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Patterns of disease

Often neurologic diseases look alike.  For instance, two diseases that look like EPM to the untrained eye. The difference between equine motor neuron disease (EMD) and equine degenerative myeloencephalopathy (EDM) can be subtle even to the expert.  The onset of age should be considered, EMD is often diagnosed in older animals while EDM is present in younger animals, although signs of EDM may not be present until the horse is 5-10 years old.  Signs are weakness and muscle loss. EMD horses show weight loss and sweating, EDM horses have a classical presentation of symmetrical ataxia.  Both diseases resemble wobbler syndrome, EPM or EHV-1 infections.  The diseases are distinguished because EMD is a neuropathy of lower motor neurons (LMN) while EDM involves upper motor neurons (UMN), it affects the brain stem and spinal cord.  A veterinarian can determine if a disease involves the LMN’s or UMN’s and this distinction weighs heavily in the potential diagnosis and treatment plan.

EMD accounts for 23% of neurological diagnosis in horses seen at major universities and has been likened to amyotrophic lateral sclerosis (ALS) in people.  A treatment for EMD is vitamin E supplementation in horses that have a deficiency.  Deficient vitamin E levels are determined by analysis of plasma levels. Forty percent of EMD horses may improve, forty percent are expected to show no improvement, and twenty percent will decline.

EDM can sometimes respond to vitamin E treatment.  It is suspected that there is a genetic cause of disease that has an environmental trigger.  The treatment may stabilize the neuropathy, but the animals don’t improve. Once diagnosed these horses should not be ridden. They are retired and can often end up in rescue facilities.

It is interesting that these diseased horses have a pigment retinopathy. The retina has a high rate of oxidative metabolism and high lipid peroxidation in the outer photoreceptors.  Oxidative stress in tissues causes damage. Horses are animals with a tapetum and the pigment deposits left  by oxidative damage are observed in the retina during an eye examination.  Recently, the etiology of a unique retinal pathology was described in a former high incidence foci of Western Pacific ALS and Parkinson dementia complex, ALS/PDC, in Guam (USA) and the Kii peninsula of Honshu Island (Japan).  It was suggested that the ALS/PDC-associated retinopathy could be due to in utero exposure of a genotoxic metabolite. It is interesting that mice with a genetically induced form of ALS (SOD 1) show retinal ganglion cell loss and microglial activation. The microglia are mediators of inflammation the central nervous system. The mouse model indicates the nervous system pathology may be a result of oxidative stress. What is an interesting finding is that some inflammatory markers can be measured in the mouse using special histopathology stains. If the mice were treated effectively for disease-associated oxidative stress it would evident on histopath.

We are continuing to developing new treatments for neurodegenerative diseases in people and horses.  One encouraging new therapy targets issues found in lower motor neuron axons and another targets multiple pathways, including neuroinflammation.  We are using the ALS mouse models initially, and thenf10-09-9781437708462.tif we will look for the disease in equine patients. We continue to build our database for potential patients, if you have a horse with EDM or EMD, or have donated a horse to a rescue diagnosed with these diseases, please let us know.

This is a picture of the normal equine eye showing the optic nerve and tapetum.