Myopathies are diseases that primarily cause damage to muscles. They may be present at birth (congenital) or occur due to nutritional imbalances, injury, or ingestion of a poisonous substance. Myositides are diseases that produce a mainly inflammatory reaction in muscle. Common causes include infections, parasitic diseases, and immune-mediated conditions.
Muscle weakness or damage can also occur as a sign of many different disorders (such as nerve trauma or influenza). Only conditions in which myopathy or myositis are primarily involved are discussed in this section.
Nutritional Myopathies of Horses
Disorders related to vitamin E, selenium (an element required in small amounts for normal nutrition), and fat metabolism can all affect the muscles, leading to inflammation and degeneration.
Selenium or Vitamin E Deficiency
Degeneration of muscle is sometimes associated with a deficiency of selenium or vitamin E. The condition may cause rapid, unexpected death in adult horses. Other affected horses may show a staggering gait, difficulty swallowing, swelling of the cheek and tongue muscles, difficulty breathing, and a rapid heartbeat. Physical changes involve the skeletal muscles and the heart muscle. Blood tests are used to confirm a selenium or vitamin E deficiency.
In foals, this nutritional myopathy may be seen at birth or shortly thereafter and may be accompanied by inflammation of fatty tissue or “yellow fat disease” (see Bone, Joint, and Muscle Disorders in Horses: Yellow Fat Disease (Steatitis)). Stiffness and pain are noticeable when feeling for the firm, fat masses below the skin, and severely affected foals may be unable to suckle. Treatment involves addressing the underlying dietary deficiency. Vitamin E supplementation appears to be effective.
Yellow Fat Disease (Steatitis)
Yellow fat disease is characterized by a noticeable inflammation of the fatty tissue, which develops a yellow tinge. This condition may occur in foals together with muscle degeneration due to vitamin E deficiency (see Bone, Joint, and Muscle Disorders in Horses: Selenium or Vitamin E Deficiency).
It is thought that an excess of unsaturated fatty acids in the food, combined with a deficiency of vitamin E or other antioxidants, causes yellow fat disease. Most known cases have involved animals whose diet consists partially or completely of fish or fish byproducts. The most effective treatment involves removing fish from the diet and restoring any dietary imbalances.
Exertional Myopathies in Horses
Exertional myopathies in horses involve muscle fatigue, pain, or cramping associated with exercise. Most exercise-associated myopathies result in death of skeletal muscle, which is called exertional rhabdomyolysis.
Signs are usually seen shortly after the horse begins to exercise. Excessive sweating, increased breathing rate, rapid heartbeat, reluctance or refusal to move, and firm, painful hindquarters are common. The severity varies between horses and even between episodes in the same horse. Severe episodes may involve muscle damage with kidney failure and reluctance to stand. A diagnosis of exertional rhabdomyolysis is confirmed using blood tests.
Exertional rhabdomyolysis can be sporadic, with single or very infrequent episodes occurring with exercise. It can also be chronic, with repeated episodes, often occurring after mild exertion. Horses of any breed may develop sporadic exertional rhabdomyolysis.
Sporadic Exertional Rhabdomyolysis (Tying Up)
The most common cause of sporadic exertional rhabdomyolysis is exercise that exceeds the horse's training. Respiratory disease and deficiencies of sodium, calcium, vitamin E, or selenium in the diet may also play a role. Affected horses generally have no previous history of the condition.
Signs include muscle cramping and stiffness following exercise. Blood tests will reveal elevated levels of certain enzymes. As soon as the condition is diagnosed, exercise should stop and the horse should be moved to a stall with comfortable bedding and access to fresh water. Treatment should aim to relieve anxiety and muscle pain and to correct dehydration and metabolic imbalances. Appropriate tranquilizers or pain relievers may be prescribed to relieve pain and inflammation. Most horses are relatively free of pain within 18 to 24 hours.
Severe rhabdomyolysis can lead to kidney problems. In severely affected animals, regular blood and urine tests are advised to assess the kidney damage. Treatments that induce urination (diuretics) are not recommended except in certain cases (such as in horses receiving intravenous fluid treatment). Your veterinarian will monitor your horse's kidney function and develop an appropriate treatment plan.
Horses should be kept on a hay diet and stall rest for a few days. The horse should continue to rest with regular access to a paddock until the blood muscle enzyme levels are normal. Because the cause is generally temporary, most horses recover with rest, a gradual return to normal training levels, and dietary changes. Horses ridden for endurance should be encouraged to drink electrolyte-supplemented water during an endurance ride. They should be watched especially closely in hot, humid weather for signs of dehydration or muscle cramping.
