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Proceedings of a Workshop on

EQUINE RECURRENT LARYNGEALNEUROPATHY

7th – 10th September 2003Stratford-upon-Avon, UK

Editors: P. Dixon, E. Robinson and J. F. Wade

Havemeyer Foundation

Havemeyer Foundation Monograph Series No. 11

© 2004 by R & W Publications (Newmarket) LimitedSuites 3 & 4, 8 Kings Court, Willie Snaith Road, Newmarket, Suffolk CB8 7SG, UK

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First published 2004

ISSN 1472-3158

Published by R & W Publications (Newmarket) Limited

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CONTENTS

EDITORS’ FOREWORD ....................................................................................................................Page vi

SESSION 1: PATHOGENESIS AND PATHOLOGY

Development and innervation of the larynxC. Hahn ..............................................................................................................................................Page 3

Neurology of recurrent laryngeal neuropathy and the thoraco-laryngeal reflexI. G. Mayhew ......................................................................................................................................Page 5

Review of the pathological changes in equine recurrent laryngeal neuropathy C. Hahn ..............................................................................................................................................Page 9

Comparison of recurrent laryngeal neuropathy with other neuropathies in horsesI. G. Mayhew ....................................................................................................................................Page 12

Laryngeal paralysis in dogsP. Dixon and K. M. Pratschke .........................................................................................................Page 16

SESSION 2: ENDOSCOPIC GRADING SYSTEMS FOR LARYNGEAL PARALYSIS

4-grade system for equine laryngeal functionN. Ducharme ....................................................................................................................................Page 21

5-point grading system of laryngeal function in horses during quiet breathingJ. G. Lane .........................................................................................................................................Page 24

Endoscopic grading system for laryngeal paralysis - 6 grade systemP. M. Dixon ......................................................................................................................................Page 26

SESSION 3: PROGRESSION AND ENDOSCOPIC VARIATION

Long-term longitudinal study of laryngeal function in 187 foalsJ. G. Lane..........................................................................................................................................Page 31

Endoscopic observations on laryngeal symmetry and movements in young racing horsesB. H. Anderson, N. J. Kannegieter and B. E. Goulden ....................................................................Page 33

Variation in laryngeal function in mature horses and progressive cases of recurrent laryngeal neuropathy (RLN)P. M. Dixon ......................................................................................................................................Page 35

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Equine Recurrent Laryngeal Neuropathy

SESSION 4: DIAGNOSIS OF RLN AND NON-RLN URT DISORDERS

Sales: Problems in diagnosis of RLN – UK perspectiveD. Ellis, T. R. C. Greet and J. G. Lane.............................................................................................Page 39

Sales: Problems in diagnosis of RLN – USA perspectiveR. M. Embertson ..............................................................................................................................Page 42

Sales: Problems in the diagnosis of RLN – Australasian perspectiveB. H. Anderson .................................................................................................................................Page 45

Differences between resting and treadmill endoscopic findings in regard to RLNJ. G. Lane .........................................................................................................................................Page 47

Non-RLN upper respiratory tract disorders found in a survey of 3,497 Thoroughbred yearlingsJ. G. Lane .........................................................................................................................................Page 49

Non-RLN URT disorders identified during post sale endoscopic examination of 5,559 TB yearlings (1997–2002) in New ZealandB. H. Anderson .................................................................................................................................1

Non-recurrent laryngeal neuropathy (RLN) causes of equine laryngeal paralysisB. McGorum and P. M. Dixon .........................................................................................................Page 55

SESSION 5: TREATMENT OF EQUINE LARYNGEAL PARALYSIS

Decision making in practice for treatment of recurrent laryngeal neuropathyT. R. C. Greet ...................................................................................................................................Page 59

Laryngeal re-innervation in the horseI. Fulton ...........................................................................................................................................Page 60

Evaluation of RLN treatment efficiency – laryngoplastyP. M. Dixon .....................................................................................................................................Page 63

Improvements in laryngoplastyE. J. Parente .....................................................................................................................................Page 66

Ventriculectomy/cordectomyN. Ducharme ....................................................................................................................................Page 68

Ventriculo-cordectomy for treatment of recurrent laryngeal neuropathy: 75 cases in a mixedpopulation of horsesS. Barakzai and P. M. Dixon ............................................................................................................Page 71

SESSION 6: EVALUATION OF RLN TREATMENT EFFICACY

Treatment of recurrent laryngeal neuropathy: Physiological and performance evaluationF. J. Derksen ...................................................................................................................................Page 77

Treatment of recurrent laryngeal neuropathy: Evaluation by respiratory sound analysisF. J. Derksen ...................................................................................................................................Page 79

Spirometric and endoscopic assessment of surgical treatment in horses with laryngeal hemiplegiaM. A. Weishaupt, R. Vogt, A. Fürst and J. A. Auer ..........................................................................Page 81

Management of canine laryngeal paralysisJ. G. Lane ........................................................................................................................................Page 83

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SESSION 7: THE FUTURE

Is RLN inherited? Newer techniques to help investigate this questionM. Binns and J. Swinburne .............................................................................................................Page 89

Multicentre trials for efficacy of treatmentN. Ducharme ....................................................................................................................................Page 90

WORKSHOP SUMMARY...................................................................................................................Page 93

LIST OF PARTICIPANTS ...................................................................................................................Page 99

AUTHOR INDEX .............................................................................................................................Page 101

EDITORS’ FOREWORD

Equine laryngeal paralysis, most commonlyattributed to the syndrome of recurrentlaryngeal neuropathy (RLN), is long

recognised as the most important equine upperairway disease of horses. It can cause exerciseintolerance and stridor during fast work and inthe rare bilateral cases, and severe respiratorydistress, even in the resting horse. Despite is,there are still large gaps in our knowledge of itsaetiology, pathogenesis, methods of assessmentand the critical evaluation of its treatment.Between 20 and 30 years ago, there wassignificant research into the disease, but therehave been few substantive studies since then.

To promote further basic and appliedresearch into this disease it seemed worthwhileto review current knowledge about this disease.This was the main purpose of the presentworkshop and we invited eminent neurologists toreview knowledge of the aetiology of RLN and tocompare it with other equine peripheralneuropathies. It was also valuable to gain anoverview of some comparative aspects of RLNwith laryngeal paralysis in other species. Byobtaining consensus on our present knowledge,we went on to suggest areas for productive futureresearch. For example, are sub-clinicalneuropathies of other long peripheral nervespresent in horses with RLN?

As well as established research scientists, ourdelegates included practitioners who undertakeupper airway examination of young horses atsales. Outlining the difficulties and practicalproblems encountered by clinicians in Europe,America and Australia, they provided insightinto the incidence and possible progression ofthis disease. Currently, endoscopy is the goldstandard for assessing laryngeal dysfunction inthe horse. For clinicians to communicateeffectively with each other on RLN cases, avariety of grading systems are in use. One aim ofthe workshop was to reach a consensus as to

which endoscopic grading system should beadvocated universally. After lengthy discussion,we reached a consensus and time will tell if theinternational community accepts the suggestedsystem. Some studies have shown that, even withwell-defined endoscopic criteria and gradingsystems, inter-observer variation can occur in theendoscopic grading of laryngeal function. Theupcoming results of an interactive videopresentation conducted at the workshop maysupport or refute this. Even allowing forindividual variation in interpretation, it is wellestablished that the endoscopic findings in somehorses (and foals) may differ from time to time.Presentations addressed the progressive nature ofthe disease, especially in some older horses.

The advent of endoscopic examinationduring exercise on a high-speed treadmill hasrevealed that assessment of laryngealdysfunction in the resting horse does not alwaysreflect what occurs during high speed exercise.In addition, upper airway obstructions in horsesare not always due to laryngeal paralysis. Theresults of large surveys of both of these topicswere presented. Recently, it was found thathorses can suffer bilateral laryngeal paralysis inthe presence of liver disease and followinggeneral anaesthesia and comparison of thesecases with RLN may cast further light on theaetiopathogenesis of both disorders.

In the last 2 decades there have been manyclinical and physiological studies of the efficacyof treatments for equine laryngeal paralysis.These have addressed both the improvement ofairway function and elimination of abnormalsounds. The various treatments currently in usewere reviewed including the promisingneuromuscular pedicle graft. Comparisons weremade with the treatment of laryngeal paralysis inthe dog.

It was agreed that future areas for researchshould include investigations into the aetio-

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pathogenesis of this disorder; possibleinvestigations of the genetics of RLN that mayeventually eliminate the disease from thebreeding population; and multi-centre assessmentof the efficacy of RLN treatment, involving largenumbers of horses.

A primary aim of the workshop was to reacha consensus on the current state of knowledge.This was particularly challenging with regard torecommendations on grading systems. Theconsensus statements are presented as the finalsection of this monograph. We hope that they will1) provide a useful review for those starting towork on recurrent laryngeal neuropathy and 2)stimulate much discussion that will lead to newinvestigations into this important disease.

Finally, we thank the participants in theworkshop, the organisers and the HavemeyerFoundation. The participants travelled longdistances and many gave up valuable time fromtheir practices in order to debate with academics.We hope that both groups gained from theexperience. Rachel Pepper and Jan Wade did asuperb job of selecting the venue and organisingthe meeting. The Havemeyer Foundationcontinues its excellent work in fostering researchand education about important equine diseases.We are very grateful for their support.

Paddy Dixonand Ed Robinson

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HAVEMEYER SCIENTIFIC WORKSHOPS

1981 First International Workshop on Lymphocyte Alloantigens of the HorseOctober - New York City, USAOrganiser: Dr D. F. Antczak

1982 Second International Workshop on Lymphocyte Alloantigens of the HorseOctober - Cornell University, Ithaca, New York, USAOrganiser: Dr D. F. Antczak

1983 Third International Workshop on Lymphocyte Alloantigens of the HorseApril - New Bolton Center, University of Pennsylvania, USAOrganiser: Dr D. F. Antczak

1984 First International Symposium on Equine Embryo TransferOctober - Cornell University, Ithaca, New York, USAOrganisers: Drs D. F. Antczak and W. R. Allen

1985 Fourth International Workshop on Lymphocyte Alloantigens of the HorseOctober - University of Kentucky, USAOrganisers: Drs D. F. Antczak and E. Bailey

1986 Workshop on Corynebacterium equi Pneumonia of FoalsJuly - University of Guelph, CanadaOrganiser: Dr J. F. Prescott

1987 Fifth International Workshop on Lymphocyte Alloantigens of the HorseOctober - Louisiana State University, USAOrganisers: Drs D. F. Antczak and J. McClure

1989 Second International Symposium on Equine Embryo TransferFebruary - Banff, Alberta, CanadaOrganisers: Drs D. F. Antczak and W. R. Allen

1990 International Workshop on Equine SarcoidsApril - Interlaken, SwitzerlandOrganisers: Dr D. F. Antczak and Professor S. Lazary

1992 Workshop on Equine Neonatal MedicineJanuary - Naples, FloridaOrganisers: Drs D. F. Antczak and P. D. Rossdale

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Third International Symposium on Equine Embryo TransferFebruary - Buenos Aires, Argentina

Organisers: Drs D. F. Antczak, W. R. Allen, J. G. Oriol and R. Pashen

1995 Equine PerinatologyJuly - Cambridge, England

Organiser: Dr P. D. Rossdale

Second International Equine Leucocyte Antigen WorkshopJuly - Lake Tahoe, California, USA

