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Some illumination on

Motor Neuron

Disease in Horses

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Equine motor neuron disease (EMND) has recently been
diagnosed as far west as the state of Oregon. It is a relatively new
condition, first diagnosed in 1990 in New York state, that
affects the nervous and muscular systems in adult horses. To
date, less than 100 horses have been diagnosed with this illness.
Affected horses demonstrate marked weight loss in the face of a
ravenous appetite. This weight loss is attributed to neurogenic
muscular atrophy. Presently there is no know cause of the

A horse with this condition appears with muscle tremors, and may
appear to be "tied up," (short-strided gait). Other signs may
include constant shifting of weight in the rear limbs and
abnormally low head carriage. The horse also has a particular
stance, with all four limbs camped (tucked) under.

The condition usually progresses with continued muscle atrophy
and debilitation over the course of one to several months.
Occasionally the condition will stabilize or even seem to improve
one to two months after the onset. Following this period in many
horses, the condition becomes progressive requiring euthanasia. A
few horses have stabilized for as long as three years, however,
none have returned to effective use.

The horse characteristically has mild elevations of the
muscle-derived enzymes, CPK and AST. Electromyography
(EMG) is frequently used as an aid in the diagnosis of this condition.

Although there is no definitive diagnostic test available for
this condition, the clinical signs, changes in muscle enzymes and
EMG findings provide strong support for the diagnosis of EMND.
Muscle and nerve biopsies have characteristic findings of EMND.

A definitive cause for EMND has not been determined; a common
toxin has not been identified and infectious agents are not
likely because of the sporadic nature of the disease. Horses
without access to pasture seem to be at higher risk for
developing the disease.

Although speculative, it is suggested that some oxidative injury
may cause the neuronal cell death leading to the clinical signs.
Vitamin E is a dietary antioxidant which may be useful in halting
the progression of the disease.

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