in friesian horses: morphological features. Vet Pathol 2015; 52(6): 1142–1147.
8 8 Wooldridge AA, Eades SC, Hosgood GL and Moore RM. in vitro effects of oxytocin, acepromazine, detomidine, xylazine, butorphanol, terbutaline, isoproterenol, and dantrolene on smooth and skeletal muscles of the equine esophagus. Am J Vet Res 2002; 63(12): 1732–1737.
9 9 Johnstone LK, Engiles JB, Aceto H, et al. Retrospective evaluation of horses diagnosed with neuroborreliosis on postmortem examination: 16 cases (2004–2015). J Vet Intern Med 2016; 30(4): 1305–1312.
10 10 Green EM, Roth JE and McClure RC. Recurrent esophageal obstruction in the horse: neurologic considerations. 32nd Ann Conf Am Assoc Equine Pract 1986.
17 Laryngeal paresis and paralysis: roaring
This is a common idiopathic disorder in most tall horses of light breed, warmblood, and draft breeds in which Wallerian‐like neuronal fiber degeneration and attempts at reinnervation occur in the recurrent laryngeal nerve (rln), the left far more so than the right, and as such is referred to as recurrent laryngeal neuropathy (RLN). These horses have degrees of neurogenic muscle atrophy in the intrinsic laryngeal muscles innervated by the rln, and a small proportion used for some kind of athletic performance will demonstrate an inspiratory noise, roaring, and/or curtailed performance at exercise.1–3
Many families of horses have a high frequency of roaring, although no specific genetic defect has been determined. One previously popular hypothesis for the idiopathic disorder in horses involves physical forces associated with the left rln having a longer course than the right nerve. The syndrome occurs most commonly on the left side in large horses with long necks and deep thoraxes. The left rln has a longer course around the aortic arch than the right nerve does around the costocervical artery. The leverage effect created by neck movement could then result in tension on the nerve and compromise to its blood supply with ischemia resulting in local and distal nerve fiber degeneration. Whether such nerve‐specific factors are more important than the presence of a generalized neuropathy with selective predisposition to damage of the rln is not known: i.e., is RLN a mononeuropathy or a polyneuropathy?2 Several toxic, metabolic, genetic, and other factors have been put forward as possible causative factors for RLN, but obviously at present the exact pathogenesis of the disease is unknown.3
Clinical evaluation of cases of RLN has been standardized by use of endoscopy during high‐speed treadmill and overground exercise, and relatively successful surgical procedures are available for palliative treatment of the condition. Denervation potentials can be recorded in left laryngeal muscles, slowing of the thoracolaryngeal response can be identified and longer left rln conduction latency (viz. reduced velocity) can be calculated with electrodiagnostic equipment, none of which really add to diagnostic accuracy and prognosis for RLN (see Chapter 38).
In addition to cases of idiopathic RLN, about 5–10% of cases of equine laryngeal paresis or paralysis have a detectable cause.4 Non‐RLN laryngeal paralysis may be a sequel to localized injury to the vagus or recurrent laryngeal nerves such as guttural pouch mycosis, rupture of the rectus capitis ventralis muscles, temporohyoid fracture, retropharyngeal abscessation, perivascular/perineural cervical injection reaction, inadvertent ventral neck intraoperative nerve damage, and retropharyngeal and cranial thoracic neoplasia. Non‐RLN paralysis may also be a manifestation of myopathy and polyneuropathy including neuroborreliosis.5 Bilateral laryngeal paralysis,6 which is considerably less common (2–6%) than unilateral paralysis, almost invariably results from generalized neuromuscular dysfunction such as hepatoencephalopathy7–9 and hyperkalemic periodic paresis. A similar array of disorders is likely associated with non‐RLN laryngeal paralysis in other large animal species.10
Pyrrolizidine alkaloid‐associated liver failure with hepatic encephalopathy frequently results in bilateral laryngeal paralysis with loud inspiratory stridor occurring at rest or with minimal exercise.7–9 The laryngeal paralysis may be temporary, worsening during exacerbations of encephalopathy and resolving with the restoration of hepatic function. No gross or histopathological abnormalities have been identified in laryngeal muscles, rln, and other peripheral nerves of affected horses. Thus, the laryngeal paralysis of liver failure in horses may reflect neuromuscular dysfunction rather than an axonopathy or myelinopathy.
