Equine motor neuron disease: findings in 28 horses and proposal of a pathophysiological mechanism for the disease
Article first published online: 23 APR 2010
© 1994 EVJ Ltd
Equine Veterinary Journal
Volume 26, Issue 5, pages 409–415, September 1994
How to Cite
DIVERS, T. J., MOHAMMED, H. O., CUMMINGS, J. F., VALENTINE, B. A., DE LAHUNTA, A., JACKSON, C. A. and SUMMERS, B. A. (1994), Equine motor neuron disease: findings in 28 horses and proposal of a pathophysiological mechanism for the disease. Equine Veterinary Journal, 26: 409–415. doi: 10.1111/j.2042-3306.1994.tb04411.x
- Issue published online: 23 APR 2010
- Article first published online: 23 APR 2010
- Received for publication: 12.11.93; Accepted: 15.4.94
- motor neuron disease
Over a three and one-half year period, 28 adult horses were diagnosed with equine motor neuron disease (EMND). The most commonly identified environmental risk factors for a horse having EMND were absence of grazing for more than a year and provision of poor quality hay. Quarter Horses were 5.4 times more at risk than other breeds but this was thought to be an epiphenomenon related to the frequency of Quarter Horses at boarding stables.
Weight loss, excessive recumbency and/or trembling were the first signs noted. Other clinical diagnostic signs included: constant shifting of the weight in the rear limbs, abnormally low head carriage and muscle fasciculations. Excellent to ravenous appetites were present in all cases and marked coprophagia in some cases.
Abnormally high serum concentration of muscle-derived enzymes was the only consistent serum chemistry abnormality found. Abnormal glucose absorption, increased cerebrospinal fluid total protein and intrathecal production of IgG were identified in a number of cases.
Euthanasia was performed on 5 horses within 4 days of hospital admission, because of inability to stand or respiratory distress, and on 18 horses after the diagnosis had been completed. Five affected horses were maintained for observational purposes for periods of 9 months to over 2 years after the onset of clinical signs. They were given access to pasture and 2 were given supplemental vitamin E as the only therapy. Marked clinical improvement occurred in the 4 more acutely affected horses.
Pathological findings, preference of type 1 muscle fibre atrophy and lipopigment accumulation within the capillary endothelium of the spinal cord of all cases, supported the hypothesis of EMND being an oxidative disease. In addition, after the absence of pasture was identified as a possible risk factor, plasma vitamin E was measured in the last 10 cases and was found to be significantly (P = .0028) lower than controls. It was hypothesised that in EMND, motor neurons with the highest oxidative activity are made susceptible to an oxidative insult by a deficiency in dietary antioxidants and if enough motor neurons are diseased, clinical signs of EMND occur. The stabilisation of clinical signs in 9 cases and the marked improvement in 4 horses suggest that, if an oxidative insult(s) is responsible for initiating the motor neuron disease, its effect is not progressive in many cases.