Miscellaneous Neurologic or Neuromuscular Disorders in Horses

Aleman, Monica R

doi:10.1016/j.cveq.2011.08.001

Cited by 16 publications

(16 citation statements)

References 100 publications

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“…Importantly, pathologic progression can be halted in affected individuals by high-dose supplementation with α-tocopherol (Harding et al, 1985, Matsuya et al, 1994, Amiel et al, 1995, Yokota et al, 1996, Cavalier et al, 1998). Similar findings were established in genetic and dietary models of vitamin E deficiency in mice (Yokota et al, 2001), rats (Einarson, 1953, Goss-Sampson et al, 1988), monkeys (Dinning and Day, 1957) and horses (Mayhew et al, 1987, Aleman, 2011). …”

Section: Discussionsupporting

confidence: 75%

Vitamin E is essential for Purkinje neuron integrity

et al. 2014

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Alpha-tocopherol (vitamin E) is an essential dietary antioxidant with important neuroprotective functions. Alpha-tocopherol deficiency manifests primarily in neurological pathologies, notably cerebellar dysfunctions such as spinocerebellar ataxia. To study the roles of α-tocopherol in the cerebellum, we used the Ttpa-/- mice which lack the tocopherol transfer protein (TTP) and are a faithful model of vitamin E deficiency and oxidative stress. When fed vitamin E deficient diet, Ttpa-/- mice had un-detectable levels of α-tocopherol in plasma and several brain regions. Dietary supplementation with α-tocopherol normalized plasma levels of the vitamin, but only modestly increased its levels in the cerebellum and prefrontal cortex, indicating a critical function of brain TTP. Vitamin E deficiency caused an increase in cerebellar oxidative stress evidenced by increased protein nitrosylation, which was prevented by dietary supplementation with the vitamin. Concomitantly, vitamin E deficiency precipitated cellular atrophy and diminished dendritic branching of Purkinje neurons, the predominant output regulator of the cerebellar cortex. The anatomic decline induced by vitamin E deficiency was paralleled by behavioral deficits in motor coordination and cognitive functions that were normalized upon vitamin E supplementation. These observations underscore the essential role of vitamin E and TTP in maintaining CNS function, and support the notion that α-tocopherol supplementation may comprise an effective intervention in oxidative stress-related neurological disorders.

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Section: Discussionsupporting

confidence: 75%

Vitamin E is essential for Purkinje neuron integrity

et al. 2014

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“…Granulomatous inflammation affecting the cranial nerves has been associated with polyneuritis equi (PNE); however, clinical experience has suggested that horses with PNE presenting primarily with cranial nerve deficits eventually also show cauda equina deficits . Moreover, the most common clinical signs reported when the cranial nerves are involved include atrophy of the muscles of mastication, dysphagia, head tilt, facial nerve paresis, and head shaking . In the present case, the neurological examination did not reveal involvement of any other cranial nerve or any signs of cauda equina dysfunction (poor tail tone, fecal and urinary incontinence, pelvic limb weakness, or pelvic limb muscle atrophy) at the time of presentation.…”

Section: Discussioncontrasting

confidence: 54%

“…The underlying cause of PNE remains unknown, but an underlying immune‐mediated process has been suggested . Corticosteroids and azathioprine have been proposed as potential treatments to slow progression of the disease …”

Section: Discussionmentioning

confidence: 99%

Imaging Diagnosis — Unilateral Trigeminal Neuritis Mimicking Peripheral Nerve Sheath Tumor in a Horse

Beltrán

Grundon

Stewart

et al. 2015

Vet Radiology Ultrasound

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A 16‐year old Warmblood gelding presented with a nonhealing corneal ulcer and absent corneal sensation in the left eye. A lesion affecting the maxillary and ophthalmic branches of the left trigeminal nerve was suspected. Magnetic resonance (MR) imaging identified marked thickening of the ophthalmic and maxillary branches of the left trigeminal nerve. The nerve was iso‐ to hypointense on T1‐weighted and T2‐weighted images with heterogeneous enhancement. A peripheral nerve sheath tumor was suspected, however granulomatous neuritis was histopathologically confirmed. These inflammatory changes can result in severe nerve enlargement and should be considered with MR findings suggestive of peripheral nerve sheath tumor.

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“…There is also potential malfunctioning of ion channels that may play a role in the pathophysiology of the condition (Cassart et al 2008 :1–16). Aleman suggests that O. megnini causes a myotonia by altering neuromuscular transmission at the postsynaptic membrane of the neuromuscular junction (Aleman 2011 :481–506). Whether the condition is a true paralysis or a myotonia remains to be shown.…”

Section: Discussionmentioning

confidence: 99%

“…Otobius megnini -associated disease in equines has been reported by Madigan et al, showing an association of the tick and clinical disease in five horses in 1995 in California (Madigan et al 1995 :74–76), whilst Zarate-Ramos et al ( 2014 ) described a similar case attributed to O. megnini in Mexico in 2014 (Zarate-Ramos et al 2014 :16–20). As yet, no neurotoxin has been described for this tick and it is possible that there may be neuromuscular dysfunction (Aleman 2011 :481–506) alone or in relation to neurotoxin involvement (Pecina 2012 :531–532). Otobius megnini is not known to transmit any pathogens (Barker & Walker 2014 ).…”

Section: Introductionmentioning

confidence: 99%

Putative Otobius megnini -associated clinical signs in horses in South Africa (2012–2018)

Miller¹

2020

Journal of the South African Veterinary Association

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Otobius megnini has been associated with certain clinical conditions in horses in both California and Mexico. A number of cases similar to those described previously have been identified by the author in South Africa. This case report summarises these cases to demonstrate that the clinical condition occurs readily in South Africa and may be increasing in occurrence. The disease has minimal coverage in the literature making it more likely that a veterinarian, unfamiliar with the disease, will miss the diagnosis. The author would like to make veterinarians aware of this as a potential differential diagnosis. This study is a retrospective review of clinical data. Clinical records of patients with similar clinical signs and treatment were reviewed and grouped together as relevant cases for this case report. Ten cases of O. megnini associated neuromuscular dysfunction are reported, suggesting a link between the occurrence of the tick and the clinical condition. Clinical signs include third eyelid prolapse, localised muscle fasciculations, elevated heart rate and limb stamping. Serum chemistry changes commonly show increased aspartate aminotransferase and creatine kinase enzymes activities. The occurrence of the ticks within South Africa and the increasing number of cases presented demonstrate the need for more investigation into the pathophysiology of this condition.

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Miscellaneous Neurologic or Neuromuscular Disorders in Horses

Cited by 16 publications

References 100 publications

Vitamin E is essential for Purkinje neuron integrity

Vitamin E is essential for Purkinje neuron integrity

Imaging Diagnosis — Unilateral Trigeminal Neuritis Mimicking Peripheral Nerve Sheath Tumor in a Horse

Putative Otobius megnini -associated clinical signs in horses in South Africa (2012–2018)

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