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  Home > Neuromuscular Diagnostic Laboratory > Other Myopathies
 

Other Myopathies

 

Other Myopathies

Virus Associated Myopathy
Equine Motor Neuron Disease

 

Virus Associated Myopathy 

Breakdown of skeletal and cardiac muscle can also occur in association with viral diseases such as equine influenza and equine infectious anemia. The viral-induced muscle damage is generally part of a larger systemic infection. Equine influenza A2, in particular, has been known to cause severe rhabdomyolosis. Other viruses have slightly different clinical presentations, such as equine herpes virus-1, which has been associated with muscle stiffness and clinical signs similar to exertional rhabdomyolysis.

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Equine Motor Neuron Disease 

Epidemiology

  1. Relatively new condition (first reported in 1990)
  2. Most cases have been in the northeastern United States
  3. Adult horses, 2 to 25 years of age
  4. Seen more commonly now that fewer horses graze on quality pastures

Pathogenesis

  1. The progressive weakness, generalized muscle wasting, and neuronal degenerative changes in these horses are similar to those described in humans with amyotrophic lateral sclerosis (Lou Gehrig's disease)
  2. Decreased antioxidant capacity is apparent in the CNS
  3. Many cases appear to be related to inadequate vitamin E in the diet over a period of years

Clinical Signs

  1. History of marked weight loss despite a ravenous appetite.  In most cases, the weight loss is preceded by an acute onset of fine muscle fasiculations, course trembling of the limb muscles, and tendency to lie down frequently.
  2. Horses in the early stages of the disease constantly shift weight from one hindlimb to the other.  Tend to stand with all four limbs closer together than normal (similar to a laminitic horse).
  3. Affected horses may have a short-strided gait, but ataxia is rarely observed.
  4. Later in the course of the disease, muscle atrophy and general debilitation become more marked.  Many affected horses are unable to carry their head and neck in the normal position.
  5. Early treatment can produce stabilization and improvement of clinical signs  Severe debilitation may necessitate euthanasia.

Diagnosis

  1. There is no definitive antemortem diagnosis - clinical signs of trembling weakness, muscle atrophy, and frequent periods of recumbency, together with mild elevations in CK and AST (1000 IU/L) and CSF protein concentration (>100 mg/dl) are suggestive of EMND.
  2. A dark reticulated bar may be seen on the retina between the tapetum and optic disc.
  3. Muscle biopsy of the sacrocaudalis muscle will show evidence of neurogenic atrophy.
  4. Serum vitamin E concentrations are often lower than 1 ppm

Pathology

Degeneration of motor neurons in the ventral horn cells and peripheral nerves and neurogenic muscle atrophy are widespread in the spinal cord.

Treatment

6000U or more of vitamin E/day may result in stabilization of clinical signs and gradual improvement.

 

 

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