South African Equine Veterinary Association Congress 2015 Protea Hotel Stellenbosch
Pathophysiology of recurrent laryngeal neuropathy
Piercy RJ*
MA VetMB MD PhD DipACVIM MRCVS
Professor of Comparative Neuromuscular Disease
Royal Veterinary College
Introduction
Some of the earliest descriptions of equine recurrent laryngeal neuropathy (RLN) were made by
Bouley, and subsequently by Dupuy in the 1820s (Bouley 1825; Dupuy 1826). Then, during the
mid 1800s, atrophy of equine laryngeal intrinsic muscles was commonly identified at necropsy in
horses that „roared‟ (Gunther 1866). Despite these early reports, and considerable interest in
recent years, the pathophysiology remains enigmatic, as does the aetiology. A discussion of the
pathophysiology of the disease can perhaps best be made in the context of the possible aetiology
and for the latter, genetic, acquired and environmental factors have each been proposed. In
summary, RLN can be described as a distal axonopathy of (predominantly) the left recurrent
laryngeal nerve with secondary neurogenic muscle atrophy of intrinsic laryngeal muscles. The
consequence is a reduced size of the rima glottis due to left cricoarytenoideus muscle paresis,
which becomes relevant at exercise and manifests as poor performance due to impaired air intake
and reduced PaO2. Although the pathophysiology (and also aetiology) remain very unclear, it is
helpful to consider certain issues that (currently) remain unresolved.
Clinically-relevant prevalence and actual disease prevalence
Estimates of RLN prevalence in horses vary widely, largely due to the manner in which diagnosis
was made. In particular, since prevalence estimates rise as the sensitivity of the technique
improves, RLN diagnosis made on the basis of results of (historical) laryngeal palpation or
perhaps the „slap test‟, historically underestimated many cases. Similarly, resting laryngoscopy
likely misses cases that might better be identified on exercising endoscopy. In recent years, my
group has continued work started elsewhere (Adreani et al. 2006; Rhee et al. 2009), which is
based on histopathological assessment of intrinsic laryngeal musculature and nerve axon density.
Somewhat surprisingly, our data, and that of others (Adreani et al. 2006; Rhee et al. 2009; Collins
et al. 2009) suggests that it is often hard to find convincing evidence of a normal (unaffected)
animal. The conclusion therefore is that whilst many horses have sub-clinical disease, it is only
those animals with the severest phenotypes that are identified clinically or that have compromised
laryngeal function– i.e. an iceberg effect. Of course, misclassification of a horse‟s phenotype (in
particular, difficulty in assigning appropriate controls) might have significant consequences on the
search for aetiology, and in particular a genetic cause, in genome wide association studies.
Furthermore, if the disease is so common (albeit often subclinically) it begs the question as to
whether the same disorder might occur in other equids, or in other long-necked mammals. The
evidence for and against RLN involvement in zebra, donkeys and ponies from our group and in
zebra and giraffe (from others) (Hahn & Mayhew 1999; Hahn and Mayhew