Equine neuroaxonal dystrophy (eNAD) and equine degenerative myeloencephalopathy (EDM) have become some of the most common postmortem diagnoses in neurologic horses in the United States. They are two diseases that can have identical clinical signs, with both conditions involving degeneration of the central nervous system. They are distinguished by the location within the central nervous system that this degeneration occurs, as eNAD affects the brainstem (specifically the medulla), and EDM affects the spinal cord in addition to the brainstem.  

The clinical signs associated with eNAD/EDM can be variable, but most commonly involve an element of proprioceptive ataxia (incoordination of limbs) and described more recently, signs may also be accompanied by behavior changes. The ataxia is typically symmetric and often has a slower onset, as opposed to beginning suddenly. The severity of the ataxia is most often mild-to-moderate. The behavior changes observed can range significantly from the horse seeming more quiet-to-dull, all the way to a horse that is extremely excitable and not one the owner or trainer can claim to behaviorally recognize. Many owner accounts describe a “switch flip” in such horses. The behavior changes may be noted under saddle and/or when handling the horse on the ground. In some cases, descriptions of changes in herd behavior, inter-horse aggression, or bouts of unpredictability and explosivity have been reported. 

Reasons for the development of eNAD/EDM are not fully understood, but may involve a variety of genetic, nutritional and/or environmental factors. The disease can affect many breeds and a variety of ages. While younger horses (less than 12 months old) were historically the classic age-of-onset description, more recently at the author’s institution, 5-15 years of age and predominantly Warmblood breeds seem overrepresented (unpublished data). Data suggest that deficiencies in antioxidant vitamin E may play a role in the development of eNAD/EDM, but the underlying mechanisms remain to be fully understood. Some horses that are diagnosed with eNAD/EDM have low blood vitamin E levels, but it is also possible that the vitamin E deficiency associated with the disease could have occurred early in the horse’s life or development, even if their blood levels are normal at the time of evaluation. Research is ongoing to better understand this aspect of eNAD/EDM.   

Unfortunately, at the time of this publication, eNAD/EDM does not have an available, definitive diagnostic test that can be performed in the living horse to confirm its presence. eNAD/EDM can only be diagnosed postmortem via microscopic evaluation of the brain and spinal cord by an experienced pathologist. This means that eNAD/EDM is a “diagnosis of exclusion” in the living horse. Put simply, we are tasked with trying to ensure that there are no alternative diseases that may be contributing to the clinical signs of concern. In horses that we suspect have eNAD/ EDM, if we are able to “rule out” these alternative diseases through diagnostics and observations, we are left with an increased suspicion of eNAD/ EDM which we then term our “working diagnosis” until it can be confirmed postmortem.  

The clinical signs observed in horses with eNAD/EDM are often similar to those seen in other neurologic conditions; ataxia is commonly attributable to cervical vertebral stenotic myelopathy (CVSM, colloquially known as Wobblers), or equine protozoal myeloencephalitis (EPM), two conditions which are also frequently diagnosed in neurologic horses in the United States. Determining if a horse has CVSM is best approached using imaging (radiographs, myelography, computed tomography). Determining if a horse has EPM or other infectious diseases is most comprehensively approached through analysis of cerebrospinal fluid (CSF) and blood, where CSF is obtained through a spinal tap. Importantly, other causes of unpredictable and abnormal behavior as well as gait abnormalities should be considered (i.e. musculoskeletal sources of pain, like lameness, back pain or muscle diseases; equine gastric ulcer syndrome, among other sources of discomfort and reactivity). Your veterinarian will use a combination of history and examination findings to determine the most likely possibilities and formulate an appropriate diagnostic plan.  

If alternative sources for the ataxia and behavior change in eNAD/EDM suspect horses have been ruled out, horses with this working diagnosis have a variable prognosis. Some horses will stabilize in their ataxia and/or behavior abnormalities for months-to-years without progression. Still others will progress in their signs. Recommendations are made based on the severity of disease and are generally limited. Depending on risks to safety of the horse and/or his handlers, a tailored exercise plan may be recommended or the horse may need to be retired from riding. Those horses with severe clinical signs may pose a safety hazard to themselves or their handlers and ultimately require euthanasia. In conclusion, eNAD/EDM is a frustrating spectrum of chronic neurodegenerative disease currently without antemortem confirmatory diagnostics, making it challenging for the horse, the horse’s connections and veterinarians alike. Research is ongoing into understanding the pathophysiology, diagnostics and, hopefully, eventual treatment and prevention options for these diseases.  

Editor’s note: This is an excerpt from Equine Disease Quarterly, Vol. 32, Issue 2, funded by underwriters at Lloyd’s, London, brokers, and their Kentucky agents. It was written by Sarah F. Colmer, VMD, DACVIM Fellow, Large Animal Neurology at the University of Pennsylvania’s New Bolton Center, in Kennett Square.