Organisers: Drs D. F. Antczak, P. Lunn and M. Holmes

First International Workshop on Equine Gene MappingOctober - Lexington, Kentucky, USA

Organisers: Drs D. F. Antczak and E. Bailey

Erection and Ejaculation in the Human Male and Stallion: A Comparative StudyOctober - Mount Joy, Pennsylvania, USA

Organiser: Dr S. M. McDonnell

Bone Remodelling WorkshopOctober - Corcord, Massachusetts, USA

Organiser: Dr H. Seeherman

1997 Second International Workshop on Equine Gene MappingOctober - San Diego, California, USA


Maternal Recognition of Pregnancy in the MareJanuary - Dominican Republic

Organisers: Drs W. R. Allen and T. A. E. Stout

Uterine ClearanceMarch - Gainesville, Florida, USA

Organiser: Dr M. M. LeBlanc

Trophoblast DifferentiationSeptember - Edinburgh, Scotland

Organisers: Drs D. F. Antczak and F. Stewart

1998 Third International Genome WorkshopJanuary - San Diego, California, USA


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Third International Workshop on Perinatology: Genesis and Post Natal Consequences of Abnormal Intrauterine Developments: Comparative AspectsFebruary - Sydney, AustraliaOrganiser: Dr P. D. Rossdale

Horse Genomics and the Genetic Factors Affecting Race Horse Performance March - Banbury Center, Cold Spring Harbor, New York, USAOrganisers: Drs D. F. Antczak, E. Bailey and J. Witkowski

Allergic Diseases of the HorseApril - Lipica, SloveniaOrganisers: Drs D. F. Antczak, S. Lazary and E. Marti

Equine Placentitis WorkshopOctober - Lexington, Kentucky, USAOrganisers: Drs D. F. Antczak, W. R. Allen and W. Zent

Septicemia II WorkshopNovember - Boston, Massachusetts, USAOrganiser: Dr M. R. Paradis

1999 Equine Genome ProjectJanuary - San Diego, California, USAOrganisers: Drs D. F. Antczak and E. Bailey

Third International Equine Genome WorkshopJune - Uppsala, SwedenOrganisers: Drs D. F. Antczak, E. Bailey and K. Sandberg

Fourth International Meeting of OIE and WHO Experts on Control of Equine InfluenzaAugust - Miami, Florida, USAOrganiser: Dr J. Mumford

European Equine Gamete WorkshopSeptember - Lopuszna, PolandOrganisers: Drs W. R. Allen and M. Tischner

Fetomaternal Control of PregnancyNovember - Barbados, West IndiesOrganisers: Drs T. Stout and W. R. Allen

2000 Equine Genome ProjectJanuary - San Diego, California, USAOrganisers: Drs D. F. Antczak and E. Bailey

Uterine Infections in Mares and Women: A Comparative StudyMarch - Naples, Florida, USAOrganiser: Dr M. M. LeBlanc

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5th International Symposium on Equine Embryo TransferJuly - Saari, FinlandOrganiser: Dr T. Katila

2001 USDA International Plant & Animal Genome ConferenceJanuary - San Diego, California

Equine Immunology in 2001January - Santa Fe, New MexicoOrganiser: Dr D. P. Lunn

Asthma and Allergies II April - HungaryOrganisers: S. Lazary and E. Marti

From Elephants to Aids June - Port Douglas, AustraliaOrganiser: Professor W. R. Allen

International Equine Gene Mapping July - Brisbane, AustraliaOrganiser: K. Bell

Second Meeting of the European Gamete Group (EEGG) September - Loosdrecht, The NetherlandsOrganiser: Dr T. A. E. Stout

Foal Septicemia IIIOctober - Tufts University European Center, Talloires, FranceOrganiser: M. R. Paradis

Infectious Disease Programme for the Equine Industry and Veterinary PractitionersOctober - Marilyn duPont Scott Medical Center, Morvan Park, Virginia, USAOrganisers: Drs J. A. Mumford and F. Fregin

From Epididymis to EmbryoOctober - Fairmont Hotel, New Orleans, USAOrganiser: Dr L. H-A. Morris

2002 USDA International Plant & Animal Genome ConferenceJanuary - San Diego, California

Comparative Neonatology/PerinatologyJanuary - Palm Springs, CaliforniaOrganiser: P. Sibbons

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Stallion Behavior IVJune - Reykjavik, IcelandOrganisers: S. McDonell and D. Miller

Rhodococcus Equi IIJuly - Pullman, WashingtonOrganiser: J. Prescott

Equine Orthopaedic InfectionAugust - Dublin, IrelandOrganiser: E. Santschi

Inflammatory Airway Disease: Defining the SyndromeSeptember - Boston, USAOrganiser: Dr E. Robinson

2003 USDA International Plant and Animal Genome ConferenceJanuary - San Diego, California

Embryonic and Fetal NutritionMay - Ravello, ItalyOrganiser: S. Wilsher

Genomics and the Equine Immunity SystemJune - Ithaca, New YorkOrganiser: D. F. Antczak

Fifth International Gene Mapping WorkshopAugust - Kreuger Park, South AfricaOrganiser: E. Baily and E. Vandyke

Equine Recurrent Laryngeal NeuropathySeptember - Stratford-upon-Avon, UKOrganisers: P. Dixon and E. Robinson

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HAVEMEYER MONOGRAPH SERIES

The following are monographs available to date at a cost of £9.95 each.

Series No 1PROCEEDINGS OF THE FIRST MEETING OF THE EUROPEAN EQUINE GAMETE GROUP (EEGG)Editors: W. R. Allen and J. F. Wade5th–8th September 1999 Lopuszna, Poland

Series No 2PROCEEDINGS OF A WORKSHOP ON FETOMATERNAL CONTROL OF PREGNANCY

Editors: T. A. E. Stout and J. F. Wade14th–16th November 1999Barbados, West Indies

Series No 3PROCEEDINGS OF THE 5TH INTERNATIONAL SYMPOSIUM ON EQUINE EMBRYO TRANSFER

Editors: T. Katila and J. F. Wade6th–9th July 2000Saari, Finland

Series No 4PROCEEDINGS OF A WORKSHOP ON EQUINE IMMUNOLOGY IN 2001 Editors: D. P. Lunn and J. F. Wade24th–28th January 2001Santa Fe, New Mexico

Series No 5PROCEEDINGS OF THE SECOND MEETING OF THE EUROPEAN GAMETE GROUP (EEGG) Editors: T. A. E. Stout and J. F. Wade26th–29th September 2001Loosdrecht, The Netherlands

Series No 6PROCEEDINGS OF A WORKSHOP ENTITLED FROM EPIDIDYMIS TO EMBRYO

Editors: L. H-A. Morris and J. F. Wade18th–21st October 2001New Orleans, USA

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Series No 7FOURTH INTERNATIONAL MEETING OF OIE AND WHO EXPERTS ON CONTROL OF EQUINE

INFLUENZA

Editors: J. A. Mumford and J. F. Wade3rd–5th August 1999Crowne Plaza Hotel, Miami, Florida USA

Series No 8PROCEEDINGS OF A WORKSHOP ON COMPARATIVE NEONATOLOGY/PERINATOLOGY

Editors: Dr P. Sibbons and J. F. Wade13th – 15th March 2002Palm Springs, California, USA

Series No 9PROCEEDINGS OF A WORKSHOP ON INFLAMMATORY AIRWAY DISEASE: DEFINING THE

SYNDROME

Editors: A. Hoffman, N. E. Robinson and J. F. Wade30th September – 3rd October 2002Boston, USA

Series No 10PROCEEDINGS OF A WORKSHOP ON EMBRYONIC AND FETAL NUTRITION

Editors: S. Wilsher and J. F. Wade15th –18th May 2003Ravello, Italy

Series No 11PROCEEDINGS OF A WORKSHOP ON EQUINE RECURRENT LARYNGEAL NEUROPATHY

Editors: P. Dixon, E. Robinson and J. F. Wade7th –10th September 2003Stratford-upon-Avon, UK

If you wish to order copies, please contact R & W Publications Ltd, Suites 3 & 4, 8 Kings Court, WillieSnaith Road, Newmarket, Suffolk CB8 7SG, UK, Tel: +44 1638 667600, Fax: +44 1638 667229, e-mail: [email protected].


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SESSION I:

Pathogenesis andpathology

Chairman: Joe Mayhew


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DEVELOPMENT AND INNERVATION OF THE LARYNX

C. Hahn

Neuromuscular Diagnostic Laboratory, Royal (Dick) School of Veterinary Studies, The University ofEdinburgh, Easter Bush, Roslin, Midlothian EH25 9RG, UK

A brief look at the evolution and development ofthe larynx goes some way to explain the curiousanatomy of this organ. About 400 million yearsago, the lungfish evolved the ability to breathe airdirectly from the external environment, perhapsbecause its watery home was periodically subjectto drought (Ewings 1949). It developed a simplelarynx-like slit behind the gills that allowed airinto the swim-bladder when the creature wasexposed to the atmosphere and that kept water outwhen it was submerged (Fig 1). As thedescendants of the lungfish moved onto land, theswim-bladder evolved into a multi-compartmentorgan with a large surface area the sole function ofwhich was gas exchange. The larynx in themeantime developed adductor and abductormuscles and lateral cartilages (such as found in theaxolotl), then separate arytenoid and cricoidcartilages (newt), primitive thyroid cartilages(alligators and their feathered relatives, the birds)and finally the complex mammalian larynx. As thesurvival of equids once depended on running longdistances to escape predators, horses evolved alarynx that when fully abducted has an aperture

that is larger than the trachea itself (this in sharpcontrast to the human larynx, where the abductedlarynx allows for speech but is only half thediameter of the trachea).

An appreciation of the neuroanatomy oflaryngeal innervation is a pre-requisite tounderstanding the pathology of recurrent laryngealneuropathy. The main source of laryngealinnervation of the equine larynx is the ipsilateralrecurrent laryngeal nerve (rln). Motor neurons ofthe rln are based in the nucleus ambiguus in thecaudal brainstem. This nucleus was recentlylocalised in the horse (Hackett 2000) and wasfound to be a loosely organised column of cells inthe ventrolateral medulla oblongata (Fig 2). Asomatotopic distribution of adductor and abductormotor neurons was not apparent but neuronsinnervating the cricoarytenoideus lateralis musclewere observed throughout the nucleus, whereasneurons innervating the cricoarytenoideusdorsalis tended to be situated more rostrally.

Nucleus ambiguous axons loop around theparasympathetic nucleus of the vagus to emergefrom the brainstem as axons of the internal branchof cranial nerve (CN) XI. They only join the vagusnerve (CN X) on leaving the skull through thejugular foramen and tympano-occipital fissure.

Cranial movement of the head duringembryogenesis, and differential degeneration ofthe 6th aortic arch, resulted in extremely longnerves with the left and right nerves havingdifferent pathways. The left nerve loops aroundthe aorta while the right takes a shorter routearound the right subclavian artery. Including itsvagal course, the total length from neuronal cellbody to larynx of the left rln can be up to 250 cmin length, making it twice as long as other motornerves in the horse and 31 cm longer than the rightrln (Cole 1946).

