Figure 2 - uploaded by Michelle L Husulak
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Electromyogram reading demonstrating fibrillation potentials in the left extensor carpi radialis muscle, which is consistent with the muscle fiber denervation that occurs with EMND. Each line represents the recording from an electrode within a muscle and the wave forms indicate spontaneous firing of the muscle due to loss of innervation.
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Two horses from Saskatchewan were presented with signs of sweating, muscle fasciculations, weight loss, and generalized weakness. The horses were diagnosed with equine motor neuron disease (EMND), by histological assessment of a spinal accessory nerve or sacrocaudalis dorsalis medialis muscle biopsy. This is the first report of EMND in western Cana...
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... by a board-certified ophthalmologist revealed incipient posterior cataracts bilaterally and normal fundi with no apparent pigment retinopathy. A serum vitamin and mineral panel revealed deficient levels of both serum magnesium at 10.10 mg/mL [RR: 18 to 35 mg/mL (16)] and a-tocopherol at 0.86 mg/mL [normal . 2 mg/mL (18)]. A muscle biopsy for histopathological evaluation was obtained from the left sacrocaudalis dorsalis medialis (SCDM) muscle (19) under stand- ing sedation with xylazine hydrochloride (Bayer Animal Health), 0.5 mg/kg BW, IV, and butorphanol (Zoetis), 0.01 mg/kg BW, IV, and local anesthesia with 2% lidocaine hydrochloride (Zoetis). The SCDM muscle contained muscle fibers with moderate size variation, anguloid atrophy, angular atrophy, centrally displaced nuclei, and sarcoplasmic masses, which is consistent with neurogenic atrophy that occurs in EMND cases (20). Electromyography (EMG) was performed under general anesthesia (21). Spontaneous fibrillation potentials consistent with muscle fiber denervation were detected in several muscles on the left side of the horse including the extensor carpi radia- lis (Figure 2), gluteal, quadriceps, triceps, and neck muscles. Complete examination of the right side was not undertaken due to the positioning of the horse in right lateral ...
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... (EMG) was performed under general anesthesia (21). Spontaneous fibrillation potentials consistent with muscle fiber denervation were detected in several muscles on the left side of the horse including the extensor carpi radialis (Figure 2), gluteal, quadriceps, triceps, and neck muscles. Complete examination of the right side was not undertaken due to the positioning of the horse in right lateral recumbency. ...
Citations
... Affected individuals are known to have previous history of little to no access to fresh grass, preventing uptake of nutritional antioxidants, for at least 18 months before onset of clinical signs (Banfield et al. 2019, Ayala et al. 2016, Husulak et al. 2016, Mohammed et al. 2007. Oxidative stress of the lower motor neurons caused by depleted nutritional antio xidants, especially vitamin E, has been suspected to play a major role in the aetiology of EMND, (Divers et al. 1997, Mohammed et al. 2007). ...
... The serum vitamin E (alpha-tocopherol) concentrations are record-ed abnormally low (<1 mg/L) (Divers et al. 1997, Banfield et al. 2019, Sasaki et al. 2016. Muscle biopsies of affected horses typically show signs of neurogenic degeneration and histological findings in central nervous system (CNS) include chromatolytic neurons in ventral horns of the spinal cord, axon swelling and degeneration, as well as eosinophilic cytoplasmic inclusion bodies (Sasaki et al. 2016, Husulak et al. 2016, Syrja et al. 2006, Finno et al. 2016, Sasaki et al. 2006). ...
... The age of affected animals also varies from 2 to 23 years old, with mean age being 9 years (Divers et al. 1997). The most common criteria for horses with EMND so far is prolonged lack of green feeds, which include sufficient amount of vitamin E in the diet (Divers et al. 1997, Divers et al. 1994, Banfield et al. 2019, Ayala et al. 2016, Husulak et al. 2016, Mohammed et al. 2007. It is experimentally proven that horses receiving vitamin-E-depleted diet (no access to green pasture and vitamin E content of less than 16.4 IU pro 1 kg feed) develop EMND in a mean time of 38.5 months (18 to 44 months) (Mohammed et al. 2007). ...
