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Immunohistochemical Analysis of Laryngeal Muscles in Normal Horses and Horses With Subclinical Recurrent Laryngeal Neuropathy

Hannah S. Rhee, Catherine M. Steel, Frederik J. Derksen, N. Edward Robinson and Joseph F.Y. Hoh

Discipline of Physiology and the Bosch Institute, School of Medical Sciences, Faculty of Medicine, The University of Sydney, Sydney, Australia (HSR,JFYH); Veterinary Clinic and Hospital, The University of Melbourne, Victoria, Australia (CMS); and Department of Large Animal Clinical Science, College of Veterinary Medicine, Michigan State University, East Lansing, Michigan (FJD,NER)

Correspondence to: Dr. J.F.Y. Hoh, Discipline of Physiology, Bldg. F13, The University of Sydney, NSW, 2006 Australia. E-mail: joeh{at}physiol.usyd.edu.au

We used immunohistochemistry to examine myosin heavy-chain (MyHC)-based fiber-type profiles of the right and left cricoarytenoideus dorsalis (CAD) and arytenoideus transversus (TrA) muscles of six horses without laryngoscopic evidence of recurrent laryngeal neuropathy (RLN). Results showed that CAD and TrA muscles have the same slow, 2a, and 2x fibers as equine limb muscles, but not the faster contracting fibers expressing extraocular and 2B MyHCs found in laryngeal muscles of small mammals. Muscles from three horses showed fiber-type grouping bilaterally in the TrA muscles, but only in the left CAD. Fiber-type grouping suggests that denervation and reinnervation of fibers had occurred, and that these horses had subclinical RLN. There was a virtual elimination of 2x fibers in these muscles, accompanied by a significant increase in the percentage of 2a and slow fibers, and hypertrophy of these fiber types. The results suggest that multiple pathophysiological mechanisms are at work in early RLN, including selective denervation and reinnervation of 2x muscle fibers, corruption of neural impulse traffic that regulates 2x and slow muscle fiber types, and compensatory hypertrophy of remaining fibers. We conclude that horses afflicted with mild RLN are able to remain subclinical by compensatory hypertrophy of surviving muscle fibers. (J Histochem Cytochem 57:787–800, 2009)

Key Words: horse • larynx • muscle fiber types • myosin heavy chain • recurrent laryngeal neuropathy • idiopathic laryngeal hemiparesis • laryngeal paralysis

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