Equine Motor Neuron Disease

Through a series of clinical studies and observations the past 10 years, researchers at Cornell University 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. Thomas J. Divers, DVM, Dipl. ACVIM, ACVECC, Department of Clinical Sciences at Cornell, said that due to getting the word out about the cause of EMND, the number of cases has dropped. Previously, researchers at Cornell were seeing 10-15 cases per year and gathering information about 20-30 cases in North America. In the past few years, they have dealt with one to two cases a year at Cornell and have heard about five to six cases elsewhere.

EMND is classified as an oxidative disorder, a cytotoxic consequence of oxygen radicals which 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 which 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, said Divers. Normal vitamin E levels should test at least 1.5 micrograms per milliliter of blood.

"We have never seen a horse with EMND with a value over one microgram per milliliter," he said. "The mean is in the 0.45 to 0.5 range. In fact, we’ve seen two horses with a value of zero. The level of vitamin E is low in the liver, fat, spinal cord, and muscles, as well as in the blood."

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.

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 a horse suffering from EMND and being fed the same diet as the affected horse. The subclinical horse might suffer from decreased strength, which might not be detectable by the owner.

The most recent study at Cornell involved 20 horses which were tracked from 1997-2000. The horses were divided into two equal groups. The first group was fed a diet deficient in vitamin E, but all other macro- and micronutrients were normal. The second group was fed a similar diet deficient in vitamin E, but copper was increased to supply a pro-oxidant to see if it would increase the risk of the disease or shorten the time in which the disease developed. Both groups developed the disease. Ten developed clinical signs, while ten were subclinically affected.

In a follow-up study funded by the Morris Animal Foundation, the 10 horses which were subclinically affected were divided into two groups based on pathological lesions from  nerve biopsies. One group is being fed a diet supplemented with 7,000 units of vitamin E per day, while the second group is continuing on a diet deficient in vitamin E. Researchers hope to discover whether supplementation of vitamin E will reverse or stop the progression of the disease. The study should be completed in January 2001.

History Of EMND

In 1990, the first report of the pathology and clinical signs was issued after 11 horses were brought to Cornell with the disease. According to Divers, at that time it was not known whether the disease was caused by toxic, infectious, or metabolic means. In 1991, Divers and his colleagues began researching EMND, the only institution to do research to this date. Based on pathologic findings, it was found that motor neurons with higher oxidative activity were preferentially diseased. Over the next two years, it was found that there was a lack of potent anti-oxidants such as vitamin E.

In 1994, there was an investigation into sporadic outbreaks of EMND in Brazil and Europe. It was found that the affected animals did not have access to pasture, green hay, and rarely had access to alfalfa.

In 1995, ocular lesions were found to be associated with EMND in antemortem biopsies. Lesions did not cause blindness, but could cause visual deficits, especially at night. However, Divers said that no owners have reported seeing a horse experience visual deficits. Post-mortem 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.

Based on the various studies, Divers said there was no genetic predisposition to the disease. "However, the incidences in Quarter Horses is higher since they are found in urban areas more than any other breed. We call this an epiphenomenon," he said.

Due to the findings, Divers recommends that owners supplement vitamin E if a horse does not have access to pasture or green, high-quality hay. He recommends feeding 2,000 units per day to horses which might have a vitamin E deficiency, and 5,000-7,000 units per day for a horse which is clinically affected by EMND.

Divers said the disease is diagnosed easily based on clinical signs, epidemiologic information such as previous cases in a stable or historical information to suggest the horse might have been without green forage for an extended period of time, measurement of plasma vitamin E and muscle enzymes, and muscle and/or nerve biopsy.

Those involved with the research at Cornell include Divers; Hussni Mohammed, BVSc, PhD; Alexander de Lahunta, DVM, PhD; Beth Valentine, DVM, PhD; Harold Hintz, PhD, MS; and the late John Cummings, DVM, PhD. The research has been funded by the Amyotrophic Lateral Sclerosis Association (ALSA), National Institute of Health (NIH), Morris Animal Foundation, American Horse Shows Association, Cornell alumni, Travers Research Committee, Zweig Research Committee, and private donations.

About the Author

Sarah Evers Conrad

Sarah Evers Conrad has a bachelor’s of arts in journalism and equine science from Western Kentucky University. As a lifelong horse lover and equestrian, Conrad started her career at The Horse: Your Guide to Equine Health Care magazine. She has also worked for the United States Equestrian Federation as the managing editor of Equestrian magazine and director of e-communications and served as content manager/travel writer for a Caribbean travel agency. When she isn’t freelancing, Conrad spends her free time enjoying her family, reading, practicing photography, traveling, crocheting, and being around animals in her Lexington, Kentucky, home.

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