Fig 1: Lungfish with modified swim bladder and dilatorand sphincter muscles (modified from Ewings, V. (1949).The Comparative Anatomy and Physiology of theLarynx. William Heinemann, Medical Books, London).

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The normal rln nerve consists of medium sizedmyelinated fibres with only scattered, smallerdiameter fibres present. Myelinated axons in therln segregate as fascicles within the vagus nerve.However, after these fascicles separate from thevagus as the rln, the axons that are targeted toinnervate a particular intrinsic laryngeal muscleare not discreetly clustered within the rln at itsorigin in the thorax, but instead are mixed amongthe fascicles throughout its length.

Although the rln is thought of classically as amotor nerve, primary afferent (‘dorsal rootganglia’) rln neurons have been demonstrated inthe proximal and distal vagal ganglia. The distalvagal ganglion is poorly described in the horse buthas recently been identified to consisthistologically of scattered neurons in the vagusnerve at its bifurcation with the cranial laryngealnerve (I.G. Mayhew, personal communication, Fig3). Involvement of sensory axons in horses withrecurrent laryngeal neuropathy has not beenestablished. Each nerve then courses cranially toprovide motor innervation to the paired intrinsic

laryngeal muscles, with the exception of thecricothyroideus muscles. These muscles have adifferent embryologic origin and are innervated bynucleus ambiguus neurons whose axons join anexternal branch of the paired cranial laryngeal orvagus nerves (de Lahunta 1983).

It is likely that the complexity and length ofthis pathway underlies the pathology of recurrentlaryngeal neuropathy

REFERENCES

Cole, C.R. (1946) Changes in the equine larynxassociated with laryngeal hemiplegia. Am. J. vet.Res. 7, 69-77.

de Lahunta, A. (1983) Veterinary Neuroanatomy andClinical Neurology. Philadelphia, W.B. SaundersCompany.

Ewings, V. (1949) The Comparative Anatomy andPhysiology of the Larynx. London, WilliamHeinemann, Medical Books.

Hackett, S. (2000) The Equine Nucleus Ambiguus:Myotopic and Neurotopic Representations of Motorand Sensory Components of the RecurrentLaryngeal Nerve. Ithaca, Cornell University.

Fig 3: Scattered neuronal cell bodies of the distal vagalganglion in the proximal vagus nerve.

Fig 2: The recurrent laryngeal nerve is supplied byaxons originating in the caudal nucleus ambiguus.(Modified from de Lahunta, A. (1983) VeterinaryNeuroanatomy and Clinical Neurology, 2nd edn.Saunders, Philadelphia, pp 105).

Glosopharyngeal(CN IX)

Vagus

Internal branchAccessory nerve

(CN XI)

Vagus n.

Recurrent laryngeal nerveCN XI

Cranial laryngeal nerve

CN IX

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NEUROLOGY OF RECURRENT LARYNGEALNEUROPATHY AND THE THORACO-LARYNGEALREFLEX

I. G. Mayhew


The neurological evaluation of a horse suspected ofhaving abnormal laryngeal function should includea complete neurological examination as left sidedrecurrent laryngeal neuropathy (RLN) may occurin conjunction with other neurological signs. Theserarely relate to brain or spinal cord lesions; moreoften to peripheral nerve involvement especiallywithin and around the guttural pouch, neck andcranial thorax. Other signs of vagosympathetictrunk involvement, especially swallowingdifficulties, Horner’s syndrome and sweating overvariable areas of the head and neck, canaccompany such signs of RLN.

The major neurological diagnostic aids thatmay be utilised in evaluating cases of RLN includethe electromyogram (EMG), nerve conductionvelocity (NCV) testing and evaluating theendoscopic and palpable thoraco-laryngeal reflex(TLR) and the electrolaryngeogram (ELG).

ELECTROMYOGRAPHY

In one study (Moore et al. 1988), EMG of thedorsal cricoarytenoidius dorsalis muscle appearedto have very high sensitivity for the diagnosis ofRLN but almost certainly would have a lowspecificity. EMG would be extremely useful inevaluation of sudden onset of signs consistent withRLN. This is where there is total paralysis of theleft (or right) side but no detectable atrophy.Immediate EMG evaluation may reveal very littleabnormality, if indeed such signs were due to anacquired lesion, such as a perivascular injection inthe cervical region. Monitoring the time course of subsequent atrophy and progression ofelectromyographic denervation abnormalitiescould help pinpoint more accurately the exact timeof onset of such an acquired disorder.

NERVE CONDUCTION VELOCITY

Steiss et al. (1989) determined the characteristicsof evoked compound muscle action potentials inthe intrinsic laryngeal muscles of control poniesand small horses. They stimulated the proximalvagus and the distal recurrent laryngeal nerve in thecranial cervical region. The mean latencies (ms),from the proximal stimulation site on the vagusnerve and the distal stimulation site on therecurrent laryngeal nerve, to the larynx for poniesand horses are shown in Table 1.

The latencies on the left side were 22% and26% longer than the right side in ponies andhorses, respectively. There was a positivecorrelation between latency and body length inponies, but not in horses. True nerve conductionvelocities are difficult to determine in such studiesbecause of the difficulty and error in measurementof the length of neural pathways being stimulated.NCV measurement is invasive and does requireheavy sedation. However, determining thesegmental latency component values could lendfurther evidence for the neuropathy present inidiopathic RLN being a distal neuropathy.

TABLE 1: Control values for vagal nerve(proximal) and recurrent laryngeal nerve (distal)conduction latencies in ponies and horses(Steiss et al. 1989)

Latency ms; mean (sd)Proximal Distal

PoniesLeft 21.7 (3.1) 3.7 (0.9)Right 17.8 (1.9) 4.0 (0.8)

HorsesLeft 29.4 (3.1) 6.8 (1.8)Right 23.4 (2.4) 5.7 (1.3)

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THORACO-LARYNGEAL REFLEX

Dr Bob Cook in the 1970s serendipitously cameup with observations that led to the publication(Greet et al. 1980) of the so called ‘slap test’. Thisperhaps more correctly is termed the thoraco-laryngeal reflex (TLR).

The pathway for this reflex is through sensoryreceptors on the skin or deeper tissues of the dorsalcranial thorax, through dorsal nerve roots to thespinal cord with an ascending pathway in thethoracic and cervical spinal cord. This pathwayappears to cross to the contralateral side at least bythe time it reaches the brachial intumescence andpossibly immediately upon entry into the spinal cordthrough dorsal nerve roots. The pathway is probablyin the lateral funiculus, but may be in the dorsalfuniculus of the spinal cord, ascending to reach thedorsal nucleus of the vagus, hence subsequently thecontralateral vagal nerve. The efferent pathwayaround major arteries in the cranial thorax is longeron the left side than the right side, as the recurrentlaryngeal nerve leaves the vagus and ascends theneck to innervate intrinsic muscles of the larynx. Inthe first report (Greet et al. 1980), 30 ataxic and 64non-ataxic horses were evaluated endoscopically forthe presence or absence of a TLR. Because 10 of the41 non-ataxic horses that had RLN demonstrated anormal TLR it was concluded that this test was veryunreliable for diagnosis of RLN. However, the datafor the horses with neurological disease indicated avery good sensitivity and an excellent specificity fordiagnosis of cervical spinal cord disease.

Subsequently, Newton-Clarke et al. (1994a)investigated the clinical value of theendoscopically-determined TLR in the diagnosis ofspinal cord and brainstem disease. This grouplooked at 15 ataxic horses (12 of whom weredetermined to have lesions to explain the signs atpost-mortem examination) and 13 control horses.They determined sensitivities in the range of

0.50–0.60 and specificities in the range of0.70–0.75. On the basis of a 50% potentialprevalence of disease this would have raised thepositive predictive value from 0.50 to 0.70 and thenegative predictive value from 0.50 to 0.64. Theirinterpretation was that this was a very poor test fordiagnosing particularly cervical spinal cord disease.

The same group studied the value of theendoscopically-determined TLR in RLN diagnosis.They evaluated 15 horses with no clinical signs ofRLN and subsequently took samples of thecrycoarytenoideus lateralis muscle forhistopathologic examination. Moderate to severeneurogenic muscle atrophy and re-innervation wasfound in 5 horses with normal TLRs. Theremaining horses also had degrees of adductormyopathy. The group determined, as did Greet(1994), that the test was useless for RLN diagnosis.It is possible that 2 of the reasons for such falsepositive results are that adductor muscle pathologyprecedes abductor muscle atrophy (Duncan andBaker 1987; Archer et al. 1989) and that goodevidence of re-innervation was found in most of thehorses by Newton-Clarke et al. (1994b).

ELECTROLARYNGEOGRAPHY

The original report by Cook and Talhammer(1991) on the electrolaryngeogram (ELR)suggested that most horses had evidence of RLN,at least on the left side. This was based on theassumption that a single pony with the samelatencies on the left and right side should beregarded as normal; this has been refuted by otherstudies (Steiss et al. 1989; Hawe et al. 2001; R.A.Curtis, unpublished data). Cook and Thalhammer(1991) also determined approximate nerveconduction velocities based on estimates of thereflex pathway length in horses of various sizes.The pony that had identical latencies on each sidehad a calculated nerve conduction velocity of 63.5m/s and this figure was used to calculate the

TABLE 2: ELG latency values for control ponies and Clydesdale horses unaffected (Grades 0–1) andaffected (Grades 2–4) with RLN (Hawe et al. 2001)

Animals Grade of RLN* n ELG latency, ms. Median (range)Left Right

Ponies 0–1 1050 (34–54) 42 (32–47)Clydesdales 0–1 7 69 (65–73) 57 (54–58)

“ 2 12 69 (60–76) 57 (52–64)“ 3–4 6 70 (65–78) 56 (53–66)

*Based on a 0–5 grading system

7


normal ranges for reflex arks varying between 250and 400 cm in length.

Hawe et al. (2001) undertook a study of 35Clydesdales and 10 ponies in which they gradedthe degree of RLN by the classical grading systemusing endoscopy at rest and post exercise, andcompared endoscopic findings with results oflaryngeal palpation for muscle mass andperformance of the TLR recorded by palpation,endoscopy and the ELG. They found that palpationfor muscle mass correlated less well with degree ofRLN than the endoscopic TLR. However, thepalpable response to the TLR did correlate with theendoscopic grade of RLN, as found by Lane(1993). It is possible that the endoscopic procedureitself or the application of a twitch may interferewith the endoscopic observation of the TLR.

Hawe et al. (2001) also determined the latencyfor the ELG in ponies to be a median of 50 ms onthe left and 42 ms on the right. In Clydesdalehorses these figures varied depending on the gradeof RLN determined and are shown in Table 2. Ineach category, the left and right latencies weresignificantly different. These workers corrected thelatency values for size of horse using variousparameters. Although it was determined that theabsolute latency values did correlate with theseverity of RLN the latency values corrected forbody size measurements did not correlate with theseverity of RLN. They concluded that the ELG isnot a simple and accurate method for the objectivediagnosis and grading of RLN as claimed by Cookand Talhammer (1991) and Cook (1995).

