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. [1] 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. [6] 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 [1], 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. [1]

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. [6]

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). [1]

Prevalence

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. [1]

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. [2]

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. [1]

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Clinical Signs

Horses that are clinically affected by EMND have both dead motor neurons and alive but dysfunctional motor neurons.[6]

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. [6]

The clinical signs of EMND typically become apparent when affected horses have lost approximately 30% of their motor neurons. [6]

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
  • Sweating
  • Hyperalert behavior

Some horse owners report that weight loss occurs before muscle trembling. [6] In some cases, trembling and constant weight shifting may not occur but muscle wasting is evident. [6]

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. [1]

EMND occurs in horses following prolonged inadequate intake of vitamin E, resulting in oxidative damage to motor neuron cells. [1]

A study at Cornell University investigated horses fed diets that were deficient in vitamin E over an average period of 38.5 months. [6] Out of 11 horses fed the deficient diet, 10 developed EMND. [6]

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. [1]

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. [10]

Horses with EMND have typically been living at the same location for at least 18 months. [6] Most horses affected by the condition have had minimal or no access to pasture and have been fed grass hay (rarely alfalfa). [6]

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. [10][6]

However, EMND has also occurred in presumed healthy horses that had access to pasture. [4]

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. [6]

Mineral Levels

It is unclear whether feeding rates for some dietary minerals might also contribute to the development of disease.

Horses with EMND have been found to have elevated copper in the spinal cord and high levels of iron in the liver. [1][11]

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). [9]

Diagnosis

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:

Blood Tests

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:

  • Low Vitamin E: Horses with EMND consistently have a low level of vitamin E (<1 g/mL) in their blood.[1][10]
  • Elevated Serum Muscle Enzymes: Creatine kinase and aspartate aminotransferase may be elevated. [1]
  • Abnormal Glucose Absorption: Horses with EMND often have a reduced rate of glucose absorption on oral glucose absorption tests. [1] The cause of reduced absorption is unknown.

Tissue Biopsy

A biopsy taken from the muscle of the tail head is valuable for confirming a diagnosis of EMND. This tissue contains a high proportion of the type I fibers that are predominantly affected by the condition.

Alternatively, a biopsy can be taken from the spinal accessory nerve (accessed via the sternocephalicus muscle). [10]

Microscopic analysis of cells obtained from these types of biopsies indicates degeneration in the lower motor nerves when EMND is present. [6]

Laboratory and Pathologic Findings

Further analyses can be done for diagnosis or during post-mortem tests which may reveal abnormalities in the following areas:

Eyes:

Despite vision remaining normal, horses with EMND may exhibit changes in the pigment of the epithelial layer of the retina, which is believed to be caused by light-generated oxidative damage. [1][5]

They may also have abnormal results on an electroretinogram (ERG) – a diagnostic test that measures the retina’s electrical activity in response to a light stimulus. [6]

Spinal Cord:

Accumulations of lipid-derived pigment (fluorescent lipopigment granules) are consistently observed in the capillaries of the spinal cord. [1] In other species, a similar type of accumulation is associated with vitamin E deficiency.

Fluorescent pigment (lipopigment) is also present in the motor nerve cells. [1]

In the spinal cord of horses affected by EMND, the copper level is increased whereas vitamin E level is low. [1]

Brainstem:

Microscopic lesions are present within some cranial nerves. [6]

Muscle Fibers:

Muscles primarily comprised of Type I fibres (slow twitch) are more significantly deteriorated compared to those predominantly consisting of Type II fibres (fast twitch). [1]

EMND Treatment

Prompt diagnosis of EMND is important as treating this condition early may help slow the progression of the disease in some horses. The only treatment available for EMND is to increase the level of vitamin E in the body.

Horses with this condition should have their baseline vitamin E levels assessed through bloodwork before starting a supplementation program.

Some horses may require higher amounts of vitamin E to effectively increase their vitamin E status.

