Vitamin Deficiency Linked to Motor Neuron Disease

Through a series of clinical studies and observations the past 10 years, researchers at Cornell University in New York have discovered that a vitamin E deficiency is the cause of equine motor neuron disease (EMND). This is a rare neurodegenerative disorder of the somatic lower motor neurons, which are found in the spinal cord, writes Sarah E. Hogwood in the October edition of The Horse.

Due to the word getting out about EMND, the number of cases has dropped, according to Dr. Thomas J. Divers of Cornell. Previously, researchers at the school were seeing 10-15 cases per year and gathering information on about 20-30 cases in North America. In the past few years, they have dealt with one or two cases a year at Cornell and have heard of about five to six cases elsewhere.

EMND is classified as an oxidative disorder, a cytotoxic consequence of oxygen radicals that are generated as byproducts of normal and aberrant metabolic processes that utilize oxygen. The disease results in preferential denervation atrophy of type one muscle fibers, whose parent motor neurons have higher oxidative activity. Horses that are deprived of pasture or green, high quality hay, and which are not supplemented with vitamin E for more than a year, are at greatest risk for EMND, Divers said. Normal vitamin E levels should test at least 1.5 micrograms per milliliter of blood.

The disease can be divided into subacute and chronic forms. Signs for the subacute form include acute onset of trembling, fasciculations (twitching), lying down, shifting of weight on the rear legs, abnormal sweating, low head carriage, inability to lock the stifles, frequent recumbency, and loss of muscle mass symmetrically throughout the body for one month prior to the trembling. Appetite and gait usually are not affected at this stage. Horses do not become uncoordinated, but walking is easier than standing. In chronic cases, the trembling and fasciculations decrease. The horse might stabilize with varying degrees of muscle atrophy, and might look emaciated. The tail usually is elevated.

Some horses with prolonged vitamin E deficiency might have the subclinical form and will not show signs of EMND. At-risk horses include those stabled with horses suffering from EMND and being fed the same diet as the affected horses. The subclinical horse might suffer from decreased strength, which might not be detectable by the owner.

In 1995, ocular lesions were found to be associated with EMND in antemortem biopsies. The lesions did not cause blindness, but could cause visual deficits, especially at night. However, Divers reported that no owners have reported seeing a horse experience visual deficits. Postmortem biopsies showed 30% of the neurons must be damaged before clinical signs appear. Out of the 30% or more, some of the neurons might be able to recover, while some are completely dead.

EMND is very similar to human motor neuron disease (amyotrophic lateral sclerosis, otherwise known as ALS or Lou Gehrig's disease). However, the human disease is more complex and the cause or causes have not been determined. EMND is the only naturally occurring animal model for ALS.

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