progressive, though sudden onset of all symptoms has been reported. In some cases inflammation and paralysis of the cranial nerves, especially cranial nerves III, VI and VII, is reported. Diagnosis of cauda equina neuritis is made through clinical signs and symptoms and CSF analysis. CSF analysis reveals yellow discolouration, cloudiness, neutrophilia and increased protein content. No bacteria or other pathogens should be present in the CSF of a horse affected by cauda equina neuritis. As the cause of cauda equine neuritis is unknown diagnosis may be difficult. EPM & EHV need to be ruled out. Treatment of cauda equina neuritis is primarily . Urinary catheters, manual removal of feces from the rectum, IV fluids and slings may be necessary depending on the severity of the symptoms. NSAID’s and DMSO may be administered in an attempt to reduce inflammation in the sacral nerves though the ability of these medications to cross the blood-brain barrier and the meninges is questionable. Prognosis is guarded to grave for horses affected by cauda equina neuritis, depending on the severity of the clinical presentation. Mild cases may spontaneously recover, though necropsy often reveals the presence of granulomas, fibrosis and calcification of the sacral neural tissue. Moderate cases may improve over time, though clinical symptoms may persist. Severe cases rarely show improvement, and euthanasia is recommended.
Equine Motor Neuron Disease
Equine motor neuron disease (EMND) is an acquired progressive, sporadic neurologic disease that is characterized by the degeneration of the motor neurons of the spine and the brain stem. EMND is considered to be idiopathic though long-term vitamin E deficiency or malabsorption leading to the oxidative damage of motor neurons is known to occur in individuals affected by EMND. The lack of dietary antioxidants allows oxidative damage & degeneration of the ventral horn of the spinal cord & specific brainstem lower motor neurons.
EMND affects
individuals, and is known to occur in Standardbreds, Thoroughbreds,
Quarter Horses and Arabian horses. Animals that are feed quality feeds and forage for extended periods and are not supplemented with vitamin E are at a higher risk of developing EMND than those allowed access to high quality green forage. , muscle atrophy and weight loss. Low head carriage, abnormal placement of the feet well under the body, weight shifting, excessive recumbency, and sweating have also been reported. Some animals may exhibit the deposition of a brown, lipofuscin-like pigment on the EMND is seen clinically as progressive muscular weakness, muscle
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