Equine Motor Neuron Disease (EMND) is a disease that causes progressive damage to nerve cells in the brain and spinal cord of adult horses.
The disease damages cells that are involved with muscle movement, rendering them dysfunctional and leading to muscle wasting.
Early signs of EMND typically include weight loss and muscle atrophy. As the disease progresses, other signs may become evident such as muscle trembling, an abnormal stance, excessive recumbency (lying down), a raised tail, and a low head and neck carriage.
The primary risk factor for EMND is vitamin E deficiency.  Other factors may also contribute to the disease but more research is needed to understand these factors.
When horses are supplemented with sufficient amounts of vitamin E, clinical symptoms improve in some cases of EMND.  However, some horses continue to deteriorate despite receiving high doses of vitamin E.
The only treatment available for horses affected by EMND is to increase vitamin E intake in the diet by providing access to green pasture or a supplemental source.
Equine Motor Neuron Disease
First identified in 1990 in the Northeastern United States , EMND is a neurodegenerative illness that affects nerve cells (neurons) located in the spinal column and brain stem of adult horses.
This condition affects the neck (cervico-thoracic) and back (lumbar-sacral) areas of the spinal cord. In particular, EMND affects a part of the spinal cord known as the ventral horn where upper motor neurons interact with lower motor neurons. 
EMND causes muscle wasting and weakness due to the deterioration of lower motor neurons of the somatic nervous system. These neurons send neural signals from the spinal cord to muscle, glands, organs and other tissues.
The condition causes degenerative changes in the nerve fibre (axon) – the part of the nerve cell that carries nerve impulses away from the cell body. EMND also results in damage to the lipid-rich material (myelin) that insulates the nerve cell and enables nerve signals to travel efficiently. 
The degeneration of motor neurons in horses with EMND is similar to what occurs in humans with amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease). 
EMND typically affects horses between 15 months and 25 years old. Both genders are equally affected. Breeds including Standardbreds, Quarter horses, and Thoroughbreds may be more likely to develop the condition for unknown reasons. 
EMND has been reported in countries around the world. In the US, cases are more prevalent in the Northeast. Based on referrals to Cornell Unversity, the prevalence was higher in the early 1990s compared to recent years. 
Increased awareness of the importance of vitamin E and increased fortification of feeds and supplements with this nutrient being may be responsible for a decline in the number of cases. 
Horses that are clinically affected by EMND have both dead motor neurons and alive but dysfunctional motor neurons.
A small proportion of clinically unaffected horses may have some deterioration of their motor neurons due to EMND, but don’t exhibit signs or symptoms of the condition. 
The clinical signs of EMND typically become apparent when affected horses have lost approximately 30% of their motor neurons. 
Common clinical signs of Equine Motor Neuron Disease include:
- Progressive weakness
- Symmetrical muscle wasting and atrophy
- Weight loss
- Abnormal stance with the hind legs positioned underneath the abdomen
- Muscle twitching and trembling
- Excessive time spent laying down (recumbency)
- Shifting the weight in the hind legs
- Short-strided gait
- Low head and neck carriage
- Elevated position of the tail head
- Discoloration on the interior surface of the eye
- Hyperalert behavior
Causes of EMND
Researchers do not yet have a complete understanding of what causes EMND. However, a dietary deficiency in vitamin E is believed to be the predominant factor that contributes to the condition. 
Vitamin E Deficiency
Vitamin E is a fat-soluble vitamin and one of several antioxidant nutrients that protect cells from harmful molecules called free radicals.
Antioxidants neutralize free radicals to prevent them from causing damage. Vitamin E helps to block the oxidative degradation of lipids that results from the accumulation of free radicals.
Horses obtain Vitamin E from grass pasture and can store this vitamin in their liver for use during times of inadequate dietary intake. This nutrient quickly degrades in cut hay so horses consuming a hay-based diet will have a low intake of Vitamin E.
However, healthy horses grazing on lush, green pasture likely get enough vitamin E which can then be used in the winter or other periods when access to pasture is limited.
If horses go long periods of time without access to pasture or have another issue that impairs their ability to store or absorb Vitamin E, they may develop a deficiency which could lead to EMND.
EMND is believed to result from oxidative damage to the somatic motor neuron cells when the level of vitamin E in the body is insufficient to mitigate free radical damage. 
Additional Risk Factors
Additional risk factors could play a role in the development of the EMND including:
- Pasture quality
- Bioavailability of vitamin E sources
- Intestinal absorption capacity
A study of 87 horses noted additional risk factors for EMND including age, breed of horse, duration of residence at the farm, not vaccinating against rabies, and certain feeding practices. 
Horses with EMND have typically been living at the same location for at least 18 months.  Most horses affected by the condition have had minimal or no access to pasture and have been fed grass hay (rarely alfalfa). 
Of horses diagnosed with EMND that have had normal access to pasture, some were diagnosed with inflammatory bowel disease or chronic liver disease that may have promoted vitamin E deficiency due to malabsorption. 
However, EMND has also occurred in presumed healthy horses that had access to pasture. 
Research suggests some horses may be individually predisposed to EMND. Horses living in the same environment, consuming identical feeds, and having similar blood levels of vitamin E are sometimes affected by the disease whereas others are not. 
It is unclear whether feeding rates for some dietary minerals might also contribute to the development of disease.
One study found that vitamin E deficient horses developed EMND at a higher rate when they were fed high levels of copper (more than 10 times the requirement) and iron (more than 5 times the requirement). 
Consult with a veterinarian if you suspect your horse has EMND. Other neuromuscular disorders including equine dysautonomia and degenerative myeloencephalopathy must be ruled out when diagnosing this condition.
The diagnosis of EMND is based on medical history, a physical and neurological assessment, clinical signs, and laboratory test results.
The following diagnostic strategies are used to confirm EMND:
Horses suspected of having EMND will undergo blood tests to determine their blood (plasma) level of vitamin E. Your veterinarian may also look for abnormalities in other nutrient levels in the blood.
Horses with EMND may have abnormal blood test results including: