Proceedings of a Workshop on - The Havemeyer Foundation

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Havemeyer Foundation Monograph Series No. 11 NON-RECURRENT LARYNGEAL NEUROPATHY (RLN) CAUSES OF EQUINE LARYNGEAL PARALYSIS B. McGorum and P. M. Dixon Department <strong>of</strong> Veterinary Clinical Studies, Easter Bush Veterinary Centre, University <strong>of</strong> Edinburgh, Roslin, Midlothian EH25 9RG, UK Non-recurrent laryngeal neuropathy (non-RLN) accounts for the small proportion (6% Goulden and Anderson 1981; 11% Dixon et al. 2001) <strong>of</strong> horses with laryngeal paralysis in which a probable cause can be identified. Conversely, RLN cases have no such detectable underlying cause. Non-RLN laryngeal paralysis may be a sequel to localised injury to the vagus or recurrent laryngeal nerves at any site along their circuitous courses. Such injury may occur in disorders <strong>of</strong> the guttural pouch (mycosis, rupture <strong>of</strong> the rectus capitis ventralis muscles, temporohyoid fracture, trauma), pharynx (trauma, abscessation, neoplasia), neck (perivascular/perineural irritant injection reactions, trauma, iatrogenic nerve damage during oesophageal and thyroid surgery) or mediastinum (neoplasia, abscessation). Non- RLN paralysis may also be a manifestation <strong>of</strong> a generalised disorder, eg a polyneuropathy or myopathy. Bilateral laryngeal paralysis, which is considerably less common (2–6%) than unilateral paralysis, almost invariably results from generalised neuromuscular disorders. Liver disease is a common cause <strong>of</strong> bilateral laryngeal paralysis (Mayhew 1989; Pearson 1991; McGorum et al. 1999). McGorum et al. (1999) recorded bilateral laryngeal paralysis in 7 <strong>of</strong> 50 horses with primary hepatic disease, all <strong>of</strong> which had hepatic encephalopathy and hyperammonaemia. All cases presented with loud inspiratory stridor and many were referred for investigation <strong>of</strong> suspected primary upper respiratory tract obstruction. In all cases, endoscopy revealed total bilateral paralysis, with both arytenoids passively adducted to the midline during inspiration. Ponies were affected more <strong>of</strong>ten than horses, but this probably reflects an increased frequency <strong>of</strong> liver failure in ponies rather than increased susceptibility. The laryngeal paralysis was <strong>of</strong>ten temporary, worsening during exacerbations <strong>of</strong> encephalopathy and resolving with restoration <strong>of</strong> hepatic function. No gross or histopathological abnormalities were identified in the laryngeal muscles, the recurrent laryngeal nerve or other peripheral nerves <strong>of</strong> affected horses. The pathogenesis <strong>of</strong> this complication remains unclear. Most reported cases are in horses with liver failure and hepatic encephalopathy, but it is unknown whether it occurs with compensated liver disease. Similarly, while it is reported in horses with pyrrolizidine alkaloid induced liver disease (Pearson 1991; McGorum et al. 1999), the role <strong>of</strong> this substance, which may be neurotoxic (Cooper and Huxtable 1999), is unclear. As the laryngeal paralysis may be temporary, and no histo-pathological lesions have been identified, it may reflect neuromuscular dysfunction rather than pathology. Such dysfunction could occur by mechanisms akin to those that cause hepatic encephalopathy. Alternatively, it may represent a form <strong>of</strong> peripheral neuropathy, a common sequel to human hepatic disease. The pathogenesis <strong>of</strong> peripheral neuropathy in human liver disease patients is unknown, but may involve metabolic inhibition <strong>of</strong> axonal membrane function, metabolic damage to Schwann cells and/or disordered insulin metabolism akin to diabetic neuropathy. Interestingly, all 3 ponies with liver disease induced bilateral laryngeal paralysis that had postmortem examinations, also had pituitary adenomas, but no overt clinical hyperadrenocorticism (McGorum et al. 1999). While pituitary adenomas are relatively common in older ponies, and may not relate to the laryngeal dysfunction, increased production <strong>of</strong> pituitary derived peptides may contribute to the pathogenesis <strong>of</strong> this complication. However, Pearson (1991) made no 55
