Vitamin E deficiency and risk of equine motor neuron disease

Abstract

BackgroundEquine motor neuron disease (EMND) is a spontaneous neurologic disorder of adult horses which results from the degeneration of motor neurons in the spinal cord and brain stem. Clinical manifestations, pathological findings, and epidemiologic attributes resemble those of human motor neuron disease (MND). As in MND the etiology of the disease is not known. We evaluated the predisposition role of vitamin E deficiency on the risk of EMND.MethodsEleven horses at risk of EMND were identified and enrolled in a field trial at different times. The horses were maintained on a diet deficient in vitamin E and monitored periodically for levels of antioxidants – α-tocopherols, vitamins A, C, β-carotene, glutathione peroxidase (GSH-Px), and erythrocytic superoxide dismutase (SOD1). In addition to the self-control another parallel control group was included. Survival analysis was used to assess the probability of developing EMND past a specific period of time.ResultsThere was large variability in the levels of vitamins A and C, β-carotene, GSH-Px, and SOD1. Plasma vitamin E levels dropped significantly over time. Ten horses developed EMND within 44 months of enrollment. The median time to develop EMND was 38.5 months. None of the controls developed EMND.ConclusionThe study elucidated the role of vitamin E deficiency on the risk of EMND. Reproducing this disease in a natural animal model for the first time will enable us to carry out studies to test specific hypotheses regarding the mechanism by which the disease occurs.

Evaluation of the risk of motor neuron disease in horses fed a diet low in vitamin E and high in copper and iron

“…High hepatic concentrations of iron and high serum concentrations of ferritin have been detected in horses with naturally occurring EMND, but the role that iron plays in the development of EMND is questionable because iron concentrations are not high in the spinal cord of those horses, 21 and in our concurrent experiment, 31 horses fed a diet that was similarly low in vitamin E content but that contained iron closer to reference range concentrations (ie, 140 ppm in concentrate feed) also developed EMND. The 4 horses in the present study with clinical signs of EMND had either unremarkable or only mildly high hepatic iron concentrations.…”

Histopathologic findings in the sacrocaudalis dorsalis medialis muscle of horses with vitamin E–responsive muscle atrophy and weakness

“…4,6,7 Limb muscles in EMND may also have fiber size variation, centrally located nuclei, and alterations in mitochondrial staining, such as dense peripheral rims and redistribution of mitochondrial enzyme stains (moth-eaten appearance). 2 Thus, it is believed that EMND is related to vitamin E deficiency, although < 45% of affected horses are reported to respond to vitamin E treatment, with 69% euthanized within 0 to 3 months following onset of clinical signs and diagnosis. 5 Clinical signs and neuropathologic lesions of EMND have been produced experimentally by feeding a vitamin E-deficient diet for 44 months.…”

Subependymal Reaction Secondary to Choroid Plexus Papilloma in a Horse

“…After-ward, because of the poor prognosis and at the owner's request, the horse was humanely euthanized, and a complete necropsy was performed. Differential diagnoses for main progressive CNS diseases in horses include infection by flavivirus (West Nile virus [WNV]), eastern equine encephalitis), Borna disease virus (BDV), rabies, leukoencephalomalacia, equine protozoal myeloencephalitis [11,12], Lyme disease [13], botulism [14], tetanus, and equine motor neuron disease [15]. Adrenocorticotropic and testosterone hormone analyses were performed from blood samples collected to evaluate the presence of a pituitary adenoma or a possible masculine aggressiveness, respectively.…”