R.A. Curtis (unpublished data) used postprocessing of digitised ELG latency and velocityestimates to determine that there was a significantassociation of the grade of RLN (Grades 1 and 2)with right peak latency. However, they found noassociation of RLN (Grades 1 and 2) with velocityestimates. This is still being prepared forpublication and it may well show statistical data toendorse the use of digitised and post processedELG recordings to categorise groups of horses ashaving different grades of RLN. However, in anindividual animal it may be very difficult todetermine statistically whether it is affected or not,let alone what grade it may have.

THE FUTURE

Regarding ELGs, it has been determined (I.G.Mayhew unpublished data) that a brain stemresponse can be detected as a short latencyresponse to the ‘slap test’ and that there also canbe an early ELG wave form of approximately thesame latency (Fig 1). It is suggested that this isactivity in laryngeal muscles via a shortened ELGresponse involving the cranial laryngeal nerve.The utility of this in determining the presence oflesions at various sites is still to be determined.

Additionally, it has also been observed (I.G.Mayhew unpublished data) that in ponies that aresedated with their head held in a normal posture theELG can be easily recorded. If the head is thenslowly lowered to an intermediate position and thento a ‘nose-near-the-ground’ position the latency of

Fig 1: An early brainstem resonse is recorded to a slaptest in the top trace. Also an early ELG waveform,possibly indicating electrical activity in the cricothyroidmuscle via the cranial laryngeal nerve is recorded in thelower trace (Note: sacle on x- axis is 20 ms).

Fig 2: ELG recorded in a pony heavily sedated withdetomidine with the head held in a normal position(lowest trace), partially lowered positions (middle 2traces) and nose-near-the-ground position (top trace).

8


the recorded ELG is prolonged (Fig 2). This mayreflect an effect on the neural pathway of the TLR,but it is extremely difficult to make sure that theneedle electrodes are indeed in exactly the sameplace as the head and neck are moved in relation tolaryngeal muscle action potential generators. Doesthis potentially indicate a mechanical component tothe pathogeneses of RLN?

Pirie et al. 2003 (personal communication)attempted to determine the influence of head andneck position on the degree of contralateralarytenoid adduction occurring during a TLR. The4 point grading system given by 5 observers wastransformed to a 0–90 ‘grade of movement’ for each head and neck position as shown inFigure 3.

There was a significant difference for the headand neck extended position (3 and 5) whencompared with the neutral position, however therewas considerable noise in the data such thatdefinitive conclusions could not be made.

Nollet et al. (2002) have data to indicate thatthe magnetic motor evoked potential in limbmuscles is useful in determining the presence andseverity of cervical spinal cord disease. It is likelythat there is a laryngeal response to corticalmagnetic stimulation and this methodology maybe applicable to service further studies of the TLRand RLN in general.

ACKNOWLEDGEMENTS

We wish to thank R.A Curtis, C.N Hahn, D.LEvans, T. Williams and L. Begg for supplying datain preparation; and R.S. Pirie for permission topresent the data in Figure 3.

REFERENCES

Archer, R.M., Lindsay, W.A. and Duncan, I.D. (1989)Equine laryngeal hemiplegia: an endoscopic surveyof 400 draft horses. Vet. Surg. 18, 62-63.

Cook, W.R. (1995) Selecting a stakes-class horse: theELG solution. Irish vet. J. 48, 240-244.

Cook, W.R. and Thalhammer, J.G. (1991)Electrodiagnostic test for the objective grading ofrecurrent laryngeal neuropathy in the horse. Proc.Am. Ass. equine Pract. 34, 275-296.

Duncan, I.D. and Baker, G.J. (1987) Experimental crushof the equine recurrent laryngeal nerve: a study ofnormal and aberrant re-innervation. Am. J. vet. Res.48, 431-438.

Greet, T.R.C. (1994) Laryngeal hemiplegia: a slap in theface for the ‘slap test’? Equine vet. J. 26, 345.

Greet, T.R.C., Jeffcott, L.B., Whitwell, K.E. and Cook,W.R. (1980) The slap test for laryngeal adductorfunction in horses with suspected cervical spinalcord damage. Equine vet. J. 12, 127-131.

Hawe, C., Dixon, P.M. and Mayhew, I.G. (2001) A studyof an electrodiagnostic technique for the evaluationof equine recurrent laryngeal neuropathy. Equinevet. J. 33, 459-465.

Lane, J.G. (1993) Recurrent laryngeal neuropathy. Proc.15th Bain-Fallon memorial Lect., Aust. equine vet.Ass. pp 173-192.

Moore, M.P., Andrews, F., Reed, S.M. and Grant B.D.(1988) Electromyographic evaluation of horses withlaryngeal hemiplegia. J. Equine vet. Sci. 8, 424-427.

Newton-Clarke, M.J., Divers, T.J., deLahunta, A. andMohammed, H.O. (1994a) Evaluation of thethoraco-laryngeal reflex (‘slap-test’) as an aid to thediagnosis of cervical spinal cord and brainstemdisease in horses. Equine vet. J. 26, 358-361.

Newton-Clarke, M.J., Divers, T.J.,Valentine, B.A. (1994b) Evaluation of the thoraco-laryngealreflex (‘slap-test’) as an indicator of laryngealadductor myopathy in the horse. Equine vet. J. 26,355-357.

Nollet, H., Deprez, P., Van Ham, L., Verschooten, F. andVanderstraeten, G. (2002) The use of magneticmotor evoked potentials in horses with cervicalspinal cord disease. Equine vet. J. 34, 156-163.

Steiss, J.E., Marshall, A.E. and Humburg, J.M. (1989)Electromyographic evaluation of conduction time ofthe recurrent laryngeal nerve: findings in clinicallynormal horses and ponies. Equine vet. J. 21, 218-220.

Head/neck position

Gra

de o

f m

ovem

ent

1009080

706050403020

100

1 2 3 4 5 6

Fig 3: Influence of head and neck position on the degreeof contralateral arytenoid adduction occurring during aTLR (Pirie et al. 2003, personal communication). Headand neck positions (time between TLR testing) were: 1)normal resting position – unsedated (5 min); 2) normalresting position, sedated (5 min); 3) head and neckextended, horizontal (8 min); 4) head and neck extendedtowards ground level (5 min); 5) head and neckextended, horizontal, as 3 (5 min); and 6) normal restingposition, sedated.

P<0.05

P<0.05

9


REVIEW OF THE PATHOLOGICAL CHANGES INEQUINE RECURRENT LARYNGEAL NEUROPATHY

C. Hahn


PATHOLOGICAL CHANGES

The lesions associated with recurrent laryngealneuropathy (RLN) have been well characterisedusing light and electron microscopy (Cole 1946;Duncan and Griffiths 1974; Duncan et al. 1978;Cahill and Goulden 1986a, b, c, d, e; Duncan et al.1991).

The primary lesions have been demonstratedin nerves, and have been found to be greatest in thedistal portions of the left and right recurrentlaryngeal nerves. Abnormalities have also beennoted proximal and distal to the aorta and in thevagus nerve. Changes noted in the right RLN areless severe than those found in the left. Thepathology is characterised by a proximal to distaldecrease in large myelinated fibres. However, thesame trend, including the presence of Renautbodies commonly reported in RLN cases, has beenshown in ‘normal’ horses (Lopez-Plana et al.1993). It is unknown if sensory fibres in therecurrent laryngeal nerves are also affected andvagal sensory ganglia should be examined forneuronal chromatolysis.

The primary lesion may be axonal in nature, asindicated by collapsed myelin sheaths without anaxis cylinder, increased myelin sheath thickness(potentially due to axonal atrophy), regeneratingSchwann cell membrane clusters and paranodaland internodal accumulations of axonal debris andorganelles. The latter may be an indication that adefect in the axonal transport systems results inthe eventual distal axonal degeneration. Inaddition there is evidence of extensive myelindamage. Büngner’s bands, representing Schwanncell membranes, and onion bulbs made up ofproliferating Schwann cells, are commonly found,as are myelin digestion chambers containing

central axon fragments. Teased fibre preparationsshow a marked variation in internodal length anddiameter indicating chronic demyelination andattempted remyelination.

Evidence of central changes have been sought,however neither Cahill and Goulden (1986) norHackett and Cummings (personal communication)were able to identify lesions in the lower motorneuron cell bodies of the recurrent laryngeal nervesin the nucleus ambiguus of affected horses.Chromatolysis of the lower motor neuron may beexpected secondary to the axonal damage, thishowever is influenced by the proximity of the lesion(Dyck and Thomas 1993). Likewise chromatolysisor neuronal loss in the nucleus ambiguus would beanticipated if the axonal changes are due to somal(cell body) pathology as has been described inBouvier des Flandres (van Haagen 1980) and theSiberian husky dogs (O’Brien and Hendriks 1986).Unfortunately, there has been no systematic work inthe horse evaluating the peripheral or centralpathological changes which accompany damage tolong axons. Ultrastructural examination of nucleusambiguus neurons has been attempted but iscomplicated greatly by the difficulty of identifyingthe boundaries of the nucleus in the medullaoblongata. It was believed that there was adifference in the number of neurons in horses withRLN compared to normal horses, but smallnumbers of animals examined did not allow astatistical comparison (Hackett personalcommunication). There have been no histochemicaltechniques applied to identify somal changessecondary to the hypothesised transport disorder.

Lesions in the laryngeal muscles innervated bythe recurrent laryngeal nerves are characteristic ofneurogenic disease. Denervation of the adductormuscles precede abductor involvement and typicalchanges include scattered angular fibres and

10


groups of atrophied fibres adjacent tohypertrophied fibres with central nuclei (Duncanand Griffiths 1974; Duncan et al. 1991). The firstmuscle groups affected appear to be the adductormuscles and within the adductor group thecricoarytenoideus lateralis is among the earliestand most severely affected muscles (Lopez Planaet al. 1993). The chronic, repetitive nature of thedisease is further exemplified by the presence ofmuscle fibre type grouping, as muscle fibre type iscontrolled by the innervating neuron.

Together, these pathological changes havebeen classified as a distal axonopathy, with thegreater pathology in the left recurrent laryngealnerve being explained by its greater length. Onehypothetical cause of distal axonopathy is a defectin the neuronal soma, as the axon depends on thecell body for metabolic support and sustaining ortrophic influences. Indeed, many of the peripheralnerve lesions that are typical in equine motorneuron disease, a disease primarily affecting thecell body, are also observed in RLN includingaxonal atrophy, proliferated Schwann cell cords(Büngner’s bands), loss of myelinated fibres andan increase in endoneurial collagen.

HYPOTHETICAL AETIOLOGIES

Despite years of work we appear to be no closer toclarifying the aetiology of this common equinedisease. Hypotheses range from mechanicalcauses such as tension and stretch to the recurrentlaryngeal nerve and its blood supply during neckmovement, growth, or the caudal shift of the heartduring embryonic development, to environmentalfactors, including toxins (reviewed by Cahill andGoulden 1987). The latter have been viewed asunlikely causes of RLN as the neuropathologicalchanges are limited to the recurrent laryngealnerves.

