BackgroundEquine neuroaxonal dystrophy/equine degenerative myeloencephalopathy (NAD/EDM) is a neurodegenerative disorder affecting genetically predisposed foals maintained on α-tocopherol (α-TP)-deficient diet.ObjectiveIntramuscular α-TP and selenium (Se) administration at 4 days of age would have no significant effect on serum or cerebrospinal fluid (CSF) α-TP in healthy foals. Serum and CSF α-TP, but not Se, would be significantly decreased in NAD/EDM-affected foals during first year of life.AnimalsFourteen Quarter horse foals; 10 healthy foals supplemented with 0.02 mL/kg injectable α-TP and Se (n = 5) or saline (n = 5) at 4 days of age and 4 unsupplemented NAD/EDM-affected foals.MethodsComplete neurologic examinations were performed, blood and CSF were collected before (4 days of age) and after supplementation at 10, 30, 60, 120, 180, 240, and 360 days of age. Additional blood collections occurred at 90, 150, 210, and 300 days. At 540 days, NAD/EDM-affected foals and 1 unsupplemented healthy foal were euthanized and necropsies performed.ResultsSignificant decreases in blood, CSF α-TP and Se found in the first year of life in all foals, with most significant changes in serum α-TP from 4–150 days. Dam α-TP and Se significantly influenced blood concentrations in foals. Injection of α-TP and Se did not significantly increase CSF Se, blood or CSF α-TP in healthy foals. NAD/EDM-affected foals had significantly lower CSF α-TP through 120 days.Conclusions and Clinical ImportanceInjection of α-TP and Se at 4 days of age does not significantly increase blood or CSF α-TP. Despite all 14 foals remaining deficient in α-TP, only the 4 genetically predisposed foals developed NAD/EDM.

BackgroundEquine neuroaxonal dystrophy/equine degenerative myeloencephalopathy (eNAD/EDM) is a neurodegenerative disorder affecting genetically predisposed foals maintained on an α‐tocopherol (α‐TOH) deficient diet. Currently no antemortem diagnostic test for eNAD/EDM is available.HypothesisBecause α‐TOH deficiency is associated with increased lipid peroxidation, it was hypothesized that F2‐isoprostanes (F2IsoP), F4‐neuroprostanes (F4NP) and oxysterols derived from free radical oxidation would be increased in the cerebrospinal fluid (CSF) and neural tissue of eNAD/EDM affected horses and could serve as potential biomarkers for disease.AnimalsIsoprostane Study A: 14 Quarter horse foals (10 healthy foals and 4 eNAD/EDM affected foals) at 1 and 6 months of age. Isoprostane Study B: 17 eNAD/EDM affected and 10 unaffected horses ≥ 1‐4 years of age. Oxysterol study: eNAD/EDM affected (n = 14, serum; n = 11, CSF; n = 10, spinal cord [SC]) and unaffected horses 1‐4 years of age (n = 12, serum; n = 10, CSF; n = 7, SC).ProceduresCerebrospinal fluid [F2IsoP] and [F4NP] were assessed using gas chromatography‐negative ion chemical ionization mass spectrometry. Serum, CSF, and cervical SC [oxysterols] were quantified using high performance liquid chromatography mass spectrometry. Results were compared with respective α‐TOH concentrations.ResultsSpinal cord [7‐ketocholesterol], [7‐hydroxycholesterol], and [7‐keto‐27‐hydrocholesterol] were higher in eNAD/EDM horses whereas [24‐ketocholesterol] was lower. No significant difference was found in CSF [F2IsoP] and [F4NP], serum [oxysterols] and CSF [oxysterols] between eNAD/EDM affected and unaffected horses. No correlation was found between [F2IsoP], [F4NP], or [oxysterols] and respective [α‐TOH].Conclusions and Clinical ImportanceIn the SC, targeted markers of cholesterol oxidation were significantly increased in horses with eNAD/EDM.

This study demonstrates that the duration of clinical signs, response to treatment and the ability of horses to use a sling are associated with survival to hospital discharge for recumbent horses.

Neuroaxonal dystrophy/EDM does not appear to cause clinical signs of ocular disease or functional ERG/EEG deficits in QHs.

Horses may develop inhibitory antibodies against factor VIII that cause acquired hemophilia A. A treatment strategy combining transfusions of whole blood and fresh-frozen plasma and administration of immunosuppressive agents was effective and induced sustained remission for at least 1 year in the mare described here.

Summary Gastrointestinal rupture is an important cause and complication of equine colic. The stomach is the most commonly affected segment in the gastrointestinal tract involved in gastrointestinal rupture. Gastric rupture can be primary or secondary; however, unless prodromal clinical signs are identified, localised and corrected, the resulting peritoneal contamination with feed, intestinal secretions and bacteria is invariably fatal. Causes for gastric rupture may be known or idiopathic; however, factors that predispose a horse to gastric rupture are poorly understood. Further research is needed to identify underlying causes and pathophysiology of gastric rupture to prevent it from occurring.

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