration and loss of motor neurons, axonal degeneration, and denervation atrophy, with changes similar to sporadic ALS.

    Conclusions:

    • A fatal equine motor neuron disease, previously unreported, has been identified.
    • The disease is characterized by progressive neurological deficits and specific neuropathological changes.
    • The similarities to human amyotrophic lateral sclerosis (ALS) suggest potential shared pathogenic mechanisms warranting further investigation.