Myelinopathies and the inherited andmetabolic primary axonopathies affect multiplenerves and in other species would be expressed aspart of a polyneuropathy and be progressive.Comparable pathology has indeed been noted infoals (Duncan 1992; Harrison et al. 1992) andclinical signs of left-sided hemiplegia have beendemonstrated to be clinically progressive (Dixonet al. 2002). Interestingly, however, there havebeen no reports of left hemiplegic horsesprogressing to develop right-sided clinical signs(Dixon, personal communication). On the otherhand, it is clear that horses affected with RLN do

not show classical clinical signs ofpolyneuropathy such as megaoesophagus,tetraparesis and muscle atrophy. Notwithstanding,involvement of other long peripheral nerves(common, deep and superficial peroneal and tibialnerves) has been reported by some workers (Cahilland Goulden 1986a; Kannegieter 1989), but wasnot found by Duncan et al. 1978). Similarly,neurogenic muscle changes have been reported toexist in the extensor digitorum longus (Cahill andGoulden 1986d) in 3 out of 4 horses sufferingfrom RLN. The above observations however havebeen isolated, uncontrolled and have not taken intoaccount that age-related pathological changes canbe demonstrated in distal limb nerves of horses(Wheeler and Plummer 1989). A detailed study ofthe peripheral nerves in RLN affected and controlanimals has not been undertaken.

It should be remembered that axonaldegeneration, characterised by distal degenerationthat spreads proximally (‘dying back’), is the mostcommon pathology seen in peripheral nervediseases caused by a wide variety of toxic,metabolic, and infectious insults. Some of theseprocesses affect the cell body, and it may be thatthe axonal dying back process may be initiated inorder to conserve energy. How a cell can eliminatepart of itself while leaving the rest intact isunknown. Localised axonal degeneration thatresembles dying back can also occur in cell cultureif the distal portion of the axon is deprived ofnerve growth factor, and a similar process may beinvolved in disease states. Other forms of axonaldegeneration that seem distinct from typical dyingback occur in various human neurodegenerativediseases such as Alzheimer’s, Parkinson’s andHuntington’s diseases.

Pathological changes of the recurrentlaryngeal nerve in RLN has been described ingreat detail using light and electron microscopybut the tools of the burgeoning science ofmolecular pathology have not been utilised. Adetailed examination of changes in generegulation and cytokine expression will have to beapplied if further details of the pathogenesis are tobe uncovered.

REFERENCES

Cahill, J.I. and Goulden, B.E. (1986a) Equine laryngealhemiplegia. I. A light microscopic study ofperipheral nerves. N. Z. vet. J. 34, 161-169.

Cahill, J.I. and Goulden, B.E. (1986b) Equine laryngeal

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hemiplegia. II. An electron microscopic study ofperipheral nerve. N. Z. vet. J. 34, 170-175.

Cahill, J.I. and Goulden, B.E. (1986c) Equine laryngealhemiplegia. III. A teased fibre study of peripheralnerves. N. Z. vet. J. 34, 181-185.

Cahill, J.I. and Goulden, B.E. (1986d) Equine laryngealhemiplegia. IV. Muscle pathology. N. Z. vet. J. 34,186-190.

Cahill, J.I. and Goulden, B.E. (1986e) Equine laryngealhemiplegia. V. Central nervous system pathology. N.Z. vet. J. 34, 191-193.

Cahill, J.I. and Goulden, B.E. (1987) The pathogenesisof equine laryngeal hemiplegia-a review. N. Z. vet. J.35, 82-90.

Cole, C.R. (1946) Changes in the equine larynxassociated with laryngeal hemiplegia. Am. J. vet.Res. 7, 69-77.

Dixon, P.M., B.C. McGorum, Railton, D.I., Hawe, C.,Tremaine, W.H., Pickles, K. and McCann, J. (2002)Clinical and endoscopic evidence of progression in152 cases of equine recurrent laryngeal neuropathy(RLN). Equine vet. J. 34, 29-34.

Duncan, I.D. (1992) Determination of the early age ofonset of equine recurrent laryngeal neuropathy. 2.Nerve pathology. Acta Neuropathol (Berl) 84, 316-321.

Duncan, I.D., J. Amundson, Cuddon, P.A., Sufit, R.,Jackson, K.F. and Lindsay, W.A. (1991) Preferentialdenervation of the adductor muscles of the equinelarynx. I: muscle pathology. Equine vet. J. 23, 94-98.

Duncan, I.D. and I.R. Griffiths (1974) Pathologicalchanges in equine laryngeal muscles and nerves.Proc. Am. Ass. equine Pract, 19.

Duncan, I.D., I.R. Griffiths, and Madrid, R.E. (1978) Alight and electron microscopic study of theneuropathy of equine idiopathic laryngealhemiplegia. Neuropathol. Appl. Neurobiol. 4, 483-501.

Duncan, I.D., P. Reifenrath, Jackson, K. F. and Clayton,M. (1991) Preferential denervation of the adductormuscles of the equine larynx. II: nerve pathology.Equine vet. J. 23, 99-103.

Dyck, P.J. and P.K. Thomas (1993) PeripheralNeuropathy. Philadelphia, W.B. Saunders Co.

Harrison, G.D., I.D. Duncan and Clayton, M.K. (1992)Determination of the early age of onset of equinerecurrent laryngeal neuropathy. 1. Musclepathology. Acta Neuropathol. (Berl) 84, 307-315.

Kannegieter, N. (1989) A Study of Distal HindlimbMuscles and Nerves in Normal and LaryngealHemiplegic Horses. PhD Thesis, Massey University,New Zealand.

Lopez-Plana, C., J.Y. Sautet, Pons, J. and Navarro, G.(1993) Morphometric study of the recurrentlaryngeal nerve in young ‘normal’ horses. Res. vet.Sci. 55, 333-337.

O'Brien, J.A. and J. Hendriks (1986) Inherited laryngealparalysis. Analysis in the husky cross. Vet. Q 8, 301-302.

van Haagen, A.J. (1980) Investigations on thePathogenesis of Hereditary Laryngeal Paralysis inthe Bouvier. Doctoral Thesis, University of Utrecht,The Netherlands.

Wheeler, S.J. and J.M. Plummer (1989) Age-relatedchanges in the fibre composition of equineperipheral nerve. J. Neurol. Sci. 90, 53-66.

12


COMPARISON OF RECURRENT LARYNGEALNEUROPATHY WITH OTHER NEUROPATHIES INHORSES

I. G. Mayhew


INTRODUCTION

This paper gives an overview of the known andsuspected neuropathies in horses, apart fromrecurrent laryngeal neuropathy (RLN). It will notdiscuss the primary traumatic neuropathies,polyneuritis equi or the neuronopathy known asequine motor neuron disease.

STRINGHALT

Stringhalt, also known as springhalt andHahnentritt, is an disease recorded from ancienttimes that is characterised by a sudden, apparentlyinvoluntary, exaggerated flexion of one or bothhind limbs during attempted movement. The hindlimb motion may be as mild as a slightly excessiveflexion to violent movements during which thefetlock or toe will contact the abdomen, thorax andoccasionally the elbow with attempted stepsleading to a peculiar ‘bunny hopping’ andplunging type gait. Ultimately marked atrophy ofmuscles of the hind limb(s), particularly distally,will occur.

Three forms of stringhalt are recognised(Huntington et al. 1989). Firstly, the sporadic formusually affects one limb and occurs worldwide.The onset can be preceded by a history of, orevidence of, trauma to the dorsal tarsal region orthe dorsoproximal metatarsus. The second formthat usually occurs as outbreaks is referred to asAustralian stringhalt, but is also seen in NewZealand (Cahill et al. 1985), United States (Gay etal. 1993), Chile (Araya et al. 1998) and Japan(Takahashi et al. 2002). Usually there issymmetrical or often asymmetrical involvement ofthe pelvic limbs, with prominent distal muscleatrophy in severe cases. This form has been

associated with exposure to several plants notablyHypochoeris radicata, Taraxicom officinal andMalva parviflora (Huntington et al. 1889, 1991;Seddon and Belschner 1926; Cahill and Goulden1985; Gay et al. 1993). These are related speciesof flat weed, Taraxicom officinal being thecommon dandelion. Finally, there is an atypicalform of stringhalt where the thoracic limbs arealso affected. There is knuckling of the forelimbfetlocks with prominent extension of moreproximal joints and atrophy of the distalmusculature, in association with prominentstringhalt in both hind limbs. It is possible thatatypical stringhalt is simply a more severe form ofAustralian stringhalt. Experimental sweet-peapoisoning (lathrysim) causes such a syndrome.Huntington et al. (1989) have graded the clinicalseverity of stringhalt from 1 to 5.

Several authors have treated sporadicstringhalt by lateral digital extensormyotenectomy, with allegedly good results.However, Crabbel et al. (1994) retrospectivelystudied 10 sporadic stringhalt cases where traumato the dorsoproximal metatarsal region had beenconfirmed. Four were conservatively treated withcontrolled exercise and turnout and 6 were treatedwith extensive myotenectomy. Although thenumbers were very small, there appeared to be noreal difference in the follow up outcomes of the 2groups.

Mephensein (Dixon and Stewart 1969),baclofen (Cahill and Goulden 1992) andparticularly phenytoin (Huntington et al. 1991)appear to be quite useful in the symptomatictreatment of Australian stringhalt cases. Whetherphenytoin is useful in the sporadic form has still tobe determined. However, at doses of 7–15 mg/kg,sid to tid, several authors (Huntington et al. 1991;Wijnberg et al. 2000; Takahashi et al. 2002) have

13


indicated substantial clinical improvements withthe drug. Notably, when the drug has beendiscontinued for a few days, signs have returned tothen abate with further treatments. In one study(Wijnberg et al. 2000), determination ofelectromyography (EMG) characteristics of‘irritability’ also indicated an improvement in themuscle function within the lateral digital extensormuscles following phenytoin treatment. AbnormalEMG patterns were also seen in stringhalt horses(Takahashi et al. 2002) but were not detectedfollowing clinical improvement with phenytointreatment.

Huntington et al. (1989) determined nerveconduction velocities (NCVs) in the peronealnerve of 4 horses affected with Australianstringhalt. The mean NCV was 19.5 ± 4.3 m/s.This compared with a NCV of 61 m/s in onecontrol horse. In one of the affected horses, theNCV was repeated after it had recovered clinicallyand was then determined to be 48.6 m/s.

It is interesting that size and age may bepredisposing factors in stringhalt, in so far as olderand taller horses tend to be affected (Slocombe etal. 1992) in preference to smaller horses such asponies and native Chilean breeds (Araya et al.1998).

The pathological lesions present in Australianstringhalt have been well studied and undoubtedlyrepresent a distal axonopathy preferentiallyaffecting large diameter axons in long nerves(Cahill et al. 1986; Slocombe et al. 1992). Thisexplains the muscle atrophy but there must also beselective involvement of γ-efferent fibres toaccount for the movement disorder with abnormalinput via the 1α-afferent fibres to the γ-efferentneurons resulting in inappropriate firing of lateraldigital extensor (and other) muscles.

The possibility that the presumed toxic factorthat produces Australian stringhalt may play a rolein RLN has fascinated several workers over theyears. One 15.3 h Thoroughbred horse from astringhalt outbreak in New Zealand was studiedintensively (Cahill et al. 1986). This horse hadsevere stringhalt and grade 5 RLN and had verysimilar, though perhaps not identical, pathologicallesions in the recurrent laryngeal as in pelvic andthoracic limb nerves. However, a more extensivestudy (Slocombe et al. 1992) showed that thechanges in long limb nerves and recurrentlaryngeal nerves in horses with stringhalt were thesame. Another study (Cahill et al. 1985) showedthat there was endoscopic evidence of abnormal

laryngeal function in 10 of 11 horses withstringhalt. Such evidence of RLN was still presentwhile these horses were recovering, or hadrecovered, over a period of a few days to 18months. Finally, in horses affected with RLN thereis a drop in the proportion of large to smalldiameter axons in the deep peroneal nerve ofaffected horses versus control horses, but no limbmuscle atrophy or signs of stringhalt (Kannegieter1989).

