title: Equine motor neuron disease: findings in 28 horses and proposal of a pathophysiological mechanism for the disease.
abstract: 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.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Clinical Sciences, New York State College of Veterinary Medicine, Cornell University, Ithaca 14853-6401.
authors.forename: T J
authors.initials: TJ
authors.lastname: Divers
authors.forename: H O
authors.initials: HO
authors.lastname: Mohammed
authors.forename: J F
authors.initials: JF
authors.lastname: Cummings
authors.forename: B A
authors.initials: BA
authors.lastname: Valentine
authors.forename: A
authors.initials: A
authors.lastname: De Lahunta
authors.forename: C A
authors.initials: CA
authors.lastname: Jackson
authors.forename: B A
authors.initials: BA
authors.lastname: Summers
mesh_terms: D000821:Animal Feed; D000818:Animals; D001947:Breeding; D004576:Electromyography / Q000662:veterinary; D005260:Female; D006734:Horse Diseases / Q000453:epidemiology / Q000209:etiology* / Q000503:physiopathology; D006736:Horses; D008297:Male; D016472:Motor Neuron Disease / Q000453:epidemiology / Q000209:etiology / Q000503:physiopathology / Q000662:veterinary*; D011446:Prospective Studies; D012307:Risk Factors; D014810:Vitamin E / Q000097:blood
chemical_list: D014810:Vitamin E