How to Increase Vitamin E Levels for Horses

Providing access to green pasture: Fresh green grass is a natural source of vitamin E for horses. Supplementation may be required for horses without access to green pasture to increase the level of vitamin E in their body.

Administering supplemental Vitamin E: Horses with EMND may benefit from supplemental d-alpha-tocopherol, the most biologically active form of vitamin E.

This natural form of vitamin E provides increased antioxidant activity and is more effective at raising the level of vitamin E in the body compared to synthetic forms of the vitamin. [12]

A dose of 2,000 to 10,000 IU (international units) of vitamin E per day is recommended. [6] The National Research Council (NRC) states the upper safe limit of dietary intake for vitamin E is 10,000 IU per 500 kg of body weight.

EMND Prognosis

The prognosis to return to normal athletic performance is poor for horses affected by EMND. All horses afflicted with the disease are not suitable for riding.

Horses with severe symptoms of EMND are often euthanized within weeks of being diagnosed. It is estimated that of horses diagnosed with EMND, 40% are euthanized due to continued deterioration. [6]

Some horses diagnosed with the condition may stabilize sufficiently to live a quality life. [6] Horses with EMND may show a significant improvement in clinical signs within four to six weeks if they are relocated to another stable and or given vitamin E supplements. [6]

However, approximately 20% of horses affected by EMND have permanent nerve damage and apparent muscle atrophy. [6]

Prevention

The best way to prevent EMND is to provide adequate Vitamin E in the diet. You can increase your horse’s Vitamin E intake by:

  • Providing access to green pasture, which supplies 2,000 IU of vitamin E per day
  • Feeding supplemental vitamin E if your horse is eating a hay-only diet
  • Always supplement with natural forms of vitamin E (d-alpha-tocopherol), which are absorbed more effectively than synthetic vitamin E
  • Consult with an equine nutritionist to help determine how much vitamin E your horse is getting per day.

Because the cause of EMND is not entirely understood, supplementation with Vitamin E is not guaranteed to completely prevent the disease.

Stay vigilant for the early warning signs of Equine Motor Neuron Disease and consult with your veterinarian right away if your horse is displaying any indications of a neurodegenerative disorder.

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References

  1. Divers, TJ. et al. Equine motor neuron disease. Vet Clin North Am Equine Pract. 1997. View Summary
  2. Divers, TJ. et al. Equine Motor Neuron Disease: A Review of Clinical and Experimental Studies. Clin Tech Equine Pract. 2006.
  3. Díez de Castro, E. et al. Eosinophilic Enteritis in Horses with Motor Neuron Disease. J Vet Intern Med. 2016. View Summary
  4. McGorum, BC. Et al. Horses on pasture may be affected by equine motor neuron disease. Equine Vet J. 2006. View Summary
  5. Riis, RC. Et al. Ocular manifestations of equine motor neuron disease. Equine Vet J. 1999. View Summary
  6. Mohammed, HO. et al. Vitamin E deficiency and risk of equine motor neuron disease. Acta Vet Scand. 2007. View Summary
  7. Banfield, J. et al. Investigating the Risk of Equine Motor Neuron Disease in a Brazilian Stable and Successful Intervention. J Equine Vet Sci. 2019. View Summary
  8. de la Rúa-Domènech, R. et al. Intrinsic, management, and nutritional factors associated with equine motor neuron disease. J Am Vet Med Assoc. 1997.View Summary
  9. Divers, TJ. Et al. Equine motor neuron disease and diet high in iron and copper. Am J Vet Res. 2005. View Summary
  10. Jackson, CA. et al. Spinal accessory nerve biopsy as an ante mortem diagnostic test for equine motor neuron disease. Equine Vet J. 1996. View Summary
  11. Polack, EW. et al. Concentrations of trace minerals in the spinal cord of horses with equine motor neuron disease. Am J Vet Res. 2000. View Summary
  12. Fagan, MM. et al. Form of Vitamin E Supplementation Affects Oxidative and Inflammatory Response in Exercising Horses. J Equine Vet Sci. 2020. View Summary