It would seem reasonable to conclude that thepresumed toxic principle in Australian stringhalt isnot the singular cause of idiopathic RLN.However, because the distal portion of long axonsin tall horses are predisposed to distal axonopathythen a further insult with the toxin associated withAustralian stringhalt could be the precipitatingfactor in inducing endoscopic and/or clinicalevidence of RLN in horses suffering fromstringhalt.

IDIOPATHIC NEUROPATHY WITH‘KNUCKLING’

Japanese workers (Furuoka et al. 1994, 1998) havestudied 3 cases of so called ‘kuckling’. Clinicallythis is, in fact, the syndrome of prominent uprightposture with flexion of the carpi and fetlocks thatoccurs as an acquired syndrome in weanlings andyearlings. These patients sometimes dragged thetoes of their forelimbs. The workers describedwidespread peripheral nerve walleriandegeneration, which was most prominent distally.The formation of bands of Büngner andregenerative axonal sprouts do make thispathological process consistent with a diffusedistal axonopathy. Neurogenic muscle atrophywith some regeneration was seen with fibre typegrouping, particularly in distal muscles. Thecomment was made that ‘laryngeal paralysis wasnot observed in the present cases’; unfortunately,the basis for this statement was not given.

SCANDINAVIAN ‘KNUCKLING’ HORSES

A detailed synopsis of 5 outbreaks of a hind limb‘knuckling’ syndrome in horses was discussed at aneurology meeting in Sweden in 2001 (K.Gustafsson et al., personal communication). Therewere a total of 24 cases occurring in an at-riskpopulation of 75 animals. Detailed clinical,paraclinical and pathological investigations wereundertaken on numerous affected cases, with only

14


3 surviving, one of which had recovered. In allcases silage was fed along with poor quality hay.

The clinical syndrome was one of varyingdegrees of sciatic nerve involvement, some horsesshowing signs of peroneal neuropathy moreprominently and others showing signs of tibialneuropathy more prominently. A total of 9,detailed postmortem examinations wereundertaken and in 2 cases there was evidence ofmild peripheral wallerian degeneration.

During discussion, 3 other outbreaks wereintroduced. In Norway, 2 horses showed similarsigns on the same property. One was examined atpost-mortem, where modest changes in myelinand axon were evident in a peroneal nerve and athoracic limb nerve. From the 1940s onwards, onepractitioner indicated that he had been aware ofnumerous cases and had seen 10 cases in the last 3years. One case at least was said to have evidenceof wallerian degeneration in sciatic and femoralnerves. Some cases with mild signs improved andin one case the forelimbs were affected and therewere lesions in forelimb nerves. Again, the dietconsisted of small bale silage, although in oneyear, in which 3 cases occurred, they were fed onlyon hay. Finally, 5 out of 6 Norwegian Fjord horseswere affected in another outbreak and 2 affectedmares gave birth to normal foals.

Further discussion extended to 2 outbreaks incattle showing evidence of sciatic/peronealneuropathy, where they would stand with thehindlimbs more caudal than normal and showedeither a tendency to stand on the dorsum of thepastern or to have considerable wearing of thehooves. In one case acrylamide was incriminatedbecause it was found in plastic feeding troughsand in the other, vanadium because of anassociation with a local steel industry producingalloy vanadium steel.

OTHER TOXIC NEUROPATHIES

Clinically, some cases of lead poisoning canpresent with laryngeal and pharyngeal paralysisthat is most probably associated with a peripheralneuropathy, but these signs are not presentconsistently (Dollahite et al. 1978; Aguilera-Tejero et al. 1996; Casteel 2001).

An outbreak of laryngeal paralysis in Arabianfoals associated with administration of anorganophosphorous anthelmintic haloxon hasbeen described in detail (Rose et al. 1981).Because of a problem of large strongyle

anthelmintic resistance, an intensive programmeof haloxon administration was given to a group ofArabian and part-Arabian foals every 2 weeksfrom 2 days of age. There was a sudden onset ofdyspnoea noted in 6 foals from 23 to 35 days ofage. Detailed pathological investigations werecarried out and revealed a distal axonopathy of therecurrent laryngeal nerves, worse on the left thanthe right, and associated bilateral neurogeniclaryngeal muscle atrophy. Unfortunately, no limbnerves or muscles were examined. Of the 6 foals,only one totally recovered, the others either wereeuthanased for other reasons, or died or wereeuthanased because of the persistent upperrespiratory embarrassment.

Additionally, 5 foals had received one or 2doses of the anthelmintic, showed no signs ofdyspnoea but when endoscoped showed Grade 2RLN. All of these 5 foals recovered normallaryngeal function.

SUSPECTED NEUROPATHIES

One investigating group has published someevidence that a primary neural lesion involving thesciatic nerve and its branches may contribute tothe acquired sporadic syndrome of equine fibroticmyopathy (Valentine et al. 1994). However, withthe weight of evidence of many cases havingprimary muscle pathology it is unlikely that sciaticnerve disease alone is responsible for many casesof this syndrome.

Numerous movement disorders, particularlyinvolving the pelvic limbs in horses, may wellinvolve a primary neuropathy. However, they havenot been investigated in detail. One of these wouldbe intermittent abduction of one pelvic limbduring the protraction phase of stride. Thissyndrome could well be explained by aninterruption to the 1α-afferent, γ-efferent pathwaythat almost certainly explains the abnormalmovements occurring in stringhalt for example.

Finally, Dr Knottenbelt from Liverpool haspresented numerous arguments that head shakersmay result from trigeminal neuritis. There doesnot appear to be a lot of evidence for aninflammatory basis to this disease. However, thepossibility that some or all of the head shakers thatare seen commonly are related to a trigeminalneuropathy is still very possible. In the authors’experience, horses with overt clinical neuritis(extensive supurative sinusitis and associatedsurgeries) or histologic evidence of neuritis of the

15


trigeminal nerve have demonstrated allodynia(painful responses to non-noxious stimuli) as wellas hypersensitivity and have not shown theclassical syndrome of head shaking but haverubbed and excoriated the side of their face.

CONCLUSION

It seems reasonable that there are many insults, asdiscussed above, including vitamin deficienciesand other toxicities, that may target distal, largediameter axons and their myelin sheaths.Therefore these could result in clinical,pathological and/or paraclinical evidence of RLN.It is unlikely that any one of these other causes ofRLN is responsible for the majority of idiopathicRLN cases.

Also, if indeed idiopathic RLN is a dying backpolyneuropathy, why is some clinical evidence ofthese other syndromes not seen in severelyaffected horses?

REFERENCES

Aguilera-Tejero, E., Mayer-Valor, R., Fernández-Gómez, M., Gómez-Villamandos, J.C. and Cano-Exposito, T. (1996) Lead poisoning, laryngealparalysis and pulmonary hemorrhage in two horses.Equine Pract. 18, 16-20.

Araya, O., Krause, A. and Solis de Ovando, M. (1998)Outbreaks of stringhalt in southern Chile. Vet. Rec.142, 426-463.

Cahill, J.I. and Goulden, B.E. (1992) Stringhalt - currentthoughts on aetiology and pathogenesis. Equine vet.J. 24, 161-162.

Cahill, J.I., Goulden, B.E. and Jolly, R.D. (1986)Stringhalt in horses: a distal axonopathy.Neuropathol. appl. Neurobiol. 12, 459-475.

Cahill, J.I., Goulden, B.E. and Pearce, H.G. (1985) Areview and some observations on stringhalt. N. Z.vet. J. 33, 101-104.

Casteel, S.W. (2001) Metal toxicosis in horses. Vet. Clin.North Am. equine Pract. 17, 517-527.

Crabill, M.R., Honnas, C.M., Taylor, D.S., Schumacher,J., Watkins, J.P. and Snyder, J.R. (1994) Stringhaltsecondary to trauma to the dorsoproximal region ofthe metatarsus in horses: 10 cases (1986-1991).

J. Am. vet. med. Ass. 205, 867-869.Dixon, R.T. and Stewart, G.A. (1969) Clinical and

pharmacological observations in a case of equinestringhalt. Aust. vet. J. 45, 127-130.

Dollahite, J.W., Younger, R.L., Crookshank, H.R., Jones,L.P. and Petersen, H.D. (1978) Chronic leadpoisoning in horses. Am. J. vet. Res. 39, 961-964.

Furuoka, H., Mizushima, M., Miyazawa, K. and Matsui,T. (1994) Idiopathic peripheral neuropathy in ahorse with knuckling. Acta Neuropathol. 88, 389-393.

Furuoka, H., Okamoto, R., Kitayama, S., Asou, S.,Matsui, T. and Miyahara, K. (1998) Idiopathicperipheral neuropathy in the horse with knuckling:muscle and nerve lesions in additional cases. ActaNeuropathol. 96, 431-437.

Gay, C.C., Fransen, S., Richards, J. and Holler, S. (1993)Hypochoeris-associated stringhalt in NorthAmerica. Equine vet. J. 25, 456-457.

Huntingdon, P.J., Jeffcott, L.B., Friend, S.C.E., Luff.(1989) Australian Stringhalt - epidemiological,clinical and neurological investigations. Equine vet.J. 21, 266-273.

Huntingdon, P.J., Seneque, S., Slocombe, R.F., Jeffcott,L.B., McLean, A. and Luff, A.R. (1991) Use ofphenytoin to treat horses with Australian stringhalt.Aust. vet. J. 68, 221-224.

Kannegieter, N.J. (1989) A Study of the Distal HindlimbMuscles and Nerves in Laryngeal HemiplegicHorses. PhD Thesis,. Massey University, NewZealand.

Rose, R.J., Hartley, W.J. and Baker, W. (1981) Laryngealparalysis in Arabian foals associated with oralhaloxone administration. Equine vet. J. 13, 171-176.

Seddon, H.R. and Belschner, H.H. (1926) Stringhalt inhorses. Agric. Gazette N.S.W. May 1st, 318-382.

Slocombe, R.F., Huntingdon, P.J., Friend, S.C.E. (1992)Pathological aspects of Australian stringhalt. Equinevet. J. 24, 174-183.

Takahashi, T., Kitamura, M., Endo, Y. (2002) Anoutbreak of stringhalt resembling Australianstringhalt in Japan. J. equine Sci. 13, 93-100.

Valentine, B.A., Rouselle, S.D., Sams, A.E. andEdwards, R.B. (1994) Denervation atrophy in threehorses with fibrotic myopathy. J. Am. vet. med Ass.25, 332-336.

Wijnberg, I.D., Back, W. and van der Kolk, J.H. (2000)The use of electromyographic examination as adiagnostic tool and phenytoin sodium as treatmentin a case of classic springhalt in a Dutch Warmbloodhorse. Tijdschr. Diergeneeskd. 125, 743-747.

