Equine Myopathy: Symptoms and Risk Factors Quiz

Monday morning disease

Fibrotic myopathy

Non-exertional myopathies

Exhaustion

Recurrent exertional rhabdomyolysis

Recurrent exertional rhabdomyolysis

Weakness, ataxia, tachypnoea, sweating (collapse)

Sporadic exertional rhabdomyolysis

Nervous/anxious horses

History of exhaustion

Recurrent Exertional Rhabdomyolysis (RER) and Polysaccharide Storage Myopathy (PSSM)

High grain diets

Quarterhorses

PSSM Type 1 (PSSM1)

Low starch diet

Muscle biopsy of semimembranosus

Rest and use anti-inflammatories/antioxidants

Quarterhorses

Increased pressure within the muscles

Mast years, wet and windy weather, and presence of Sycamore trees

Elevated muscle enzymes (CK>10,000iu/L), myoglobinuria, and submission of plasma for acylcarnitine profile and serum for hypoglycin A and conjugated MCPA

Guarded, with up to 84% mortality reported

Muscle rigidity, high body temperature, tachycardia, and tachypnoea

Genetic testing, avoiding fasting, anesthesia and stress, and ensuring adequate magnesium and potassium levels

Fluid therapy, glucose supplementation or high CBH meals, analgesia, multivitamins, and removal of co-grazing horses from pasture

Weakness, muscle tremors, painful muscles, myoglobinuria, tachycardia, tachypnoea, and colic-like symptoms

'Gene mutation affecting voltage-dependent skeletal muscle sodium channels'

Selenium

Trembling and muscle fasciculations

Elevated creatinine kinase (CK) levels

Selenium injections IM

Pale, oedematous muscle, calcification

Myopathic changes

Naylor, R. (2017). Atypical myopathy. UK-Vet Equine.

Scavenge free radicals and prevent lipid peroxidation

'Equine atypical myopathy in the UK: Epidemiological characteristics of cases reported from 2011 to 2015'

Bedford HE, Valberg SJ, Firshman AM, Lucio M, Boyce MK, Trumble TN. Histopathologic findings in the sacrocaudalis dorsalis medialis muscle of horses with vitamin E-responsive muscle atrophy and weakness.

Dyspnoea, weakness, stiffness, trembling, recumbency, sudden death, irregular tachydysrhythmia

Tongue, gastrocnemius, semimembranosus/tendinosus, biceps femoris, lumbar, gluteals, neck

CK/AST elevation, myoglobinuria, electrolyte derangements, low selenium (whole blood), low GSH-Px, low α-tocopherol (vit E) (plasma)

Selenium injections IM, oral α-tocopherol supplementation, supportive nursing

Weakness, toe dragging, narrow-base stance, muscle atrophy, trembling, muscle fasciculations, weight shifting

Presence of myopathic not neuropathic change in SCDM biopsy

To scavenge free radicals and prevent the formation of lipid hydroperoxides

Pale, oedematous muscle, calcification, hypercontracted muscle fibers on histology

Weakness, atrophy, trembling, and muscle fasciculations

CK/AST elevation, myoglobinuria, electrolyte derangements

Mast years, pasture access, wet and windy weather, presence of Sycamore trees

Hyperkalemic periodic paralysis (HYPP) and Malignant Hyperthermia (MH)

Strenuous exercise

Fluid therapy, glucose supplementation or high CBH meals, analgesia, multivitamins, removal of co-grazing horses from pasture

Guarded, with up to 84% mortality reported

Thoroughbred horses

Atypical Myopathy (AM), Hyperkalemic periodic paralysis (HYPP), Malignant Hyperthermia (MH), Recurrent Exertional Rhabdomyolysis (RER), Post-anesthetic myopathy, Polysaccharide Storage Myopathy (PSSM)

Avoiding fasting, anesthesia, and stress; ensuring adequate magnesium and potassium levels

Sycamore trees

Muscle rigidity, high body temperature, tachycardia, tachypnoea

Common myopathies affecting horses include exertional and non-exertional myopathies. They can be differentiated based on the association with exercise.

Appropriate interventions include a combination of therapeutic strategies such as medication, exercise management, and dietary changes, along with optimal husbandry practices.

The prognosis of myopathies affecting horses varies depending on the specific type of myopathy and its severity.

Clinical signs include weakness, ataxia, tachypnea, sweating, collapse, and possible hyperthermia, along with myoglobinuria and elevated CK levels.

RER is also known as Monday morning disease or Azoturia, with a higher prevalence in nervous/anxious horses, especially in racing Thoroughbreds, and the exact etiology and pathogenesis are still unknown.

The possible cause of atypical myopathy is unknown, and it presents with episodic/progressive weakness, muscle wasting/atrophy, and a historical link to ingestion of Sycamore seeds.

EMND presents with muscle wasting/atrophy, peripheral neuropathies, and autoantibodies against neuronal antigens.

During this period, atypical myopathy was associated with ingestion of Sycamore seeds, particularly in grazing horses.

HYPP is characterized by episodes of muscle tremors, weakness, and intermittent paralysis, often triggered by stress or high potassium intake.

