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Histologic analysis of horses afflicted with idiopathic laryngeal hemiplegia: nerve and muscular properties
Author(s) -
Hermanson John W,
Svoboda Sarah M.,
Cheetham Jonathan,
Ducharme Normand G.
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.448.1
Subject(s) - medicine , laryngeal paralysis , atrophy , recurrent laryngeal nerve , paralysis , reinnervation , anatomy , muscle hypertrophy , vocal cord paralysis , pathology , denervation , cardiology , surgery , thyroid
Equine idiopathic laryngeal hemiplegia (ILH), is characterized by respiratory distress at exercise due to paralysis of a muscle, the cricoarytenoideus dorsalis (CAD), that abducts the vocal folds during inspiration. Degeneration of the left recurrent laryngeal nerve (RLN) has been linked to paralysis in affected horses. Histology of this nerve and the CAD muscle in 18 horses was evaluated after endoscopic grading. Samples were evaluated for signs of degeneration, including differences in myelinated axons in the RLN or its laryngeal branches, as well as for fiber type grouping and muscle fiber hypertrophy and muscle atrophy in CAD muscles. There were more (p≤0.05) myelinated axons in the right RLN (601±29)than in the left (426±29). There was no significant difference in fiber type percentages (type I vs. II) in left vs. right CAD. However, there was more fiber type grouping in the left vs. the right CAD. In grade 1 horses, those without any functional deficit in movement of the vocal folds (subclinical disease), there were regions of fiber type grouping, suggesting reinnervation of those regions. In grade 4 horses (the worst cases) there was nearly total atrophy of the CAD, while nerves showed loss of myelinated axons. Results demonstrate that the RLN and CAD degenerate concomitantly in horses with both mild and severe laryngeal dysfunction. Funding was provided in part by the Zweig Fund and by Med‐El.