Chronic Exertional Rhabdomyolysis
Some horses have multiple episodes of rhabdomyolysis that occur after even light exercise. Two forms of chronic exertional rhabdomyolysis have been identified from samples of muscle tissue (biopsies)—polysaccharide storage myopathy and recurrent exertional rhabdomyolysis.
Polysaccharide storage myopathy is most often seen in Warmbloods, draft horses, and breeds related to the Quarter Horse. It is an inherited disorder in Quarter Horse-related breeds. Light-breed horses with this condition often have episodes of rhabdomyolysis at a young age with little exercise. Resting for several days prior to exercise increases the risk of an episode. Signs include a tucked-up abdomen, a camped-out stance (in which the cannon and fetlock are further back rather than in line with the point of the buttock), muscle twitching, sweating, irregular gait, hindlimb stiffness, and reluctance to move. Some horses paw or roll in a way that resembles colic. Certain blood enzyme levels are increased during an episode. Signs in draft horses may include loss of muscle mass, difficulty standing with a hindleg raised, difficulty backing up without hindlimb shaking, progressive weakness, and reluctance to stand. Blood tests, urinalysis, exercise testing, muscle biopsy, and an analysis of the diet may all be useful in diagnosing this condition.
When fed a high-starch meal, Quarter Horses with polysaccharide storage myopathy store a higher proportion of absorbed glucose in their muscles than do healthy horses. Your veterinarian can recommend a diet for a horse with polysaccharide storage myopathy, adjusting the amount of forage and grain or replacing it with a fat supplement. Caloric needs should be assessed first to prevent horses becoming obese on a high-fat diet. Improvement in horses with this condition requires both dietary changes and gradual increases in the amount of daily exercise and turn-out.
Recurrent exertional rhabdomyolysis is most often seen in Thoroughbreds (in which it may be an inherited condition), Standardbreds, and Arabian horses. It is likely due to problems with regulation of calcium within muscle cells. Muscle contraction is intermittently disrupted in otherwise healthy horses.
Your veterinarian can perform tests to determine the cause of the condition, including blood and urine tests, dietary analysis, exercise testing, and muscle biopsy. An exercise challenge test is useful to detect less severe cases. Determining the severity of the condition during mild exercise is helpful in deciding how quickly to resume training.
Management of this condition is best done by minimizing the factors that lead to an episode and regulating calcium within muscle cells through the use of medication. Techniques include decreasing stall confinement by using turn-out or a hot walker, exercising and feeding horses with this condition before other horses, providing the company of compatible horses, and careful use of low-dose tranquilizers during training. A high-fat, low-starch diet is helpful.
Unlike horses with polysaccharide storage myopathy, horses that have recurrent exertional rhabdomyolysis often require higher-calorie diets. At these high caloric intakes, specialized feeds designed for horses with this condition are necessary. Simply adding vegetable oil or rice bran cannot supply enough calories for athletes in intense training. Your veterinarian can recommend a diet for a horse with recurrent exertional rhabdomyolysis.
Hyperkalemic Periodic Paralysis
Hyperkalemic periodic paralysis is a hereditary condition that affects American Paint horses, Appaloosas, Quarter Horses, and Quarter Horse crossbreeds. About 4% of Quarter Horses are affected by this condition, which results from an abnormally high level of potassium in the blood.
Signs are not always obvious but may include intermittent muscle spasms and weakness. They are usually first identified in foals and young horses up to 3 years of age. A brief period in which muscles stay contracted for much longer than normal and have difficulty in relaxing is often the first sign. In some horses, the third eyelid also slips out of place. Muscle spasms begin on the flanks, neck, and shoulders and may spread to other parts of the body. Most horses remain standing during mild attacks, but weakness with swaying, staggering, dogsitting, or lying down may be seen. Severe attacks last anywhere from 15 minutes to an hour or longer. Breathing and heart rate may increase, but horses remain alert and attentive. Some horses have difficulty breathing due to upper respiratory muscle paralysis. Once an episode is over, the horse can walk or stand normally.
Episodes can be triggered by sudden dietary changes or foods with high potassium content, such as those containing alfalfa hay, molasses, electrolyte supplements, and kelp-based supplements. Lack of food, anesthesia or heavy sedation, trailer rides, and stress may also cause an episode. However, the condition is often unpredictable. Exercise does not appear to trigger episodes.