Muscle wasting/atrophy is a common feature of equine motor neuron disease and autoimmune-mediated myositis among other myopathies.

Muscle pain, weakness, tremors or fasciculations, shifting lameness, sweating, myoglobinuria

Quarterhorses, Appaloosa, Paint, European draft breeds

A single dominant missense mutation in the equine muscle glycogen synthase gene, affecting glycogen synthesis and glycogenolysis

Trainers often recognize the signs, elevated muscle enzymes, muscle biopsy of semimembranosus, in vitro contracture studies on intercostal muscle

High grain diets

Minimize continued muscle damage (rest, anti-inflammatories/antioxidants), analgesia, correct fluid deficit/induce diuresis, and correct electrolyte abnormalities

Localized rather than generalized myopathy, hard, hot, swollen muscles (gluteals, epaxial muscles, triceps), onset may be delayed, compartment syndrome

Selenium

Rest, anti-inflammatories/antioxidants

Avoid triggering agents such as halothane, isoflurane, and other inhalation anesthetics

Recurrent exertional rhabdomyolysis, PSSM 1&2, atypical myopathy, permanent gait abnormalities, fibrotic myopathy, episodic/progressive weakness, equine motor neuron disease, hyperkalaemic periodic paralysis, muscle wasting/atrophy, peripheral neuropathies, and autoimmune-mediated myositis

The prognosis can vary depending on the specific myopathy, but it is essential to assess the severity, progression, and potential for management of each condition.

Recurrent exertional rhabdomyolysis (RER)

Monday morning disease

Intermittent episodes of muscle tremors, weakness, and temporary paralysis.

Provide immediate supportive care, including rest, fluid therapy, and electrolyte management.

Muscle biopsy

Selenium

Quarter Horses

Muscle weakness, stiffness, dark urine, and respiratory distress.

Dyspnoea, weakness, stiffness, trembling, recumbency, sudden death, irregular tachydysrhythmia

CK/AST elevation, myoglobinuria, electrolyte derangements, low selenium (whole blood), low GSH-Px, low α-tocopherol (vit E) (plasma)

Selenium injections IM, oral α-tocopherol supplementation, supportive nursing

Tongue, gastrocnemius, semimembranosus/tendinosus, biceps femoris, lumbar, gluteals, neck

Poor prognosis

Better prognosis, usually see improvement quickly

Presence of myopathic (not neuropathic) change in SCDM biopsy

Weakness, toe dragging, narrow-base stance, muscle atrophy, trembling, muscle fasciculations, weight shifting

Hypercontracted muscle fibres

Selenium

Recurrent episodes, muscle pain, weakness, tremors or fasciculations, shifting lameness, sweating, myoglobinuria.

Limit glycogen synthesis (reduce insulin activity) and promote glycogen breakdown through low starch, high fat diet, supplemental vitamin E, maintain regular work/turn out routine, avoid days off, minimize stress, minimize changes in management.

Low starch diet, use fat for extra calories, access to a salt block, reduce caloric intake when not in work, feed smaller, more frequent meals, minimize stress.

Minimize continued muscle damage (rest, anti-inflammatories/antioxidants), analgesia (NSAIDs, opioids, paracetamol, lidocaine infusion, ketamine infusion), correct fluid deficit/induce diuresis (oral or IV fluid therapy, correct electrolyte abnormalities).

Localized rather than generalized myopathy, hard, hot, swollen muscles (gluteals, epaxial muscles, triceps), onset may be delayed, compartment syndrome.

Marked elevation of muscle enzymes (CK and AST), myoglobinuria in more severe cases, muscle biopsy of semimembranosus revealing abnormal polysaccharide in myofibres, not all cases have the GYS1 mutation.

A single dominant missense mutation in the equine muscle glycogen synthase gene.

Likely linked to calcium homeostasis, autosomal dominant inheritance, chronic non-specific changes associated with muscle regeneration.

Localized rather than generalized myopathy, hard, hot, swollen muscles (gluteals, epaxial muscles, triceps), onset may be delayed, compartment syndrome.

Stiff, painful muscles (large muscle groups- gluteals, triceps), myoglobinuria, usually appears on the day following a rest day.

Mast years, pasture access, wet and windy weather, and presence of Sycamore trees

Weakness, muscle tremors, painful muscles, myoglobinuria, tachycardia, tachypnoea, and colic-like symptoms

Guarded, with up to 84% mortality reported

Fluid therapy, glucose supplementation or high CBH meals, analgesia, multivitamins, and removal of co-grazing horses from pasture

Muscle rigidity, high body temperature, tachycardia, and tachypnoea

Genetic testing, avoiding fasting, anesthesia and stress, and ensuring adequate magnesium and potassium levels

Gene mutation affecting voltage-dependent skeletal muscle sodium channels

Elevated muscle enzymes (CK>10,000iu/L) and myoglobinuria, submission of plasma for acylcarnitine profile and serum for hypoglycin A and conjugated MCPA

Muscle wasting/atrophy

Muscle stiffness, reluctance to move, and muscle atrophy