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New Zealand veterinary journal1986; 34(10); 170-175; doi: 10.1080/00480169.1986.35335

Equine laryngeal hemiplegia. Part II. An electron microscopic study of peripheral nerves.

Abstract: The recurrent laryngeal nerves were examined by electron microscopy in five control, four subclinical and four clinical laryngeal hemiplegic horses. In addition, the peroneal nerve was examined in two horses in the latter group. The distally distributed loss of large myelinated fibres in the left recurrent laryngeal nerve seen by light microscopy was confirmed. In addition, active axonal pathology was found to be more evident than indicated by light microscopic investigations. The onion bulb formations observed indicated the repetitive nature of the damaging influence to nerve fibres. Although the pathological changes were most obvious in the distal left recurrent laryngeal nerve, alterations similar in type and distribution were present in other areas of the left and right nerves, and in the distal hindlimb nerves. The observation of fibres with inappropriately thick myelin sheaths relative to their axonal calibre, was confirmed statistically by determining the regressions of axis cylinder perimeter against the number of myelin lamellae. In conclusion, the peripheral nerve pathology of equine laryngeal hemiplegia was demonstrated to be a distally distributed loss of myelinated fibres, with considerable active axonal damage, in conjunction with axonal atrophy. These features suggest that this disease may be classified as a distal axonopathy.
Publication Date: 1986-10-01 PubMed ID: 16031225DOI: 10.1080/00480169.1986.35335Google Scholar: Lookup
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  • Journal Article

Summary

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The research focused on the microscopic study of peripheral nerves in horses afflicted with laryngeal hemiplegia, a condition affecting horses’ voicebox. The study finds that this disease leads to a significant loss of myelinated fibres in the peripheral nerves, among other damaging effects, and suggests it can be classified as a distal axonopathy.

Methodology and Findings

  • The research involved the examination of the recurrent laryngeal nerves in various horses, including four with subclinical and four with clinical laryngeal hemiplegia, and also in five control horses.
  • The analysis was conducted using electron microscopy, a powerful tool for viewing extremely small structures like tissues and cells. This was complemented with light microscopy, which provided general imaging of the nerves.
  • The myelinated fibres in the left recurrent laryngeal nerve in horses with laryngeal hemiplegia were found to have distally distributed loss. This was aligned with previous observations from light microscopy.
  • Furthermore, the study discovered the presence of active axonal pathology, a nerve damage condition, which was more prevalent than initial observations from light microscopic studies suggested.
  • The research also noted onion bulb formations, indicating repetitive damage to nerve fibres, a characteristic of certain pathological conditions.

Further Observations and Conclusions

  • Pathological changes were not only localized. They were evident within the distal left recurrent laryngeal nerve, in other parts of the left and right nerves, and also in the distal hindlimb nerves.
  • The study confirmed the presence of fibres with unusually thick myelin sheaths compared to their axonal size. This confirmation came from statistical comparison of the axis cylinder perimeter against the number of myelin lamellae.
  • The peripheral nerve pathology in equine laryngeal hemiplegia appears to be characterized by the distal loss of myelinated fibres, significant active axonal damage, and axonal atrophy.
  • Given these findings, the research concludes that equine laryngeal hemiplegia could potentially be classified as a ‘distal axonopathy’, a type of disease that primarily affects the peripheral regions of axons, the long threadlike part of a nerve cell.

Cite This Article

APA
Cahill JI, Goulden BE. (1986). Equine laryngeal hemiplegia. Part II. An electron microscopic study of peripheral nerves. N Z Vet J, 34(10), 170-175. https://doi.org/10.1080/00480169.1986.35335

Publication

ISSN: 0048-0169
NlmUniqueID: 0021406
Country: England
Language: English
Volume: 34
Issue: 10
Pages: 170-175

Researcher Affiliations

Cahill, J I
  • Department of Veterinary Clinical Sciences, Massey University, New Zealand.
Goulden, B E

    Citations

    This article has been cited 6 times.
    1. Cercone M, Hokanson CM, Olsen E, Ducharme NG, Mitchell LM, Piercy RJ, Cheetham J. Asymmetric recurrent laryngeal nerve conduction velocities and dorsal cricoarytenoid muscle electromyographic characteristics in clinically normal horses.. Sci Rep 2019 Feb 25;9(1):2713.
      doi: 10.1038/s41598-019-39189-zpubmed: 30804428google scholar: lookup
    2. Cheetham J, Regner A, Jarvis JC, Priest D, Sanders I, Soderholm LV, Mitchell LM, Ducharme NG. Functional electrical stimulation of intrinsic laryngeal muscles under varying loads in exercising horses.. PLoS One 2011;6(8):e24258.
      doi: 10.1371/journal.pone.0024258pubmed: 21904620google scholar: lookup
    3. Collins N, Milne E, Hahn C, Dixon P. Correlation of the Havemeyer endoscopic laryngeal grading system with histopathological changes in equine Cricoarytenoideus dorsalis muscles.. Ir Vet J 2009 May 1;62(5):334-8.
      doi: 10.1186/2046-0481-62-5-334pubmed: 21851734google scholar: lookup
    4. Dupuis MC, Zhang Z, Druet T, Denoix JM, Charlier C, Lekeux P, Georges M. Results of a haplotype-based GWAS for recurrent laryngeal neuropathy in the horse.. Mamm Genome 2011 Oct;22(9-10):613-20.
      doi: 10.1007/s00335-011-9337-3pubmed: 21698472google scholar: lookup
    5. Harrison GD, Duncan ID, Clayton MK. Determination of the early age of onset of equine recurrent laryngeal neuropathy. 1. Muscle pathology.. Acta Neuropathol 1992;84(3):307-15.
      doi: 10.1007/BF00227824pubmed: 1384268google scholar: lookup
    6. Duncan ID. Determination of the early age of onset of equine recurrent laryngeal neuropathy. 2. Nerve pathology.. Acta Neuropathol 1992;84(3):316-21.
      doi: 10.1007/BF00227825pubmed: 1329430google scholar: lookup