Many horses recover from episodes of hyperkalemic periodic paralysis without treatment. Owners may treat early mild episodes with light exercise or feeding of grain or corn syrup. In severe cases, emergency treatment from a veterinarian is necessary. If breathing is severely obstructed due to upper respiratory muscle paralysis, a veterinarian may need to perform a tracheostomy (create a hole in the trachea) to allow the horse to breathe. Sudden death is common in severe cases.
To prevent episodes in affected horses, the level of potassium in the body should be reduced. High-potassium feeds, such as alfalfa hay, brome hay, canola oil, soybean meal or oil, sugar molasses, and beet molasses, should be avoided. Grains such as oats, corn, wheat, and barley; beet pulp; and late cuts of timothy and bermuda grass should be fed in small meals several times a day. Horses should also have regular exercise and frequent access to a large paddock or yard. Pasture is ideal for horses with this condition, because the high water content of live grass reduces potassium intake. Special feeds for horses with this condition are available without a prescription. For horses with recurrent episodes even with dietary changes, there are some drugs that may be helpful. However, use of these drugs during competition is restricted.
Some myopathies in horses are caused by ingestion of certain plants, drugs, or other toxins.
Certain feed additives (of a type called ionophores) that are often added to feeds for poultry or livestock other than horses may cause muscle disease. Usually this is the result of exposure to feeding or mixing errors of these drugs. The toxic effects may be compounded due to various other drugs incorporated into feeds. Signs include persistent loss of appetite, heart failure with rapid heartbeat, difficulty breathing, diarrhea, stiffness, muscle weakness, and reluctance to stand. Diagnosis requires history of exposure to these drugs and physical signs, along with appropriate laboratory tests.
Degeneration of skeletal and heart muscles results when some animals consume the toxic portions (often the leaves, fruit, or beans) of certain plants. Coyotillo (Karwinskia humboldtiana), sennas (Cassia species), and white snakeroot (Eupatorium rugosum) have been suggested, but other species also may cause similar damage. Sennas (such as coffee senna and sickle-pod) are common in fields and pastures. Affected animals show weakness and trouble walking, and severely affected animals have unhealthy-looking, degenerated muscles and a strong reluctance to stand. Treatment consists of supplemental feeding and removal of animals from the area in which they ingested the toxic plants.
Some myopathies in horses are caused by problems in the animal's circulatory system. In ischemic myopathy, the formation of blood clots that block the iliac artery results in extensive damage and death of muscle tissue of the hindlimb due to a lack of blood supply. In post-anesthetic myopathy, complications of general anesthesia may cause changes to muscle tissue due to abnormally low arterial blood pressure induced by gas anesthesia.
Fibrotic and Ossifying Myopathy in Quarter Horses
This condition is seen primarily in working Quarter Horses as a result of injury to the inner thigh muscles. Usually, it affects one leg at a time and involves thickening and scarring of connective tissue that progressively worsens. The muscles bond together and eventually harden. The gait is distinctive in affected horses; the forward stride is jerky, and the foot is pulled back a short distance before being placed back on the ground. The hardening of the muscles can be felt in some cases. X-rays and ultrasonography help to establish the degree of bonding and hardening. Treatment involves surgery to cut out the thickened and scarred tissue or to cut the ligament attached at the stifle. Most horses improve after surgery but only about half make a full recovery.
Ruptured blood vessels and death of skeletal muscle accompanied by injury to blood vessels may be an immune-mediated consequence of equine respiratory diseases associated with Streptococcus equi (the bacteria that cause strangles in horses).
Last full review/revision July 2011 by Russell R. Hanson, DVM, DACVS, DACVECC; Joerg A. Auer, DrMedVet, Dr h c, MS, DACVS, DECVS; Andrew P. Bathe, MA, VetMB, DACVS, DEO, MRCVS; Leo B. Jeffcott, MA, BVM, PhD, FRCVS, DVSc, VD; Svend E. Kold, DMV, MRCVS, RCVS Specialist in Equine Surgery (Orthopedics); C. Wayne McIlwraith, BVSc, PhD, DSc, FRCVS, DACVS; Dale A. Moore, MS, DVM, MPVM, PhD; Sheldon Padgett, DVM, MS, DACVS; Tracy A. Turner, DVM, MS, DACVS, DABT; Stephanie J. Valberg, DVM, PhD, DACVIM; John F. Van Vleet, DVM, PhD