Equine Recurrent Laryngeal Neuropathy reference to pituitary adenomas in 2 ponies with liver failure and inspiratory dyspnoea, which were subjected to detailed post mortem examination. Rarely, horses may develop post operative laryngeal paralysis, sometimes complicated by secondary severe pulmonary oedema and/or haemorrhage (Abrahamsen et al. 1990; Dixon et al. 1993, 2001). These cases had variable recovery <strong>of</strong> laryngeal function, with one horse showing complete resolution within 24 h, while another had residual laryngeal dysfunction after one year. Post-operative laryngeal paralysis was most likely to have resulted from excessive head/neck extension, which could induce neural stretch injury or cause neural hypoxia via occlusion <strong>of</strong> the vasa nervorum. Alternatively, laryngeal paralysis may have resulted from compression <strong>of</strong> the recurrent laryngeal nerve against a rigid structure in the neck. Myopathy, persistent hypoxia and preexisting laryngeal dysfunction are additional factors that may contribute to development <strong>of</strong> this complication. Temporary post operative laryngeal paralysis has also been reported in a dog. A variety <strong>of</strong> toxic peripheral neuropathies may cause equine laryngeal paralysis including delayed organophosphate induced toxicity, Australian stringhalt, lead poisoning and plant poisoning. However in all such cases, laryngeal paralysis is clearly part <strong>of</strong> generalised disorder that affects multiple nerves, and so presents little diagnostic problem. Delayed organophosphate induced toxicity leads predominantly to degeneration <strong>of</strong> long axons in peripheral nerves and spinal cord, and results from covalent binding <strong>of</strong> organophosphates to ‘neuropathy target esterase’. Organophosphate induced laryngeal paralysis may be permanent (Rose et al. 1981; Duncan and Brook 1985). Ingestion <strong>of</strong> Lathyrus spp. and Cicer arietinum (chick pea) may cause equine laryngeal paralysis. The toxic principles include beta-N- oxalylamino- L-alanine, an excitatory amino acid which causes neuropathy with distal axonal degeneration. Feeding experiments with Lathyrus sativus (Indian vetch) indicated that, even with prolonged feeding, only a minority <strong>of</strong> horses were affected. Lead toxicosis primarily targets peripheral nerves, and approximately 13% <strong>of</strong> horses with lead toxicosis develop laryngeal dysfunction (Sojka et al. 1996), which may or may not recover with time. The pathogenesis <strong>of</strong> lead neurotoxicosis is multifactorial and includes inactivation <strong>of</strong> thiol and cysteine-containing enzymes, and Zn-, Cu-, Fedependent enzymes, resulting in neural oxidative stress, and toxicity <strong>of</strong> cell membranes resulting in increased membrane permeability. Hyperkalaemic periodic paresis, a generalised myasthenic disorder, commonly presents with episodic upper airway obstruction. While airway obstruction in this disorder is multi-factorial, laryngeal spasm or paralysis occurs in approximately half <strong>of</strong> affected horses. The severity and incidence <strong>of</strong> upper airway dysfunction may be reduced by medical treatment (Carr et al. 1996). REFERENCES Abrahamsen, E.J., Bonahon, T.C., Bednarski, R.M., Hubbell, J.A.E., and Muir, W.W. (1990) Bilateral arytenoid cartilage paralysis after inhalation anaesthesia in a horse. J. Am. vet. med. Ass. 197, 1363-1365. Carr, E.A., Spier, S.J., Kortz, G.D., and H<strong>of</strong>fman, E.P. (1996) Laryngeal and pharyngeal dysfunction in horses homozygous for hyperkalemic periodic paralysis. J. Am. vet. med. Ass. 209, 798-803. Cooper, R.A. and Huxtable, R.J. (1999) The relationship between reactivity <strong>of</strong> metabolites <strong>of</strong> pyrrolizidine alkaloids and extrahepatic toxicity. Proc. West Pharmacol. Soc. 42, 13-16. Dixon, P.M., Railton, D.I., and McGorum, B.C. (1993) Temporary bilateral laryngeal paralysis in a horse associated with general-anaesthesia and post anesthetic myositis. Vet. Rec. 132, 29-32. Dixon, P.M., McGorum, B.C., Railton, D.I., Hawe, C., Tremaine, W.H., Pickles, K., and McCann, J. (2001) Laryngeal paralysis: a study <strong>of</strong> 375 cases in a mixed-breed population <strong>of</strong> horses. Equine vet. J. 33, 452-458. Duncan, I.D. and Brook, D. (1985) Bilateral laryngeal paralysis in the horse. Equine vet. J. 17, 228-233. Goulden, B.E. and Anderson, L.J. (1981) Equine laryngeal hemiplegia part II: some clinical observations. N. Z. vet. J, 29, 194-198. Mayhew, I.G. (1989) Large Animal Neurology. Lea and Febiger, London. McGorum, B.C., Murphy, D., Love, S., and Milne, E.M. (1999) Clinicopathological features <strong>of</strong> equine primary hepatic disease: a review <strong>of</strong> 50 cases. Vet. Rec. 145, 134-139. Pearson, E.G. (1991) Liver failure attributable to pyrrolizidine alkaloid toxicity and associated with inspiratory dyspnea in ponies: Three cases (1982- 1988). J. Am. vet. med. Ass. 9, 1651-1654. Rose, R.J., Hartley, W.J., and Baker, W. (1981) Laryngeal paralysis in Arabian foals associated with oral haloxon administration. Equine vet. J. 13, 171- 176. Sojka, J.E., Hope, W., and Pearson, D. (1996) Lead toxicosis in 2 horses: similarity to equine degenerative lower motor neuron disease. JVIM 10, 420-423. 56
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