16


LARYNGEAL PARALYSIS IN DOGS

P. M. Dixon and K. M. Pratschke

Division of Veterinary Clinical Studies, The University of Edinburgh, Easter Bush Veterinary Centre,Easter Bush, Midlothian EH25 9RG, UK

NON-IDIOPATHIC LARYNGEAL PARALYSIS

Hereditary forms of laryngeal paralysis, that arepart of a general neuropathy, are described in theBouvier des Flandres, Dalmation, Rottweiler,Siberian husky (and crosses) and white coatedGerman shepherd (van Haagen et al. 1978; Braundet al. 1994; Mahony et al. 1998; Ridyard et al.2000). Inheritance patterns have been establishedin Bouvier des Flandres (van Haagen et al. 1981)and Dalmation (Braund et al. 1994). Dogs affectedwith congenital laryngeal paralysis are typicallyless than 7 months old at presentation and as theyare part of a more generalised polyneuropathy ormyopathy, they carry a poor prognosis. Congenitallaryngeal paralysis has been less commonlydescribed in other breeds, including toy breeds.

In older dogs, acquired laryngeal paralysis mayalso manifest as part of a peripheral diffuseneuropathy (Braund et al. 1989), in association withmyasthenia gravis, hypothyroidism (Gaber et al.1985), hypoadrenocorticism and lead ororganophosphate poisoning. Laryngeal paralysiscan also follow direct trauma to the recurrentlaryngeal nerves, eg bite wounds, aggressive use ofchoke chains; or during thyroid, oesophageal,tracheal (prosthetic ring implants) or cervical spinesurgery. It can also occur following damage to therecurrent laryngeal nerves by aggressive necktumours (eg thyroid neoplasms) or mediastinum (eglymphosarcoma). Ankylosis of the cricoarytenoidjoint has also been described as a cause of laryngealdysfunction in the dog, (but not the horse).

IDIOPATHIC LARYNGEAL PARALYSIS

Despite the extensive lists of aetiologies of caninelaryngeal paralysis, most are due to unknowncauses, as is the case with horses and are termed

canine idiopathic laryngeal paralysis. Thistypically affects large breeds, such as Labradors,retrievers, Afghans, and Irish setters and has beenrecorded less commonly in smaller breeds and cats.One study showed that subclinical, unilateral orbilateral laryngeal paresis or paralysis was presentin 25% of dogs undergoing general anaesthesia fornon-related reasons (Broome et al. 2000).

In equine recurrent laryngeal neuropathy(RLN), pathological changes in laryngeal adductormuscle are more severe than abductor musclechanges. As dysphonia is one of the earliest signs ofcanine laryngeal paralysis, it may be thatpreferential adductor compromise also occurs earlyin the equivalent canine disease in dogs (Braund etal. 1988b). Dogs with idiopathic laryngeal paralysishowever are generally not presented until theadvanced stages of the disease process, not beingsubject to equivalent athletic demands of horses.

Idiopathic canine laryngeal paralysis is oftenbilateral and usually affects middle aged to olderdogs (median age of 9.5 years in some clinical casestudies). This is in contrast to equine RLN, which isprimarily unilateral and usually diagnosed inyounger horses. As is the case with horses, it hasbeen suggested that male dogs are affected morefrequently with idiopathic laryngeal paralysis.Clinical signs in acquired laryngeal paralysis aresimilar to those of the congenital form, but usuallyhave a more gradual onset than the former. Inaddition to altered or absent barking (dysphonia), asoft non-productive cough is also common inaffected dogs, which may be due to aspiration. Othercommonly recorded signs in severely affected dogsinclude inspiratory stridor and dyspnoea duringexercise, excitement or hot weather; and even life-threatening respiratory obstruction (syncope) inmore severe cases. These signs are due to theseverity and frequent bilateral nature of the

17


laryngeal paralysis. Older pet dogs with unilaterallaryngeal paralysis are seldom presented withclinical signs but working or racing dogs withunilateral paralysis may present with clinical signsthat interfere with their work (Greenfield 1987).

Greenfield et al. (1997) showed that clinicalsigns and measurable airflow changes associatedwith bilateral laryngeal paralysis did not develop indogs until a median of 38 days following bilateraldenervation of the recurrent laryngeal nerves. Thereason for such a delay is unclear. It has beensuggested that slow development of clinical signs inmany naturally occurring cases of canine idiopathiclaryngeal paralysis is due to progressivedeterioration of the recurrent laryngeal nerve.However, progressive anatomical changes in thelaryngeal structures may also be necessary fordevelopment of severe clinical signs.

Canine idiopathic laryngeal paralysis can beconfirmed by ultrasonography in the consciousdog or laryngoscopy in the lightly anaesthetisedsubject (deeper anaesthesia will cause immobilityof even the normal larynx), taking care todistinguish passive laryngeal abduction associatedwith deep expiration from normal active laryngealabduction that occurs during inspiration.

Most publications on idiopathic caninelaryngeal paralysis report the diagnosis andtreatment of this disorder, or the use of dogs asmodels to treat human laryngeal paralysis. Fewcomment on the pathogenesis or epidemiology.Early work suggested involvement of a neurogenicor denervation atrophy of the laryngeal muscles(such as occurs in horses) and this has becomewidely accepted as the most likely aetiopathogenesis(O’Brien et al. 1973). Most studies have either usedretrospective case analysis (O’Brien et al. 1973);have been restricted to congenital laryngealparalysis (van Haagen et al. 1978, 1981) or haveanalysed laryngeal innervation in normal dogs(Braund et al. 1988 a,b), and so their data andconclusions can be difficult to extrapolate toidiopathic canine laryngeal paralysis. For example,van Haagen et al. (1978, 1981) have describedhistological evidence of neurogenic axonaldegeneration of the right and left recurrent laryngealnerves in cases of congenital laryngeal paralysis

Biopsies of intrinsic laryngeal muscles in casesof idiopathic canine laryngeal paralysis have shownevidence of neurogenic atrophy (O’Brien et al.1973; Love et al. 1987). A comparative study of theneuropathology of canine and equine ‘RLN’ couldprovide much useful information for both species.

REFERENCES

Braund, K.G., Steiss, J.E., Marshall A.E., Mehta, J.G.,Toivio-Kinnucan, M. and Amling, K.A. (1988a)Morphologic and morphometric studies of the vagusand recurrent laryngeal nerves in clinically normaladult dogs. Am. J. vet. Res. 49, 2111-2116.

Braund, K.G., Steiss, J.E., Marshall A.E., Mehta, J.R.and Amling, K.A. (1988b) Morphologic andmorphometric studies of the intrinsic laryngealmuscles in clinically normal adult dogs. Am. J. vet.Res. 49, 2105-2110.

Braund, K.G., Steinberg, H.S., Shores, A., Steiss, J.E.,Mehta, J.G., Toivio-Kinnucan, M. and Amling, K.A.(1989) Laryngeal paralysis in immature and maturedogs as one sign of a more diffuse polyneuropathy.J. Am. vet. med. Ass. 12, 1735-1740.

Braund, K.G., Shores, A., Cochrane, S., Forester, D.,Kwicien, J.M. and Steiss, J.E. (1994) Laryngealparalysis-polyneuropathy complex in youngDalmations. Am. J. vet. Res. 55, 534-542.

Broome, C., Burbidge, H.M. and Pfeiffer, D.U. (2000)Prevalence of laryngeal paresis in dogs undergoinggeneral anaesthesia. Aust. vet. J. 78, 769-772.

Burbidge, H.M., Goulden, B.E. and Jones, B.R. (1993)Laryngeal paralysis in dogs: an evaluation of thebilateral arytenoid lateralisation procedure. J. smallAnim. Pract. 34, 515-519.

Gaber C.E., Amis, T.C., LeCouteur, R.A. (1985)Laryngeal paralysis in dogs: A review of 23 cases. J.Am. vet. med. Ass. 186, 377-380.

Greenfield, C.L. (1987) Canine laryngeal paralysis.Comp. cont. Educ. pract. Vet. 9, 1011-1020.

Greenfield, C.L., Alsup, J.C., Hungerford, L.L. andMcKiernan B.C. (1997) Bilateral recurrentlaryngeal neurectomy as a model for the study ofidiopathic canine laryngeal paralysis. Can. vet. J.38, 163-167.

Mahony, O.M., Knowles, K.E., Braund, K.G., Averill,D.G. and Frimbeerger, A.E. (1998) Laryngealparalysis-polyneuropathy complex in youngRottweilers. JVIM 12, 330-337.

Love, S., Waterman, A.E. and Lane, J.G (1987) Theassessment of corrective surgery for caninelaryngeal paralysis by blood-gas analysis – a reviewof 35 cases. J. small Anim. Pract. 28, 597-604.

O’Brien, J.A., Harvey, C.E., Kelly, A.M. and Tucker,J.A. (1973). Neurogenic atrophy of the laryngealmuscles of the dog. J. small Anim. Pract. 14, 551-532.

Ridyard, A.E., Corcoran, B.M., Tasker, S., Willis, R.,Welsh, E.M. Demetriou, J.L. and Griffiths, L.G.(2000) Spontaneous laryngeal paralysis in fourwhite-coated German shepherd dogs. J. small Anim.Pract. 41, 558-561.

van Haagen, A.J., Hartmann, W. and Goedegebuure, S.A.(1978) Spontaneous laryngeal paralysis in youngBouviers. J. Am. anim. Hosp. Ass. 14, 714-720.

van Haagen, A.J., Bouw, J. and Hartman, W. (1981)Hereditary transmission of laryngeal paralysis inBouviers. J. Am. anim. Hosp. Ass. 17, 75-76.

18

Equine Laryngeal Neuropathy

19


SESSION 2:

Endoscopic gradingsystems for laryngealparalysis

Chairman: Paddy Dixon

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21


4-GRADE SYSTEM FOR EQUINE LARYNGEALFUNCTION

N. Ducharme

College of Veterinary Medicine, Cornell University, Ithaca, New York, USA

The impetus for this grading system was thecontroversy regarding the clinical significance ofvarious forms of asynchrony and/or asymmetry ofthe arytenoid cartilage during examination at restor after exercise. The 4-grade system forassessment of resting laryngeal function waspublished in 1991 (Hackett et al. 1991; Ducharmeet al. 1991) to meet 3 objectives: 1) a simplepractical system; 2) correlation with evaluation atexercise; and 3) a system that was consistentbetween observers and during re-examination. Inthis aspect of laryngeal evaluation, the focus is onthe respiratory function and more specifically theabductor function of the arytenoid cartilages. It iswell known that laryngeal adductors are generallymore severely affected when compared to theabductors (Duncan et al. 1991). However,adductor deficit is not of clinical significanceeither for the respiratory or digestive role of thelarynx except perhaps from its recognition in theslap test. Although the grade is used in referenceto the left arytenoid cartilage, it has also been usedto describe the more rare form of failure of rightarytenoid cartilage abduction.

