Equine Motor Neuron Disease: A Review of Clinical and Experimental Studies
Section snippets
Clinical Findings
Horses with acquired EMND are 2 years of age or older.2, 3 There is generally an acute onset of muscle trembling, a short-strided gait, almost constant shifting of weight in the pelvic limbs when standing, and excessive recumbency (Fig. 1). Muscle wasting is noticeable, and, in retrospect, owners frequently remark that weight loss was apparent before the trembling being observed.2 Ocular fundus examination reveals brown reticular discoloration (Fig. 2) in nearly 40% of cases, although visual
Laboratory Findings
The only consistently abnormal laboratory finding on routine hematologic and serum chemical analyses is a mild to moderate elevation in serum muscle enzyme (creatine kinase and aspartate aminotransferase) activity.2 Plasma vitamin E values are consistently low (<1 μg/mL), selenium is normal, vitamin A is slightly low to normal, and serum ferritin is frequently high in horses with EMND.7
In the spinal cord of EMND affected horses, copper is increased compared with controls,8 and vitamin E is low (
Pathology
Pathologic findings are generally limited to the lower motor neuron system.1, 10 In acute cases, there is noticeable neuronal degeneration (swollen, chromatolytic somata with distorted nuclei) and loss of somatic motor neurons in the spinal cord ventral horns. In more chronic, “arrested” cases, glial scars, consisting of astrocytes and lipofuscin-laden microglia and a paucity of motor neurons, may be the only noticeable microscopic finding. Loss of approximately 30% of somatic motor neurons
Epidemiology
Horses with EMND have almost always been housed at the same location for at least 18 months.3, 15, 16 There is no sex predilection, but Quarter Horses and Thoroughbreds are over-represented in the patient population.15 There is minimal or no access to pasture for the great majority of cases seen in the U.S.17 The few U.S. horses having EMND and a history of normal access to pasture had infiltrative bowel disease and/or chronic hepatic disease, presumably causing malabsorption.2 Almost all EMND
Experimental Disease
Four of 8 horses fed a low vitamin E and high copper and iron diet (all other NRC nutrient recommendations being normal) developed EMND. These 4 had both characteristic clinical signs and pathological findings that developed 22 or more months after the diet was started.20 In a separate study, 10 additional horses were fed a similarly low vitamin E diet but normal (NRC recommended) copper and iron diet; 5 of the 10 horses developed EMND beginning at 18 months.21 There was no difference between
Discussion
EMND is a devastating neurodegenerative disease, frequently resulting in either death of the affected horse or chronic debilitation. Some horses can have a dramatic improvement in clinical signs, but undoubtedly have permanent loss of some motor neurons.2 It seems plausible that when horses are clinically affected with EMND, there are both dead motor neurons and alive but dysfunctional motor neurons. If there are enough dysfunctional motor neurons that recover, then the clinical signs will
Summary
Epidemiological, pathological, and laboratory data and experimental studies all support the hypothesis that EMND occurs after prolonged vitamin E deficiency. Oxidative injury to the neurons is believed to be the cause of the neuronal cell injury and death. Experimental and clinical studies also suggest that there is an individual predisposition to this neurodegenerative disease, as many horses kept in the same environment, fed identical feeds, and having similar blood vitamin E levels remain
References (24)
- et al.
Association between plasma vitamin E concentration and the risk of equine motor neuron disease
Equine Vet J
(1997) - et al.
Equine motor neuron disease is not linked to Cu/Zn superoxide dismutase mutationssequence analysis of the equine Cu/Zn superoxide dismutase cDNA
Gene
(1996) - et al.
Equine motor neuron disease; a preliminary report
Cornell Vet
(1990) - et al.
Equine motor neuron diseasefindings in 28 horses and proposal of a pathophysiological mechanism for the disease
Equine Vet J
(1994) - et al.
Epidemiology of equine motor neuron disease
Vet Res
(1994) - et al.
Ocular manifestations of equine motor neuron disease
Equine Vet J
(1999) - et al.
Simple and practical muscle biopsy test for Equine Motor Neuron Disease
Proc Am Assoc Equine Pract
(1996) - et al.
Spinal accessory nerve biopsy as an antemortem diagnostic test for equine motor neuron disease
Equine Vet J
(1996) - et al.
Concentrations of trace minerals in the spinal cord of horses with equine motor neuron disease
Am J Vet Res
(2000) - et al.
Eosinophilic cytoplasmic inclusions in sporadic equine motor neuron diseasean electron microscopic study
Acta Neuropathol (Berl)
(1993)
Quantitative assessment of motor neuron loss in equine motor neuron disease (EMND)
Equine Vet J
Acquired equine motor neuron disease
Vet Pathol
Cited by (14)
Diseases of the Nervous System
2019, Large Animal Internal MedicinePasture-related diseases and disorders
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2018, Equine Internal Medicine: Fourth EditionDisorders of the Neurologic System
2018, Equine Internal Medicine: Fourth EditionThe role of diet in the prevention and management of several equine diseases
2012, Animal Feed Science and TechnologyCitation Excerpt :Around 40% of horses will deteriorate quickly in around 1 month after diagnosis, 40% will show improvement within a similar time period with environmental change and/or vitamin E supplementation (2000–10,000 U/day), and the remaining 20% of animals will have permanent muscle atrophy. Each outcome is dictated by the extent of motor neuron death (Divers et al., 2006b). Laboratory findings often found in EMND cases are mild increases in CK and AST, and reduced plasma vitamin E concentrations <1 μg/mL (Divers et al., 1994).
Large Animal Neurology, Third edition
2022, Large Animal Neurology, Third edition
Supported by the Jack Lowe Equine Research Fund.