Equine Motor Neuron Disease - Vitamin E Deficiency
With the prolonged drought, heat stressed grass and the anticipated shortness of quality of hay, horse owners should be aware of a uncommon syndrome termed Equine Motor Neuron Disease or EMND.
BACKGROUND: Vitamin E is an important vitamin for the horse. It is a powerful antioxidant essential for normal muscle function. Antioxidants prevent free radicals from damaging cellular membranes and a lack of Vitamin E can lead to muscular problems and neurologic problems. EMND is a well described but uncommonly seen disorder in horses characterized by muscle wasting, muscle dysfunction, muscle fasiculations, and neurologic dysfunction. It develops in response to chronic Vitamin E deficiency (>6 months) which allows oxidative damage to nerves and muscles. The disease affects primarily the motor neurons of the spinal cord ventral horn and brain stem and type 1 muscle fibers. Vitamin E is present in fresh grass, and fresh cut hay but not in dried hay. Additionally diets supplemented with fish or plant oils, and grain that has been stored too long or is rancid may all contribute to a Vitamin E deficiency.
CLINICAL SIGNS: Clinical signs depend on the chronicity of the problem, the age of the horse, and the genetic makeup of the horse. Three forms of EMND are described: 1. subacute, 2. chronic, and 3. subclinical.
In the subacute form of EMND, horses may present for trembling, muscle fasiculations, shifting of weight, abnormal sweating, excessive recumbency, muscle atrophy, and weight loss despite an aggressive appetite. Classically the adult horse exhibits weight loss and neurogenic muscle atrophy first. The gluteal muscles, triceps, and quadriceps are the most affected muscle groups. The muscle atrophy is followed by gait abnormalities and muscle fasiculations, usually within 30 days. Eventually the damage to the postural muscles leads to a abnormal base narrow stance, frequent shifting of weight, a low head carriage, partial prolapse of the penis and/or a slight tail elevation. When moving the horse may appear normal, but the clinical signs will return when the horse stops. Some horses will not stop walking or when forced to stop will lay down. Due to this behavior (trembling and laying down) horses will frequently present to a veterinarian for evaluation of abdominal pain. Ultimately the condition can deteriorate to recumbency.
In the chronic form horses present for poor performance, gait abnormalities, and failure to gain weight. Horses may have gone through a subacute phase, but some horses just develop a chronic form. The horses do not show the same level of trembling and muscle fasiculations as the subacute form. The degree of muscle atrophy may vary from mild to emaciated.
In the subclinical form horses present for performance problems due to low levels of muscle damage.
DIAGNOSIS: Horses affected with EMND frequently have mild elevation of CK and AST. Complete Blood Cell (CBC) counts are normal. A muscle biopsy is the definitive test, but a postural muscle must be sampled. The most frequently biopsied muscle is the sacrocaudalis dorsalis muscle along the tail head. Serum Vitamin E levels may be low or normal. A low Vitamin E with clinical signs is diagnostic, but the disease should not be ruled out based on a normal Vitamin E level. Some horses with EMND will also have an abnormal glucose absorption test although the reasons for and significance of this is not understood.
DIFFERENTIALS: The most important differentials to consider include laminitis, rhabdomyolysis (tying up), and colic. Additionally EPM, PSSM, botulism, and lead toxicity can cause similar symptoms
PREVENTION: Horses being fed poor quality hay with no pasture access should have their Vitamin E levels monitored. Horses that have limited access to pasture should receive at least 2000 IU/day of Vitamin E (dl-a-tocopherol). If this level is not in the grain being fed, or if no grain is being fed, additional supplementation is recommended.
RISK: EMND typically occurs in adult horses beginning around 9 years of age and peaking at 15 years of age. In the few published case series Quarter Horses appear to be at a higher risk.
TREATMENT: Aggressive treatment with oral Vitamin E early in the course can reverse the damage. A water soluble form of Vitamin E should be supplemented based on serum Vitamin E levels. Aggressive supplementation may be necessary for 6 to 8 weeks. Once clinical signs abate and serum Vitamin E levels are normal a lower quality or lesser amounts of Vitamin E can be supplemented. In addition to Vitamin E supplementation, acutely affected horses will need supportive care.
PROGNOSIS: The prognosis depends on the level of damage. Severe cases may not ever return to the same level of performance. Slightly less than half of horses with the subacute or chronic form treated will regain all muscle mass and return to normal function. Many horses will stabilize but will not regain the muscle mass lost without appropriate rehabilitation. A low percentage of horses will continue to deteriorate despite treatment.
REFERENCE: Reed, Bayly, Sellon editors. Equine Internal Medicine 3rd edition. Pages 521-522 and 634 - 637.
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