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Overview of Myopathies in Horses


Stephanie J. Valberg

, DVM, PhD, DACVIM, ACVSMR, McPhail Equine Performance Center, Michigan State University

Last full review/revision Feb 2014 | Content last modified Feb 2014
Topic Resources

Muscle disorders in horses present with a variety of clinical signs ranging from muscle stiffness and pain to muscle atrophy, weakness, exercise intolerance, and muscle fasciculations. The most common clinical presentation is muscle pain, stiffness, and reluctance to move due to rhabdomyolysis. Rhabdomyolysis, defined as disruption of striated skeletal muscle, can broadly be grouped into causes associated with exercise (exertional rhabdomyolysis) and causes unrelated to exercise.

Differential diagnoses for reluctance to move, acute recumbency, and discolored urine include lameness, colic, laminitis, fracture, pleuropneumonia, tetanus, aorto-iliac thrombosis, neurologic diseases resulting in recumbency or reluctance to move, intravascular hemolysis, and bilirubinuria. Causes of non-exercise-associated rhabdomyolysis include infectious (eg, Clostridium sp, influenza, Streptococcus equi, Sarcocystis) and immune-mediated myopathies, nutritional myodegeneration (vitamin E or selenium deficiency), traumatic or compressive myopathy, idiopathic pasture myopathy, and toxic muscle damage from the ingestion of ionophores (eg, monensin, lasalocid, rumensin). Plants, including white snake root and vitamin D–stimulating species, should also be considered (see Differential Diagnoses of Equine Myopathies). Genetic causes of nonexertional rhabdomyolysis include glycogen branching enzyme deficiency (foals), malignant hyperthermia (Quarter horses), and polysaccharide storage myopathy.


Differential Diagnoses of Equine Myopathies

Non-exercise-associated Rhabdomyolysis

Inflammatory myopathies

Clostridial myositis

Influenza myositis

Sarcocystis myositis

Immune-mediated myopathy

Nutritional myopathy

Vitamin E and selenium deficiency

Toxic myopathies

Ionophore toxicity

Senna occidentalis

Pasture myopathies

Rayless goldenrod/white snakeroot

Hypoglycin A in box elder and European sycamore trees

Traumatic myopathies

Compressive anesthetic myopathy


Genetic myopathies

Glycogen branching enzyme deficiency in Quarter horses

Polysaccharide storage myopathy types 1 and 2

Malignant hyperthermia in Quarter horses

Exertional Rhabdomyolysis

Focal muscle strain

Sporadic tying-up (overexertion)

Chronic tying-up

Dietary imbalances, vitamins, minerals, electrolytes

Polysaccharide storage myopathy types 1 and 2

Malignant hyperthermia

Recurrent exertional rhabdomyolysis

Idiopathic chronic exertional rhabdomyolysis

Exertional Myopathy with Normal CK

Mitochondrial myopathy

Polysaccharide storage myopathy type 2

Muscle Atrophy

Myogenic atrophy

Severe rhabdomyolysis


Cushing disease

Immune-mediated myositis (rapid atrophy)

Vitamin E–deficient myopathy

Homozygous polysaccharide storage myopathy type 1

Polysaccharide storage myopathy type 2

Neurogenic atrophy

Equine protozoal myelitis

Local nerve trauma

Equine motor neuron disease

Idiopathic peripheral neuropathy

Toxic peripheral neuropathies

Muscle Fasciculations

Pain, fear

Weakness (botulism, chronic debilitation)

Electrolyte abnormalities

Equine motor neuron disease

Hyperkalemic periodic paralysis


Otobius megnini (ear tick) infestation

Myotonic dystrophy

Stiff horse syndrome


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In all animals, the motor unit of skeletal muscle consists of the motor neuron, the neuromuscular junction, and muscle fibers. Muscle dysfunction—such as ataxia, paresis, or paralysis—most commonly originates in which of the following locations?
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