Equine neuroaxonal dystrophy (eNAD) and equine degenerative myeloencephalopathy (EDM) are similar central nervous system diseases related to vitamin E deficiency. eNAD lesions are restricted to the brain stem, while EDM lesions are more diffuse but clinically indistinguishable. Both conditions can only be diagnosed through necropsy of the brain and spinal cord.
At the 2023 AAEP Convention, Sarah Colmer, VMD, DACVIM-LAIM, from University of Pennsylvania’s New Bolton Center, described typical clinical signs of vitamin E deficiency: general proprioceptive ataxia, muscle atrophy, trembling, weakness, behavioral changes, and decline in performance. The condition is most common in relatively young horses, especially those ages 8-12. Diagnosis is often by exclusion to rule out alternatives like cervical vertebral stenotic myopathy (CVSM) or equine protozoal myeloencephalitis (EPM).
Indicators for eNAD and EDM in Horses
Green grass provides horses’ main source of natural vitamin E and serves as a potent antioxidant that plays an important role in neuromuscular function. Horses with EDM don’t usually respond to improved blood vitamin E levels from vitamin E supplementation. Colmer noted there is a subset of vitamin E-responsive myopathy (VEM) that responds to high doses of vitamin E supplementation for six months. However, those individuals with mitochondrial alterations in the sacrocaudalis dorsalis medialis (SCDM, the tailhead) had irreversible changes.
Some biomarkers might be indicative of eNAD or EDM, such as increased pNF-H (phosphorylated neurofilament heavy, identified on post-mortem in blood and CSF) and low serum vitamin E.
Research on eNAD/EDM, Serum Vitamin E, and CSF pNF-H
Colmer’s retrospective and prospective study (2021-2023) aimed to determine what percentage of horses with eNAD/EDM also exhibit histopathologic changes in the tailhead and to compare the percentage of those animals to horses with low serum vitamin E or increases in serum and CSF pNF-H.
Of horses with eNAD/EDM plus a tailhead biopsy, 75% were Warmbloods, 16% Thoroughbreds, and 9% other breeds. They ranged in age from 2-18, with an average age of 8. Findings indicate:
- 41% (28/68) of horses had concurrent SCDM mitochondrial aberrations associated with VEM.
- 8% (3/36) had elevated serum pNF-H concentrations.
- 22% (8/36) had elevated CSF pNF-H concentrations.
- 19% (11/59) had low serum vitamin E.
Biopsy of the tailhead can identify VEM if there are SCDM mitochondrial alterations that increase antemortem suspicion of neurodegenerative disease. Colmer suggested future studies of VEM frequency in normal and neurologic horses to estimate specificity. In this study, blood and CSF pNF-H and serum vitamin E testing revealed poor sensitivity.
Colmer cited a 2013 study (Bedford) suggesting the duration rather than temporal vitamin E deficiency results in SCDM mitochondrial alterations, with only 21% of the study population exhibiting low serum vitamin E at the time of euthanasia. Changes in the tailhead muscle seem to be an irreversible “snapshot” of vitamin E signifying an affected horse experiences oxidative damage from global vitamin E deficiency. She noted this study did not use a control population or a population with differential diagnoses such as CVSM or EPM for comparison. It is possible that vitamin E is not the whole story.
Treatment and Management Recommendations
Colmer recommends treating horses with vitamin E-responsive myopathy. Then, “optimize them holistically to compensate for some of their clinical signs,” she said. Even if a horse is supplemented with appropriate amounts of vitamin E throughout their lifetime, damage from vitamin E deficiency can occur in utero. Therefore, she recommends vitamin E supplementation for pregnant mares in high-risk areas. She also noted that horses on the same farm with the same management strategies might have vastly different vitamin E levels, possibly due to absorption or metabolic variations. It is best to test and change supplementation as needed, then test again in one to two months.
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