The importance of good equine management is constantly being stressed, and there is a seemingly endless stream of literature available advising on all aspects of this huge subject – from diet and worming to the latest “must have” rug or accessory.

As the role of owning a horse has moved from that of necessity to one of pure pleasure, so it would appear that people are keener to invest more time and money on improving their standards of horsemastership, as well as horsemanship.

It is therefore somewhat alarming that a relatively new condition, which appears to be linked to inadequate or inappropriate horse care, has become recognised in the past 15 years.

Equine motor neurone disease (EMND) is a condition in which the sporadic degeneration of muscle nerves in mature horses leads ultimately to excessive muscle weakness and wastage.

It is characterised as a generalised weight loss (due to muscle wastage, or atrophy) despite a normal or even increased appetite. Affected horses become unsafe to ride and because there is currently no known cure, they may have to be put down in the end.

EMND bears certain similarities to human motor neurone disease, but is actually more closely comparable to the human disorder amyotrophic lateral sclerosis. It was first described in literature back in 1990, with these early cases occurring mainly in North America. Since then it has been diagnosed occasionally in South America, Europe and Japan.

The exact cause of EMND remains unclear. The damage to the motor neurons, which supply the muscles, appears to be related to periods of oxidative stress created by imbalances between pro-oxidants and anti-oxidants in the blood.

The prime factors appear to be invariably a lack of grazing opportunity (ie through constant stabling), together with a diet based mainly on grain, with poor-quality grass or hay as a fibre source.

This explains why it appears to be more prevalent in housed animals such as Thoroughbreds, as opposed to ponies. The diet of stabled horses is likely to be deficient in Vitamin E, a powerful anti-oxidant, and it is here that most current research is concentrating.

The disease itself tends to fluctuate between two states, the active phase and the arrested phase, with most owners becoming alerted to a problem during the initial active phase.

There are a number of ways of diagnosing this condition but, because of its relative rareness, many vets will want to investigate a whole range of other possibilities first.

There is no specific treatment for EMND. It certainly makes sense to supplement the diet with Vitamin E right from the start, and it may also be worth using an anti-oxidant treatment, such as DMSO, or corticosteroids during the active phase.

The long-term outlook remains poor, however many cases can survive for several years.

One study showed that up to 40% of EMND sufferers improved after the first six weeks, with some of them appearing almost normal in three months, but if they were put back into work there was a rapid deterioration.

A further 40% stabilised but stayed permanently disfigured, and the remaining 20% went downhill rapidly throughout the initial active phase until they became recumbent and had to be euthanized.

The evidence therefore suggests that this distressing condition is essentially a nutritionally derived anti-oxidant deficiency, and, as such, should be easy to prevent.
Green forage is high in Vitamin E, which is the single most common and accessible natural anti-oxidant freely available.

In an ideal world, all horses should be allowed to graze for significant periods of the day, and if that is not possible, their diets should be supplemented with high-quality green forage (at the expense of some grain) or a commercially produced Vitamin E supplement.

Happily, fewer cases of EMND are being reported these days. Hopefully this is due to an increased awareness of the need for a balanced diet with plenty of access to grass.

Complacency should not be encouraged, however, and many vets remain concerned that clinical EMND is just the tip of the iceberg, with many cases of horses in poor condition or not performing quite up to expectations being ignored.

The active phase

  • Normal appetite
  • Trembling and generalised weakness of muscles, especially when standing still
  • Symmetrical loss of muscle mass, especially along topline
  • Reluctance to stand, with symmetrical buckling of forelimbs
  • Odd limb posture when standing, with all four limbs held close together and the weight shifted back on to the hind limbs
  • An almost normal gait when walking or trotting, but much-reduced exercise tolerance (affected horses move better than they stand)
  • An increased tendency to lie down
  • Pigmentation and degeneration of the retina of the eye, with some visual impairment possible
  • Sweating
  • Elevation of tail head
  • Some central nervous system signs
  • Recumbency and respiratory distress in the final stages

    The arrested phase

  • No significant weight gain despite increased food intake
  • Easily fatigued
  • Tail head elevation
  • Not sweating, trembling or lying down as much
  • Gait may be normal or a little stiff, with a stringhalt-type action in many cases

    The diagnosis

  • Laboratory findings (eg muscle enzymes, gut and liver function tests, plasma Vitamin E levels)
  • Tail head muscle biopsy
  • Spinal accessory nerve biopsy
  • EMG (electromyography — showing widespread denervation responses)
  • Ophthalmic examination (retinal changes)
  • CSF analysis (cerebrospinal fluid)
  • This article first appeared in Horse & Hound (2 September 2004)

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