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