Monday Morning Disease : Introduction Muscle disorders are a common cause of disability in….

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Review A review of equine muscle disorders M.

Aleman * Department of Medicine and Epidemiology, Tupper Hall 2108, One Shields Avenue, School of Veterinary Medicine, University of California, Davis, CA 95616, USA Received 8 September 2007; received in revised form 17 December 2007; accepted 6 January 2008 Abstract Muscle disorders are a common cause of disability in horses.

For many years, clinical manifestations such as muscle pain, exercise intolerance, weakness, and stiffness were believed to be caused by a single syndrome.

However, in the past years a broad spectrum of muscle disorders have been recognized including glycogen and polysaccharide storage myopathies, malignant hyperthermia, mitochondrial myopathy, hyperkalemic periodic paralysis and others.

For some, a specific mutation has been identified.

Recognition of the myopathic clinical phenotype and thorough clinical, electrodiagnostic, and histological evaluations are essential to further our understanding of equine myopathies.

Advances in understanding equine myopathies may potentially benefit other species including humans. Ó 2008 Elsevier B.V.

All rights reserved. Keywords: Equine; Exertional; Myopathy; Myotonia; Rhabdomyolysis 1.

Introduction Muscle disorders are a common cause of disability in affected horses, and in the past, have been known by several names including tying up, Monday morning disease, azoturia, equine rhabdomyolysis, and equine myoglobinuria.

Although originally thought to be a single clinical syndrome, it is now clear that these clinical manifestations are common to several different muscle disorders with different etiologies [1].

In 1992 the first hereditary muscle disease, hyperkalemic periodic paralysis in Quarter Horses, was reported [2,3] and a genetic test is available for diagnosis.

Recently metabolic, inflammatory, dystrophic and other inherited muscle diseases have been described in horses [4–10].

A specific genetic defect and mode of inheritance have only been identified in hyperkalemic periodic paralysis [3], glycogen branching enzyme deficiency [7], and malignant hyperthermia [8].

Horses have a number of muscle disorders which share similar clinical, histopathological and in some cases molecular features with humans.

Thus the horse can be considered * Tel.: +1 530 752 0290; fax: +1 530 752 9815.

E-mail address: mraleman@ucdavis.edu as an animal model for human muscle diseases.

Disorders that affect horses and man include equine motor neuron disease [11] with many similarities to human amyotrophic lateral sclerosis [12], malignant hyperthermia in Quarter Horses with a mutation in the calcium release channel of the skeletal muscle sarcoplasmic reticulum, RyR1 gene [8], hyperkalemic periodic paralysis in Quarter Horses caused by a mutation in the a-subunit of the skeletal muscle sodium channel, SCN4A gene [2], and glycogen branching enzyme 1 deficiency in Quarter Horse and Paint foals due to a mutation in the glycogen branching enzyme 1, GBE1 gene [7].

With increased recognition of the myopathic phenotype in horses by veterinarians, and use of state-of-the-art histological, biochemical and molecular techniques, the spectrum of myopathies affecting the horse will be greatly expanded.

Known causes of equine myopathies are shown in Table 1.

This classification separates myopathies into non-exertional and exertional categories.

These categories are further divided into whether or not they are associated with rhabdomyolysis.

A final category covers diseases associated with altered membrane conduction.

This review highlights the most important recognized muscle disorders in horses with an emphasis on inherited, metabolic, toxic, and inflammatory myopathies. 0960-8966/$ – see front matter Ó 2008 Elsevier B.V.

All rights reserved.

Doi:10.1016/j.nmd.2008.01.001 278 Table 1 Classification of myopathies in horses I.

Non-exertional myopathies M.

Aleman / Neuromuscular Disorders 18 (2008) 277–287 II.

Exertional myopathies A.

Rhabdomyolysis Sporadic Lack of training Overexertion Heat exhaustion Electrolyte imbalances Chronic Dietary imbalances Polysaccharide storage myopathy Recurrent exertional rhabdomyolysis Idiopathic Trauma B.

No rhabdomyolysis Mitochondrial myopathy Complex I respiratory chain enzyme deficiency Pituitary pars intermedia dysfunction myopathy III.

Altered muscle membrane conduction Electrolyte abnormalities Tetany (severe hypocalcemia) Others Hyperkalemic periodic paralysis Myotonic dystrophy Tick myotonia (ear tick: Otobius megnini) A.

Rhabdomyolysis Nutritional Vitamin E/selenium deficiency Metabolic Glycogen branching enzyme deficiency Polysaccharide storage myopathy Anesthesia associated Compartmental myopathy Malignant hyperthermia Toxic Pasture associated Drug/chemical associated Ionophore toxicosis Organophosphate toxicity Trauma Inflammatory Infectious Viral, bacterial, parasitic Immune-mediated B.

No rhabdomyolysis Pituitary pars intermedia dysfunction myopathy Steroid induced Disuse atrophy Muscle wasting associated with neoplasia Neoplasia (rare)

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