Evaluation of epidemiological, clinical, and pathological features of neuroaxonal dystrophy in Quarter Horses

Monica Aleman William R. Pritchard Veterinary Medical Teaching Hospital, School of Medicine, University of California-Davis, Davis, CA 95616.

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Carrie J. Finno William R. Pritchard Veterinary Medical Teaching Hospital, School of Medicine, University of California-Davis, Davis, CA 95616.

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Robert J. Higgins Department of Pathology, Microbiology and Immunology, School of Medicine, University of California-Davis, Davis, CA 95616.

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Birgit Puschner Department of Molecular Biosciences, School of Medicine, University of California-Davis, Davis, CA 95616.

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Barbara Gericota William R. Pritchard Veterinary Medical Teaching Hospital, School of Medicine, University of California-Davis, Davis, CA 95616.

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Kishorchandra Gohil Department of Internal Medicine, School of Medicine, University of California-Davis, Davis, CA 95616.

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Richard A. LeCouteur Department of Surgical and Radiological Sciences, School of Medicine, University of California-Davis, Davis, CA 95616.

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John E. Madigan Department of Medicine and Epidemiology, School of Veterinary Medicine, School of Medicine, University of California-Davis, Davis, CA 95616.

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Abstract

Objective—To describe epidemiological, clinical, and pathological features of neuroaxonal dystrophy in Quarter Horses (QHs) on a single farm.

Design—Prospective case series.

Animals—148 horses.

Procedures—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 and Clinical Relevance—Neuroaxonal dystrophy should be considered in evaluation of young horses with ataxia and proprioceptive positioning deficits. Vitamin E deficiency may contribute to disease severity.

Abstract

Objective—To describe epidemiological, clinical, and pathological features of neuroaxonal dystrophy in Quarter Horses (QHs) on a single farm.

Design—Prospective case series.

Animals—148 horses.

Procedures—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 and Clinical Relevance—Neuroaxonal dystrophy should be considered in evaluation of young horses with ataxia and proprioceptive positioning deficits. Vitamin E deficiency may contribute to disease severity.

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