Non-exertional myopathies, atropy, and fasciculations (Proceedings)


Non-exertional myopathies, atropy, and fasciculations (Proceedings)

Nov 01, 2010

Muscle atrophy refers to a decrease in muscle size, particularly in muscle fiber diameter. Atrophy can reflect a disorder of the muscle cells (myogenic atrophy) or loss of neural stimulation to the muscle cells (neurogenic atrophy). Trauma, infection and nervous disorders are all causes of atrophy in horses.

     o Neurogenic atrophy affects both type 1 (slow twitch) and type II (fast twitch) muscle fibers. Complete denervation such as peripheral nerve trauma results in rapid loss of muscle mass (50% in 14-21 days). Equine Protozoal Myelitis (EPM) can also be associated with rapid focal atrophy. However, more generalized syndromes such as ELMN disease display a slower onset of generalized atrophy. Neurogenic atrophy can be determined by muscle biopsy (both fiber types affected – small, angular fibers with concave sides) and the presence of EMG abnormalities.
     o Myogenic atrophy can be caused by malnutrition, cachexia associated with disease, disuse, and corticosteroid exposure (pituitary dysfunction). Myogenic atrophy can be distinguished from neurogenic atrophy on the basis of slower progression, absence of EMG abnormalities and specific atrophy of type 2 fibers on muscle biopsy. Rapid myogenic atrophy (30% loss of muscle mass within 48 hours) does occur occasionally following severe rhabdomyolysis or muscle trauma, and in association with immune mediated muscle disorders.

ELMN disease can cause profound generalized atrophy and fasciculations in horses kept in dry lot situations or on a vitamin E deficient diet for a prolonged period of time. Affected horses display constant shifting in the hind limbs with mildly elevated serum CK activity and low plasma vitamin E concentrations. Biopsy of the sacrocaudalis dorsalis muscle (selected due to a high concentration of slow twitch fibers) usually provides a definitive diagnosis.

Muscle fasciculations can be a physiological response to pain, fear and anxiety. They also arise from viral encephalitis (west nile virus), electrolyte abnormalities (hypocalcemia), parasitic infections (Otobius Megnini ear ticks) and hereditary disorders of muscle (HYPP, myotonia).
          • Otobius ear ticks: These ticks can infest the external ear canal of horses and excrete a toxin which alters acetylcholine release from the presynaptic terminals. Horses with heavy infestations display intermittent painful cramping of the pectoral, triceps, abdominal and hindlimb muscles and may fall over when stimulated. Myotonic cramping is observed on percussion of the muscles. Colic signs and significant elevations in serum CK (> 4000 U/L) are also reported. Topical treatment utilizing pyrethrin and piperonal butoxide results in recovery in 12-36 hours. Acepromazine may reduce painful cramping during this period.
          • Myotonia: Myotonic disorders comprise a group of diseases characterized by delayed muscle relaxation following mechanical stimulation or voluntary contraction. A key feature is abnormal muscle membrane excitability caused by ion channel dysfunction.
          • Congenital myotonia has been reported in horses and goats and usually presents in the first year of life.
     o Affected foals have well developed musculature, particularly in the hindlimbs, and display characteristic 'dimpling' on percussion of the muscle due to delayed relaxation of the muscle.
     o Mild hind limb stiffness may inhibit ability to rise and is typically most prominent immediately after rising and diminishes with movement.
     o The condition is likely linked to a disorder of a muscle ion channel (sodium or chloride) resulting in abnormal membrane excitability (not yet proven)
     o Electromyography reveals a characteristic abnormality (dive-bomber pattern) and muscle biopsies may display fiber hypertrophy, splitting and central nuclei. Clinical signs usually plateau before a year of age with no further progression of signs.