Vitamin E and Equine Motor Neuron Disease

Thomas J. Divers, DVM, Dipl. ACVIM, ACVECC, reported at the Cornell at Saratoga Symposium on Equine Health Care that many of the questions about equine motor neuron disease (EMND) have been answered. EMND was first reported in 1990 by the late John Cummings, DVM, PhD. It is an acquired neurodegenerative disease of adult horses that is similar to amyotrophic lateral sclerosis (Lou Gehrig's disease) in humans. Divers said the clinical signs in horses vary according to the form of the disease.

Subacute Form

Horses develop acute onset of trembling, fasciculations (brief, spontaneous muscle contractions), lying down more than normal, frequent shifting of weight in the rear legs, and abnormal sweating. Head carriage might be abnormally low. Appetite and gait usually are not noticeably affected. The owner might mention that the horseshad been losing weight (loss of muscle mass) for one month prior to the trembling.

Chronic Form

The trembling and fasciculations subside and the horse stabilizes, but with varying degrees of muscle atrophy. In some cases, the atrophy is so severe that the horse looks emaciated. In other cases, there is noticeable improvement in muscle mass and/or fat deposition. The tail head frequently is in an abnormally high resting position.

Subclinical Form

Research has proven that horses maintained on prolonged low vitamin E diets might have subclinical (underlying) disease. This could have significant implications since affected horses would, unknowingly to the rider or owner, have decreased strength. Divers and his colleagues have demonstrated that the damage to the neurons is caused by an oxidative disorder. They also have shown that all horses with EMND have a low plasma concentration of vitamin E.

Since the relationship of vitamin E to EMND has been discovered, the incidence of EMND has greatly decreased.

Cause And Treatment

Vitamin E can be a very effective antioxidant. That is, it is well known to protect against oxidative damage. All affected horses had a history of being off pasture for an extended period of time. Pasture is an excellent source of vitamin E, but the vitamin E content of hay can be deficient because of losses of vitamin E during harvest and storage.

The disease was produced experimentally at Cornell in 10 horses which for more than a year were fed a diet containing a low concentration of vitamin E. The research clearly showed that the lack of dietary vitamin E is a primary factor in the development of EMND. The studies were supported by the Morris Animal Foundation and the Amyotrophic Lateral Sclerosis Association.

Treatment of affected animals with vitamin E can lead to some improvement, but complete recovery is unlikely. Studies supported by the Morris Animal Foundation are underway at Cornell to further define the role of vitamin E as a treatment.

Prevention Is Key

The disease can be prevented by access to pasture. Divers recommended that all horses without access to green forage for more than a year be routinely tested for plasma vitamin E, then supplemented with vitamin E if needed.

"If this were a standard policy, most, if not all cases of EMND could be prevented," Divers stated. "If only the human disease were this simple."

About the Author

Harold Hintz, PhD, MS

Harold Hintz, PhD, MS, retired from teaching animal nutrition at Cornell University in 2005 and is now a professor emeritus there. He is also a member of The Horse’s Editorial Advisory Board. His main research interest is equine nutrition, particularly mineral and energy metabolism. He has authored 190 peer-reviewed journal articles, 615 articles in non-refereed publications, and has authored or co-authored four books and contributed to 36 books.

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