Vitamin E-Related Neuromuscular Equine Disorders

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lf was a 20-year-old Percheron-Morgan cross who had been a resident of Madison County, N.Y., his entire life. Alf started having problems with laminitis related to insulin resistance and Cushing’s disease about six years ago, but he was doing well on a low-carbohydrate diet with mineral balancing. The only change in his feeding, medications and supplements was that he stopped eating his CocoSoya oil in midwinter. CocoSoya (www.uckele.com, 800-248-0330) is a highly palatable high-fat oil that also contains natural vitamin E.

Alf’s problems began when, late spring 2007, he couldn’t hold his hind legs up for the farrier to work on his feet. In just a few weeks, he had gone from a horse that cantered around the field in play to one that was barely able to walk quickly.

In retrospect, he had been losing weight and top-line definition for a while and had shown some trembling and trouble moving to the side in his stall. It was noted that his winter diet was providing far more calories than he should have needed to maintain his weight.

In addition to the trouble holding up his legs and balancing for the farrier, he developed a wide stance behind, had to ”bunny hop” to get over the ledge of his stall and could easily be pushed off balance. He was showing rapidly worsening muscle atrophy. His hind legs would sometimes be pulled up tight against his belly when he tried to move, then be slapped down again. His hind legs were swung wide when he walked. The overall impression was that his hind end was ”disconnected.”

Several veterinarians saw Alf, but there was no consensus on what his problem was. He didn’t have any convincing neurological exam abnormalities, although the atrophy was suspicious for EPM (equine protozoal myeloencephalitis) and his gait was definitely strange. Some veterinarians thought stringhalt or shivers, others mentioned EPSM (equine polysaccharide storage myopathy). Spinal stenosis was considered, as was a vitamin E/selenium deficiency. Before all was said and done he was tested for Lyme disease, too.

All of these guesses were reasonable, but none fit as a clear-cut classical explanation for all his symptoms. It was finally decided that a muscle biopsy was needed to try to rule out a primary muscle problem like EPSM.

In the meantime, Alf’s owner had read about EPSM and started him back on a small amount of oil (4 oz./day), syringing it into him. Extra vitamin E was also given on recommendation of his vets, although nobody expected it to help much.

The veterinarian who did Alf’s biopsy noted that the muscle tissue was unusual. The tissue tore easily, and they expected abnormal results, but the biopsy sent to Dr. Stephanie Valberg’s Neuromuscular Diagnostic Laboratory at the University of Minnesota turned out to be normal, with no evidence at all of EPSM or glycogen abnormalities, and no primary muscle problem. Meanwhile, within just a few days of restarting oil and an increased dose of vitamin E, Alf was showing a dramatic improvement.

The trembling and abnormal gaits decreased. He was stronger and steadier. Within less than three weeks, he was again walking more normally, making some small attempts at a trot or canter. Although Alf’s balance and movement improved, he continued to lose muscle. Odd loose skin appeared on his hindquarters, then his head, neck and chest. His chest muscles were shrinking. His lower hind legs were also swollen, assumed to be edema from not moving as much. He was also dropping more in the ankles and getting a post-legged look. He moved better when given phenylbutazone, which shouldn’t be the case with EMND (equine motor neuron disease) and suggested he had pain. He was beginning to look more and more like a DSLD (degenerative suspensory ligament desmitis) horse.

Ultrasounds showed, sure enough, extensive lesions in his suspensory ligaments and the branches at the ankle were enlarged. Alf had no history of a suspensory injury.

He was started on Jiaogulan and arginine alpha-ketoglutarate experimental treatment even before the ultrasounds were completed, because of the strong suspicion of DSLD. Within days he was happier and more comfortable. The edema left his lower legs. Muscle loss stopped and his skin was tightening up. L-carnitine was added for further muscle and nerve support. A year and half later, Alf looks like a 5-year-old.

Bottom Line

Alf’s leg swelling and ultrasound findings are typical for DSLD, a degenerative connective tissue problem that classically involves the suspensories but it’s really body-wide (systemic). The wide-based gait, rapid muscle/weight loss and sudden appearance of sagging skin have also been reported with DSLD. His rapid response to Jiaogulan and arginine alpha-ketoglutarate has been seen in many horses with DSLD, and in people with similar problems treated with topical nitric oxide donors. The treatment is designed to boost nitric-oxide levels.

On the other hand, his initial partial response to vitamin E and a small amount of oil looked like EMND and the muscle trembling he was showing aren’t typical of DSLD. He may have both problems.

DSLD and EMND are both rare. Because they also have symptoms that overlap with more common diseases, horses are often misdiagnosed, as happened to Alf.

Article by Dr. Eleanor Kellon, Veterinary Editor.