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  Home > Neuromuscular Diagnostic Laboratory > Neuroaxonal Dystrophy/Equine Degenerative Myeloencephalopathy

Neuroaxonal Dystrophy/Equine Degenerative Myeloencephalopathy

An important differential diagnosis for Wobbler’s disease in horses

If a horse is has clinical signs compatible with Wobbler’s disease (cervical vertebral compressive myelopathy or CVCM), it is important to consider neuroaxonal dystrophy as another possible diagnosis as the two diseases share a similar age of onset, occur in all breeds of horses and are associated with similar neurologic deficits.

Neuroaxonal dystrophy (NAD) is an abnormality of selected cells in the central nervous system. The condition has been associated with neurologic disease in humans, sheep, cats, dogs and horses. In all these species, an underlying genetic basis for disease has either been identified (humans) or suspected (sheep, cats, dogs). In horses, a familial tendency has been suggested by pedigree analysis and supported by breeding studies in Morgans and Appaloosa horses. Equine NAD is considered the underlying basis of equine degenerative myeloencephalopathy (EDM) and clinically, the two diseases are indistinguishable. EDM can be considered a more severe variant of NAD.


• NAD/EDM reported in the following breeds:

o Quarter horses / Paints/ Appaloosa
o Haflingers
o Standardbreds
o Thoroughbreds
o Pony of the Americas
o Lusitano/Andalusians
o Morgans
o Paso Finos
o Arabians
o Tennessee Walking Horse
o Norwegian Fjord
o Various Mixed Breeds

• Males and females equally affected
• Age of onset ranges from birth up to 3 years of age although most cases demonstrate clinical signs by six to twelve months of age

***Clinical signs can be subtle and may be missed for many years unless an experienced veterinarian examines the horse specifically for neurologic disease***

Clinical signs: Symmetric ataxia (incoordination) that is often more severe in the hind limbs than the front limbs, abnormal stance at rest with front or hind limbs placed abnormally- either too wide or too narrow (Figures 1-3), 


and proprioceptive deficits, which means that the horses do not know where their limbs are as they walk. These clinical signs may be subtle and horses should be evaluated walking in slow tight circles and stopping frequently, backing, walking with their head elevated, and walking up and down hills and curbs. Ataxia, or incoordination, is graded on a 5-point scale:

0= Normal; no neurologic abnormalities identified
1= Mild and inconsistent abnormalities
2= Mild consistent abnormalities
3= Moderate consistent abnormalities
4= Severe consistent abnormalities
5= Recumbent

Quarter horses affected with NAD/EDM may also be abnormally quiet and dull. This often makes these horses particularly easy to handle.

A video demonstrating different grades of ataxia due to NAD/EDM

Prevalence: The ataxia observed with NAD/EDM are very similar to that seen with Wobblers syndrome, or cervical vertebral malformation/malarticulation (CVM), where neurologic signs are caused by compression of the spinal cord in the neck, typically due to developmental abnormalities or osteoarthritis. In a study performed at Cornell University, EDM was the second most common neurologic disease diagnosed in horses:

CVM UMEC NAD Mayhewchart
Mayhew, et al.1

Typically, horses are affected with NAD or EDM early in life (6-12 months of age); however, these neurologic abnormalities can be subtle and may be missed for years unless the horse is specifically examined for neurologic disease. Mild cases may present with performance-related issues, where the horse is just not performing up to the standard expected for its breeding and training. Males and females are equally affected and the disease has been reported in the following breeds:

o Quarter horses / Paints/ Appaloosa
o Haflingers
o Standardbreds
o Thoroughbreds
o Pony of the Americas
o Lusitano/Andalusians
o Morgans
o Paso Finos
o Arabians
o Tennessee Walking Horse
o Norwegian Fjord
o Various Mixed Breeds

Role of Vitamin E in NAD/EDM: A vitamin E (alpha-tocopherol) deficiency has been reported in some cases of NAD/EDM. Previous research has concluded that vitamin E is a factor in the development of EDM in the first year of life in genetically predisposed foals. It was previously determined that foals with EDM do not demonstrate significant differences in oral vitamin E absorption as compared to normal foals.2 Overall, there is very strong evidence that NAD/EDM is an inherited disorder and it may be that vitamin E acts as a modifier to determine the overall severity of the disease in horses affected with NAD/ EDM. This theory has been supported by the NAD/EDM research to date.

DIAGNOSIS: At this time, a definitive diagnosis of NAD requires examination of the spinal cord on post-mortem examination. Without a necropsy (post-mortem examination), we cannot definitively diagnose the disease. We suspect cases of NAD/EDM in horses that meet the following criteria:

• Age of onset of symmetric neurologic signs at 6-36 months of age that either stabilize or are very slowly progressive
• History of other related horses that appear to be affected with similar signs
• History of low vitamin E or poor nutrition during the first year of life
• NEGATIVE EPM titer (blood and spinal fluid)
• NORMAL neck x-rays +/- NORMAL myelogram
• NEGATIVE for West Nile Virus

TREATMENT: At this time, there is no effective treatment for NAD/EDM. Supplementation of affected cases with Vitamin E does NOT appear to improve clinical cases. In genetically predisposed animals, supplementing broodmares and foals (at least 2000 IU/day of natural alpha-tocopherol) does appear to result in less severe neurologic signs but does not entirely eliminate the disease. It appears that the disease may be inherited in an autosomal dominant manner, meaning that only one parent needs to be affected to produce an affected foal. Therefore, it is difficult to make breeding recommendations until a genetic test is available. Although horses do not appear to recover from this disorder, the disease is often either non-progressive or very slowly progressive and horses do not become substantially more neurologic during their lifetime. The neurologic deficits present by 3 years of age generally remain unchanged throughout the life of the horse.

***Horses do not appear to recover from this disorder ***

Vitamin E Supplementation

• Form of Vitamin E: Natural sources have great biological activity and are retained for longer duration in tissues than synthetic supplemental sources

o Kentucky Equine Research Product: NanoE


o Kentucky Performance Product: Elevate



• NRC Recommended dose for normal horses is 1000 IU/day (1.6-2 U of d-alpha-tocopherol/kg/d)

**Important to measure serum vitamin E concentrations BEFORE implementing a supplementation program to determine if there is an underlying deficiency ***

o Pregnant broodmares

♦ 5000 IU/day 1st two trimesters (8.5-10.5 IU/kg/d)
♦ 10,000 IU/day Last trimester (17-21 IU/kg/d)

o Foals

♦ E-Se (Schering Plough) injection at birth (1 ml/100 lbs)
♦ 5000 IU/day through 1 year of age (8.5-10.5 IU/kg/d)
♦ 2000 IU/day > 1yr

o Affected Cases **Supplementation will not improve neurologic status **

♦ 5000 IU/day (2.2-4 IU/kg/d)

o Feed Levels of Vitamin E

♦ Recommend having hay analyzed

RESEARCH: A genetic test to identify NAD/EDM would enable veterinarians to diagnose the disease without requiring euthanasia and assist breeders in selecting against the mutation. Currently, we have mapped the potential mutation to a specific chromosome and we need additional cases to further define the candidate region.

1. Mayhew IG, deLahunta A, Whitlock RH, et al. Spinal cord disease in the horse. Cornell Vet 1978;68 Suppl 6:1-207.
2. Blythe LL, Craig AM, Lassen ED, et al. Serially determined plasma alpha-tocopherol concentrations and results of the oral vitamin E absorption test in clinically normal horses and in horses with degenerative myeloencephalopathy. Am J Vet Res 1991;52:908-911.


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