... Primary, noninflammatory, neurodegenerative disorders with varying degrees of spinal cord involvement are an entity of genetic, toxic, nutritional, or unestablished etiology in humans (Salachas and Meininger 2001;Arbesman et al. 2014) and domestic animals (de Lahunta 1983;de Lahunta 1990;Jubb and Huxtable 1993;Storts 1995). The disorders have been previously described in many domestic animal species, including dogs (Palmer et al. 1984;Sheahan et al. 1991;Levine and Levine 2012), cats (Caulfield et al. 2009;Rohdin et al. 2010), sheep (Storts 1995;Siso et al. 2006), goats (Cordy and Knight 1978;Storts 1995;Ohfuji 2015b), horses (Finno et al. 2011;Husulak et al. 2016), cattle (Kennedy et al. 1986;Richard and Edwards 1986;Baird et al. 1988;Ohfuji 2015a), and swine (McGavin et al. 1962;Higgins et al. 1983;Pletcher and Banting 1983;O'Toole et al. 1994;Davies et al. 1996;Penrith and Robinson 1996;Nathues et al. 2010;Delgado et al. 2011;Wohlsein et al. 2012). In swine, occurrence of neurodegenerative disorders such as those that involve more specifically and gravely the spinal cord than the brain is relatively uncommon compared to other domestic animal species. ...
... Spinal cord lesions of this report, evidently identified through routine, special, and immunohistochemical staining techniques, were characterized by the presence of Walleriantype degeneration of myelinated axons in the white matter. White matter lesions were not accompanied or preceded by the presence of demyelinated areas, and many survived axons were in a normally myelinated state indicative of full development of myelin sheaths (myelination), perhaps ruling out a myelinopathic (demyelinating or hypomyelinating) entity that has been documented in humans (Faro 2000;Liblau et al. 2001) and domestic animals (de Lahunta 1983;Sheahan et al. 1991;Storts 1995;Husulak et al. 2016). In addition, there were no preexisting or underlying inflammatory, vascular, or traumatic lesions in the spinal cord. ...
Spinal cord degeneration was identified in nine swine consisting of four fattening pigs (5 months old) and five adult sows (2 to 3 years old). These animals were raised on nine different farms and culled over a 1.5-year period on account of similar clinical signs encompassing ataxia and paresis progressing to paraplegia. Histopathologically, the spinal cord exhibited white matter degeneration with no predilection for specific tracts, which was more severe in five swine and less severe in the others. White matter lesions were characterized by Wallerian-type degeneration of myelinated axons, exhibiting axonal swelling/loss and myelin sheath dilation/disintegration associated with occasional macrophage reaction and little fibrous astrogliosis. Gray horn neurons were unremarkable. In the brain examined in three cases, similar but minimal degenerative lesions were observed in the marginal areas of the brainstem in one case. Significant lesions were absent in the hind limb nerves, including sciatic nerve, femoral nerve, and obturator nerve, in seven cases. The spinal lesions were regarded as being a variant of neurodegenerative disorder. The pathogenesis appeared to involve a primary impairment of myelinated axons in the spinal white matter (central axonopathy). The pattern and extent of this disease were considered different from those reported previously in swine with neurodegenerative or myelinopathic disorders of inherited, toxic, or nutritional origin. The etiology remains unknown, though a metabolic abnormality was suspected to be one of the likeliest possibilities.
We carried out an investigation to identify the factors that predispose to the risk of equine motor neuron disease (EMND) and evaluated the long-term impact of an intervention. Data on several biomarkers, including antioxidants (α-tocopherols, β-carotenes, glutathione peroxidase (GSHPx)), and superoxide dismutase (SOD1), neurofilaments, and other putative risk factors hypothesized to associate with the likelihood of EMND were collected. The data were analyzed for their significance of association with the condition. The EMND outbreak started in 1991 and continued until 1998. A total of 69 EMND cases and 64 control horses met the inclusion criteria and were enrolled in the study. Most cases (74%) occurred in 1996 and 1997. Horses afflicted with EMND had significantly lower plasma levels of vitamin E than control horses (0.381 vs. 1.148 μg/mL). There were no significant differences in the levels of vitamin A, β-carotenes, GSHPx, or the activities of SOD1 between EMND cases and control horses. Horses afflicted with EMND had significantly higher serum levels of phosphorylated neurofilament heavy than controls (2.85 vs. 0.27 ng/mL). The probability of EMND diagnosis increased above 50% when the serum levels of phosphorylated neurofilament heavy increased beyond 2.54 ng/mL. Mixed and Brazilian breeds had a significantly higher risk of EMND in comparison to Standardbred horse among the study population. In 1997, there was a change in the diet where better quality green hay was used. The incidence of EMND dropped to 0 in 1 year after intervention and remained at that level for the past 20 years.
