EDM diagnosis, treatment
Equine degenerative myeloencephalopathy (EDM) is a diffuse degenerative disease of the spinal cord and brain stem, with signs
of slowly progressive ataxia and weakness. Though first observed in the Northeast, several breeds of horses with ataxia and
neuroaxonal dystrophy were subsequently noted throughout the United States, including Appaloosas, Arabians, Quarterhorses,
Thoroughbreds, Standardbreds, Paso Fino horses, Morgan horses, Paint horses, Norwegian Fjord horses, Welsh ponies and mules.
The disease also was seen in Grant zebras (E. burchelli) and Mongolian wild horses (E. przewalskii) in captivity. Horses with ataxia and the neuronal dystrophy characteristic of EDM as well as atactic wild horses and zebras
responsive to therapy with vitamin E have been identified in Europe. Most EDM-affected horses exhibit ataxia during their
first year, with onset of clinical signs prior to 6 months of age. The initial clinical signs were upper motor neuron signs
with general proprioceptive deficits as well as a tendency for generalized hyporeflexia and hypometria. Signs of EDM include
clumsiness, inability to do complicated movements, malpositioning of limbs at rest and during movement and obvious ataxia
EDM, commonly seen in young horses, was shown to have a familial component, but is also linked to low serum vitamin E levels
and/or vitamin E deficiency.
Several factors suggest vitamin E deficiency. Pathologic findings of neuroaxonal dystrophy and lipofuscin-like pigment accumulation
are common features in experimentally induced vitamin E deficiency in several species and in EDM-affected horses.
Low to deficient serum or plasma alpha-tocopherol values were reported in several studies of EDM. Supplementary administration
of vitamin E to foals from sires known to produce EDM decreased the incidence of the disease, and adult horses with EDM treated
with 6,000 IU/day of alpha-tocopheryl acetate for one or more years showed neurologic improvement.
It was found that foals showing signs of incoordination, supplemented with 6,000 IU vitamin E per day appeared normal by 2
years of age. (The EDM work is by Linda Blythe, DVM, PhD, and Morrie Craig, PhD, researchers at Oregon State University, 1991-1992.)
It is highly recommended that horses at risk be supplemented with the vitamin. The incidence of EDM on one farm was reduced
from 40 percent to zero via supplementation of 1,000 IU to 2,000 IU per day of d,l alpha-tocopheryl acetate. Horses fed 6,000
IU of d,l alpha-tocopheryl acetate per day, mixed with 60 ml of corn oil, mixed in a liter of sweet feed or grain, showed
improved neurologic scores.
In children with neurologic deficits caused by malabsorption of vitamin E, therapy with massive doses of vitamin E before
5 years of age resulted in return to normalcy. Young horses respond better to vitamin E supplementation if their gait deficits
are appreciated sooner, the UC researchers say.
The reasons for the low alpha-tocopherol values may include inadequate vitamin E in the feed; reduced absorption of vitamin
E due to lack of bile acids or intestinal malfunction; failure to make chylomicrons in the enterocytes necessary to carry
the vitamin E via the lymphatic system to the blood and liver; the absence of specific hepatic protein (tocopherol transfer
protein, TPP) postulated to transfer the vitamin E from the chylomicrons to the LDL and HDL; an inadequate number of cellular
vitamin E receptors; and increased utilization and/or excretion of the vitamin.
Vitamin E is valued for its prime role as a scavenger of free-radicals and therefore its antioxidant protection of neuronal
lipid membranes. The disease often is confirmed, not only by the ataxia seen in young horses, but also by low plasma or serum
α-tocopherol status (< 3 µg/ml), though these low values also are seen in horses without neurologic disease. A known history
of EDM within the horse's bloodline can help confirm the diagnosis.
Supplementing stallions with 1,500 IU vitamin E per day decreases the incidence of EDM in their foals from 40 percent to 10
percent. A vitamin-E-responsive EDM in Standardbred and Paso Fino horses from 3 to 30 months of age has been described. Symmetric
ataxia and paresis, along with laryngeal adductor, cervicofacial, local cervical and cutaneous trunci hyporeflexia, were characteristic.
No clinical signs were observed before 3 months of age.
The onset of gait abnormality is usually abrupt. Clinical signs have been seen to remain static or progressed for weeks or
months. Severely affected animals often fall while running. In one study, the mean (± SD) serum alpha-tocopherol concentration
of 13 ataxic weanlings was 0.62 ± 0.13 (range 0.47 to 0.84) µg/ml.
A number of non-ataxic weanlings had similar values, although vitamin E supplementation reduced the incidence of the syndrome
on affected farms. Based on genetic studies, this disorder seems to have a familial disposition.
To reach a tentative diagnosis of EDM, a neurologic exam and a CSF exam are recommended. Measuring various parameters within
the CSF are suggested, and analysis of CSF alpha-tocopherol may be of value as shown by the results of a 2008 study by Higgins
EMND diagnosis, treatment
Equine motor neuron disease (EMND) is a naturally occurring neurodegenerative disease, an oxidative disorder of the somatic
motor neuron system in adult horses.
Clinical signs include weight loss from muscle wasting, trembling, muscle fasciculations and prolonged periods of recumbency.
Pathologic changes are primarily limited to the somatic lower motor neurons of the spinal cord and brainstem nuclei, and their
corresponding efferent nerves and innervated muscle groups and the retinal pigment epithelium.
Vitamin E deficiency is a primary factor, as studies show that horses without access to green forage/pasture for 18 months
or more, high-grain diets and coprophagia and/or geophagia are at high risk for the disease.
Low plasma/serum alpha-tocopherol is a consistent laboratory finding in horses with EMND, along with increased amounts of
potential pro-oxidants, copper in the spinal cord and of hepatic iron.
The lack of access to pasture, dietary deficiency of vitamin E, or excessive dietary copper have been confirmed as likely
risk factors for the disease.
Four of eight horses fed low-vitamin-E diets (hay stored for > 1 yr. 19.8 IU/kg; grain, 25.7 IU/kg) with excess copper (>
4,000 ppm) and iron (> 2,000 ppm) exhibited signs of EMND at 21, 27 and 28 months, with mean plasma alpha-tocopherol concentrations
of 0.255 µg/ml. (EMND work is by Thomas J. Divers, DVM, Dipl. ACVIM, Dipl. AVECC, professor of medicine and chief of the Section
of Large Animal Medicine at Cornell University College of Veterinary Medicine, and colleagues, 2006).
The other four horses, though they did not show signs of EMND within 30 months, did show decreased plasma alpha-tocopherol
levels (mean, 0.39 µg/ml). Histological changes in the spinal cord, peripheral nerves and muscles were characteristic of EMND
in all four affected horses. The other four horses, though they had no clinical signs of EMND, did show some nerve lesions
histologically. Mean hepatic alpha-tocopherol concentration was significantly low (2.57 ug/g, dry weight) in EMND affected
horses compared to control horses (21.1 ug/g).
Mean hepatic copper concentrations (503 ppm) of horses with EMND were excessively higher, more than 50 times the value of
It was concluded that vitamin E deficiency plays a major causative role in EMND. Vitamin E was not measured in the spinal
cord tissue of the horses, but in humans tocopherol concentrations in CSF are highly correlated with serum concentrations.