Equine Motor Neuron Disease (EMND) is a disease characterized by weakness and weight loss. Though an uncommon problem in horses, a specific disease entity has been identified as the cause in some cases. This disease resembles human sporadic amyotrophic lateral sclerosis (ALS). This article discusses causes, diagnosis, treatment and prognosis.

EMND and was first described in 1990 by John Cummings and colleagues at Cornell University. The majority of initial cases appeared to cluster in the Northeastern United States. By 1998 150 horses have been definitively diagnosed with EMND at Cornell University with another 50 or so cases reported worldwide. EMND closely resembles a human progressive muscular atrophy (Lou Gehrig?s disease), a form of human motor neuron disease. Symptoms result from destruction of lower motor neurons in the brainstem and spinal cord.

EMND is a rare condition of horses. Currently the cause is unknown but Vitamin E plays an important role in this disease. Vitamin E is an antioxidant that helps the body deal with noxious byproducts of metabolism. There is strong evidence affected horses are not receiving enough vitamin E though deficiency in the diet is not always present. It appears that some horses have an increased need for vitamin E in the diet and this may be a genetic disorder for some horses. The most common source of vitamin E is fresh green grass, ...more.

Risk factors associated with the disease include increasing age, high copper diets, and limited pasture access. However there have been a group of horses on grass, with vitamin E content exceeding recommended amounts that have developed this disease. Quarter horses, Appaloosas, and Standardbreds and older horses are at a higher risk. The most common age for symptoms to begin is 16 years and then declines.

Clinical signs are chiefly characterized by tremors and postural weakness. Early there is weight loss and a normal to increased appetite and laying down. Weight loss often precedes the onset of trembling by several weeks. Trembling usually is most evident when the horse stands. Other consistent findings are:

• Inability to lock their stifles
• shifting weight from one hind limb to another constantly
• an abnormally low head carriage
• rest their head on fixed objects

Clinical signs progress over one to several months and included generalized weakness, trembling and shivering, muscle atrophy and weight loss. The horse remains bright and has an increased appetite. Frequently the tail head is held away from the body. It is often said about these horses that they walk better than they stand.

There are several important diseases that should be considered and ruled out:

• botulism
• chronic organophosphate toxicity
• myositis, tying up, shivers (equine polysaccaride storage myopathy)
• malabsorptive disorders
• neglect
• grass sickness (is this the same as botulism?)
• ionophore poisoning
• selenium deficiency or toxicity

Clinical signs, increase muscle enzymes, and biopsy of the spinal accessory nerve provide definitive diagnosis. Biopsy of the sacrocaudalis dorsalis medialis muscle, one of the tail head muscles is easy and is 90% accurate for diagnosing EMND. Microscopic examination of the biopsy reveals axonal degeneration and denervation atrophy of skeletal muscle. The histopathological lesion is muscle degeneration due to denervation. This change can be caused by other factors, tail blocking, other diseases, but when combined with clinical signs and increase muscle enzymes it can be very accurate.

Plasma vitamin E concentrations for 53 affected horses (0.76 +/- 0.70 ug/ml) were significantly lower than 69 control horses (2.15 +/- 1.66 ug/ml).

Needle electromyographic studies have proved to be a useful diagnostic test as they are consistently abnormal in affected animals but require general anesthesia for accurate interpretation. Prolonged insertional activity and positive sharp waves are frequently recorded, particularly in the proximal thoracic appendicular muscles.

Recently a distinctive retinopathy has been recognized in horses with EMND. A mosaic pattern of dark brown to yellow-brown pigment deposition in the tapetal zone, coupled with a horizontal band of pigment at the junction of the tapetum and nontapetum. In one study this technique was as accurately as biopsy, identifying 90% of the EMND affected horses.

Large doses of vitamin E has resulted in improvement particularly when the disease is recognized early. 6000 IU per day per horse (between 600 and 1200 lbs.) in the feed is recommended for treatment. The diet should be evaluated for excessive minerals, especially copper, and if found eliminated. Improvement is usually seen in two to three weeks and progress can be made for up to a year. Vitamin E is safe even at these high levels but care must be taken that selenium is not in your E supplement. The high levels of the supplement may result in selenium toxicity...more

On farms or in familial lines where the problem has occurred in the past, vitamin E should be supplemented at the rate of 2.25 IU / kg of bodyweight and a check for excessive minerals, especially copper done.

Search the National Library of Medicine for all the summaries on this topic. Just push the button the search fields have been already filled in: