title: Evaluation of epidemiological, clinical, and pathological features of neuroaxonal dystrophy in Quarter Horses.
abstract: OBJECTIVE
  To describe epidemiological, clinical, and pathological features of neuroaxonal dystrophy in Quarter Horses (QHs) on a single farm.
  
  
  METHODS
  Prospective case series. Animals-148 horses.
  
  
  METHODS
  Neurologic, pathological, and toxicological evaluations were completed in selected neurologically affected horses over a 2-year period. Descriptive statistical analysis was performed.
  
  
  RESULTS
  87 QHs and 1 QH-crossbred horse were affected. Most (50/88 [56.8%]) affected horses were 1 to 2 years old (median age, 2 years [range, 2 months to 34 years]). Neurologic deficits included obtundation (53/88 [60%] horses), decreased to absent menace response (33/88 [37.5%]), proprioceptive positioning deficits, wide-based stance, ataxia, and dysmetria (88/88 [100%]). Most (78/88 [88.6%]) horses had mild ataxia, but some (10/88 [11.4%]) had moderate to severe ataxia. Low serum concentrations of vitamin E (≤ 2 mg/L) were detected in 3 index case horses and 16 of 17 randomly selected horses (13/14 affected and 3/3 unaffected) during study year 1. Dietary vitamin E supplementation did not improve neurologic deficits in affected horses; vitamin E administration in pregnant mares appeared to decrease but not prevent disease development among offspring born the following year. Lesions detected at necropsy included bilaterally symmetric neuroaxonal degeneration with axonal spheroids in the nucleus gracilis, nucleus cuneatus medialis, nucleus cuneatus lateralis, and nucleus thoracicus (5/5 horses).
  
  
  CONCLUSIONS
  Neuroaxonal dystrophy should be considered in evaluation of young horses with ataxia and proprioceptive positioning deficits. Vitamin E deficiency may contribute to disease severity.
authors.affiliation: William R. Pritchard Veterinary Medical Teaching Hospital, School of Medicine, University of California-Davis, Davis, CA 95616, USA. mraleman@ucdavis.edu
authors.forename: Monica
authors.initials: M
authors.lastname: Aleman
authors.forename: Carrie J
authors.initials: CJ
authors.lastname: Finno
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Higgins
authors.forename: Birgit
authors.initials: B
authors.lastname: Puschner
authors.forename: Barbara
authors.initials: B
authors.lastname: Gericota
authors.forename: Kishorchandra
authors.initials: K
authors.lastname: Gohil
authors.forename: Richard A
authors.initials: RA
authors.lastname: LeCouteur
authors.forename: John E
authors.initials: JE
authors.lastname: Madigan
mesh_terms: D000375:Aging; D000818:Animals; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism; D019587:Dietary Supplements; D004569:Electroencephalography / Q000662:veterinary; D005260:Female; D005786:Gene Expression Regulation / Q000502:physiology; D006734:Horse Diseases / Q000188:drug therapy / Q000209:etiology* / Q000473:pathology; D006736:Horses; D008297:Male; D019150:Neuroaxonal Dystrophies / Q000209:etiology / Q000473:pathology / Q000662:veterinary*; D011247:Pregnancy; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D014810:Vitamin E / Q000627:therapeutic use*; D014811:Vitamin E Deficiency / Q000150:complications / Q000175:diagnosis / Q000473:pathology / Q000662:veterinary*
chemical_list: D002352:Carrier Proteins; D012333:RNA, Messenger; C017763:alpha-tocopherol transfer protein; D014810:Vitamin E