Uncommonly, following general anesthesia, horses may develop postanesthetic laryngeal paralysis with variable recovery of laryngeal function. This may result from excessive head and neck extension compromising nerve blood flow or from compression and/or stretching of the recurrent laryngeal nerve over a rigid structure in the neck. Myopathy, persistent hypoxia, and pre‐existing laryngeal dysfunction are additional factors that may contribute to the development of this complication.
Several toxic peripheral neuropathies cause equine laryngeal paralysis including intermediate and delayed organophosphate induced toxicity,11–13 pasture‐associated stringhalt, lead poisoning, ingestion of Lathyrus spp. and Cicer arietinum (chick pea), and other plant poisonings, all with evidence of a generalized disorder that affects multiple nerves and so presents little diagnostic problem. Finally, a syndrome of bilateral rln neuropathy can accompany the more general lesions of copper deficiency, at least in goats.14
As an aside, diaphragmatic paralysis can be mentioned here as a very unusual neurologic disease resulting in variable signs of respiratory distress with no evidence of respiratory tract obstruction or of pulmonary lesions and can result from mid cervical (C3‐5) spinal cord or bilateral nerve root, or phrenic nerve, or diaphragmatic muscle lesions. Abdominal collapse during inspiration and thoracic expansion, is the characteristic syndrome.15–19
References
1 1 Dixon PM, Robinson E and Wade JF. Equine recurrent laryngeal neuropathy. Havemeyer Foundation Monograph Series No. 11: R & W Publications. 2004.
2 2 Draper ACE and Piercy RJ. Pathological classification of equine recurrent laryngeal neuropathy. J Vet Intern Med 2018; 32(4): 1397–1409.
3 3 Parente EJ. Fifty years of recurring struggles with recurrent laryngeal neuropathy. Equine Vet J 2018; 50(2): 155–158.
4 4 McGorum B and Dixon PM. Non‐recurrent laryngeal neuropathy (RLN) causes of equine laryngeal paralysis. In Equine Recurrent Laryngeal Neuropathy, Dixon PM, Robinson E, Wade JF, Editors. Havemeyer Foundation Monograph Series No 11: R & W Publications. 2004; 55–56.
5 5 Johnstone LK, Engiles JB, Aceto H, et al. Retrospective evaluation of horses diagnosed with neuroborreliosis on postmortem examination: 16 cases (2004–2015). J Vet Intern Med 2016; 30(4): 1305–1312.
6 6 Duncan ID and Brook D. Bilateral laryngeal paralysis in the horse. Equine Vet J 1985; 17(3): 228–233.
7 7 Hughes KJ, McGorum BC, Love S and Dixon PM. Bilateral laryngeal paralysis associated with hepatic dysfunction and hepatic encephalopathy in six ponies and four horses. Vet Rec 2009; 164(5): 142–147.
8 8 McGorum BC, Murphy D, Love S and Milne EM. Clinicopathological features of equine primary hepatic disease: a review of 50 cases. Vet Rec 1999; 145(5): 134–139.
9 9 Pearson EG. Liver failure attributable to pyrrolizidine alkaloid toxicosis and associated with inspiratory dyspnea in ponies: three cases (1982–1988). J Am Vet Med Assoc 1991; 198(9): 1651–1654.
10 10 Bushby VE, Woodford NS and Little DR, Huxley JN. Laryngeal hemiplegia in a heifer. Vet Rec 2004; 155(22): 715.
11 11 Rose RJ, Hartley WJ and Baker W. Laryngeal paralysis in Arabian foals associated with oral haloxon administration. Equine Vet J 1981; 13(3): 171–176.
12 12 Coppock RW, Mostrom MS, Khan AA and Stair EL. A review of