The resting 4–Grade laryngeal examinationwas developed using a population of 108 horses(61 SB, 38 TB, and 9 other breeds that consistedof 66 females, 34 geldings and 8 entire males (6years ± 3.6 SD). In the early development of the4–Grade system, 3 main criteria were used: degreeof symmetry, degree of synchrony, and degree ofabduction. Degree of laryngeal asymmetry was acriterion used in the grading, but was abandonedbecause of the low intra-observer agreement rate(37%). It was found that in the initial population,all 108 horses could be classified in one of 4grades (Table 1) summarised in the gradingsystem. A second conclusion was that most of thediscrepancies in classification between observers

and within observers were due to lack ofagreement on the degree of asynchronousmovement of the left arytenoid cartilage. Incontrast, there was substantial agreement on theability to recognise full arytenoid cartilageabduction. This criterion (ability to identify fullarytenoid cartilage abduction) is therefore, thefoundation of the 4-Grade system and, as time hasproved, the criterion with the most clinicalsignificance.

A second major issue to resolve regarding anylaryngeal grading system is identifying the correctlaryngeal grade. Therefore, we and others (Archeret al. 1991; Ducharme et al. 1991) evaluatedvarious conditions during examination. It wasdiscovered that full abduction could be inducedconsistently by nasal occlusion or by inducing aswallow by touching the tip of the epiglottis witha video-endoscope. In addition, in many cases, theuse of a respiratory stimulant was found not onlyto increase the respiratory frequency, but also thedegree of abduction of the arytenoid cartilages. Itwas also determined that the use of sedation suchas xylazine hydrochloride decreases the degree ofabduction and affects the degree of laryngealasynchrony (Valdez-Valquez et al. 199). The nasalside that the endoscope is passed influences theviewer’s perspective of the larynx and decreasesthe repeatability of the grading system. Therefore,it was recommended that laryngeal grading shouldbe performed in the resting animal withoutsedation, always using the same nostril and ifneeded, with the use of the twitch (Ducharme etal. 1991).

The real value of any resting grading system isits correlation with laryngeal function at exerciseand performance. Four studies have correlated theresting laryngeal grade to the degree of abductionof the arytenoid cartilage during strenuous

22


exercise on high-speed treadmill. In the initialstudy (Rakestraw et al. 1991), 49 horses wereevaluated while exercising on a 5% inclined high-speed treadmill for 8 min at a maximum speed of8.5 m/s. Hammer et al. (1998) compared theoutcome of 26 Grade III horses to exercising gradein horses travelling up to 14 m/s. Martin et al.(2000) described the correlation of 73 horses withGrade II, III and IV to exercising grade in horsestravelling up to 14 m/s. Finally, we reviewed theoutcome of 313 horses exercising on the treadmillat our hospital at speeds up to 16 m/s (Rakestrawet al. 1991). These 4 studies were combined for ananalysis to establish the results of the comparisonof the resting laryngeal Grade in 461 horses: 204horses had a laryngeal Grade I, 114 had alaryngeal Grade II, 126 had a laryngeal Grade III,and 17 had a laryngeal Grade IV. The results aresummarised in Figure 1. It was found that 100% ofhorses with a laryngeal Grade I, and 96% of horseswith a laryngeal Grade II had full arytenoidcartilage abduction (Grade A) throughout

exercise. All horses without significant movementof the arytenoid cartilage at rest (Grade IV),experienced collapse of the arytenoid cartilage(Grade C). Most horses (85%) with laryngealGrade III had some degree of arytenoid cartilagecollapse. Furthermore they were a range ofoutcome in horses with laryngeal Grade III,indicating that horses with this type of laryngealgrade need further evaluation, such as examinationduring exercise. The results of this study indicatethat failure to obtain and maintain arytenoidabduction at rest is the major criterion to triagehorses that probably have an abnormal arytenoidcartilage function at exercise. This finding wascollaborated further by another group ofinvestigators (Christley et al. 1997) who looked atindices of ventilation during exercise. They foundthat the only criterion in the resting laryngealgrade at rest that differentiates horses withabnormal indices of ventilation at exercise was thepresence or absence of full arytenoid cartilageabduction. Indeed, horses that did not have full

TABLE 1: 4-Grade classification system for assessment of equine laryngeal respiratory function inunsedated horses examined at rest*

Laryngeal grade Definition

I Synchronous and full abduction of the arytenoid cartilages.

II Asynchronous movement (hesitation, flutter, abduction weakness, etc.) of theleft arytenoid cartilage during any phase of respiration. Full abduction of the leftarytenoid cartilages (when referenced to the right) is observed either byswallowing, nasal occlusion or the use of respiratory stimulants.

III Asynchronous movement (hesitation, flutter, abduction weakness, etc.) of theleft arytenoid cartilage during any phase of respiration. Full abduction of the leftarytenoid cartilages (when referenced to the right) cannot be induced either byswallowing, nasal occlusion or the use of respiratory stimulants.

IV Midline or paramedian position of the left arytenoid cartilage and no substantialmovement of the left arytenoid cartilage can be induced by swallowing, nasalocclusion or the use of respiratory stimulants.

*Update from Hackett et al. (1991)

TABLE 2: 3-Grade classification system for assessment of equine laryngeal respiratory function inhorses examined during exercise*


A Full abduction of the arytenoid cartilages during inspiration.

B Partial abduction of the left arytenoid cartilages between full abduction andthe resting position.

C Abduction less than resting position including collapse into the right half ofthe rima glottidis.

*Update from Rakestraw et al. (1991)

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arytenoid cartilage abduction at rest experiencedstatistically more severe exercise-inducedhypoxemia and hypercarbia. And finally, whenStick et al. (2001), studied the correlation betweenresting laryngeal grade in yearlings and futureperformance in Thoroughbred racehorses, theyfound that yearlings with laryngeal Grade-I and -II had significantly better racing performance asadults, compared with yearlings with Grade-IIIarytenoid cartilage movements.

In summary, since its introduction 12 yearsago, the 4-grade system has been validated usingcorrelation between resting examination andtreadmill examination, as well as between restingexamination and future performance. This allowsthe equine practitioner an accurate, repeatablemean to identify horses that are likely toexperience clinical disease during exercise (GradeIII and IV) and those whose laryngeal function isnormal (Grade I and II).

REFERENCES

Archer, R.M., Lindsay, W.A., Duncan, I.D. (1991) Acomparison of techniques to enhance the evaluationof equine laryngeal function. Equine vet. J. 23,104-107.

Christley, R.M., Hodgson, D.R., Evans, D.L., Rose, R.J.(1997) Cardiorespiratory responses to exercise inhorses with different grade of idiopathic laryngealhemiplegia. Equine vet. J. 29, 6-10.

Ducharme, N.G., Hackett, R.P., Fubini, S.L., Erb, H.N.(1991) The Reliability of Endoscopic Examinationin Assessment of Laryngeal Function in Horses. Part II: Side of Examination, Influence of Re-examination, and Sedation. Vet. Surg. 20, 180-184.

Duncan, I.D., Reifenrath, P., Jackson, K.F., Clayton, M.(1991) Preferential denervation of the adductormuscles of the equine larynx. II: Nerve pathology.Equine vet. J. 23, 99-103.

Hackett, R.P., Ducharme, N.G., Fubini, S.L., Erb, H.N.(1991) The Reliability of Endoscopic Examinationin Assessment of Laryngeal Function in Horses. PartI: Development of a Laryngeal Grading System. Vet.Surg. 20, 174-179.

Hammer, E.J., Tuleners, E.P., Parente, E.J., Martin, B.B.(1998) Videoendoscopic assessment of dynamiclaryngeal function during exercise in horses withgrade III left laryngeal hemiparesis at rest: 26 cases(1992-1995). J. Am. vet. med. Ass., 212:399-403.

Martin, B.B., Reef, V.B., Parente, E.J., Sage, A.D.(2000) Causes of poor performance of horses duringtraining, racing, or showing: 348 cases (1992-1996).J. Am. vet. med. Ass., 216, 554-558.

Rakestraw, P.C., Hackett, R.P., Ducharme, N.G. Nielan,G.J., Erb, H.N. (1991) A comparison of arytenoidcartilage movement in resting and exercising horses.Vet. Surg. 20;122-127.

Stick, J.A., Peloso, J.G., Morehead, J.P., Lloyd, J.,Eberhart. S., Padungtod, P., Derksen, F.J. (2001)Endoscopic assessment of airway function as apredictor of racing performance in Thoroughbredyearlings: 427 cases (1997-2000). J. Am. vet. med.Ass. 1, 219; 962-967.

Valdes-Valquez, M.A., Aguilera-Tejero, E., Mayer-Valor, R. (1993) Effects of Xylazine duringendoscopic evaluation of functional upperrespiratory disorders in horses. Equine vet. Sci. 13,84-86.

100

80

60

40

20

0I II III IV

%

0

100

37

96

6515

15

100

Fig 1: Correlation of 4-grade resting laryngeal grade toexercising grade in 443 horses.

Exercising grade

Resting grade

A

B

C

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5-POINT GRADING SYSTEM OF LARYNGEALFUNCTION IN HORSES DURING QUIET BREATHING

J. G. Lane

Department of Clinical Veterinary Science, University of Bristol, Langford House, Langford, Bristol,BS40 5DU, UK

Clinicians are generally obsessed with scoring orgrading disorders which they encounter, whether itbe the severity of feather pecking in chickens, hipdysplasia in dogs or function of the equine larynx.The purpose is invariably to provide an objectiveand repeatable method to document observations.This 5-point scheme to grade the endoscopicperception of equine laryngeal motility at rest inthe stable, including on return from exercise – quietbreathing has been used at Bristol since the early1980s and in Australasia since 1993 (Lane 1993;Kannegeiter and Dore 1995). It is not very differentfrom the 4-point scale used in North America(Rakestraw et al. 1991) and has been continuedsimply because it has been found to be workable ineveryday equine laryngological practice.

Grade 1: All movements, both adductory andabductory are synchronised and symmetricalregardless of whether sedated or examined beforeor after exercise. A ‘mirror’ effect is achievedthrough a perspective artifact whereby the rightarytenoid appears less abducted when theendoscopy is performed through the right nostril,and the left is similarly less abducted when thelarynx is viewed via the left nasal chamber.

Grade 2: All major movements are symmetricaland a full range is achieved. Transient asynchrony,flutter or delayed opening may be seen (Baker1983).

Grade 3: Asymmetry of the rima glottidis at restdue to reduced motility by the left arytenoidcartilage and vocal fold. On occasions, typicallyafter swallowing or during the nostril closuremanoeuvre, full symmetrical abduction is achieved.

Grade 4: There is consistent asymmetry of therima glottidis but with some residual activemotility by the left arytenoid cartilage and vocalfold. Full abduction is not achieved at any stage.

Grade 5: True hemiplegia. There is obvious andconsistent asymmetry of the rima glottidis with noresidual active motility by the left arytenoidcartilage and vocal fold. No responses to the ‘slap’test are provoked.

At the request of a major owner/breeder video-endoscopic recordings were made of the upperrespiratory tracts of 3,497 yearlings during a 15 yearstudy and the findings have been reviewed. Thestudy has provided a unique opportunity to estimatethe prevalence of laryngeal disorders as and to assessthe distribution of functional anomalies in theThoroughbred. Although the subjects represent anelite group of horses on the basis of geneticselection, unlike previous investigations (Pascoe etal. 1981; Raphael 1982; Baker 1983; Lane et al.1987; Sweeney et al. 1991), these were unbrokenand, therefore untried animals. Initially,approximately half of the yearlings had beenpurchased, some privately and some at auction, andhalf were homebred. In recent years the majority ofthe yearlings examined have been homebred and yetthe distribution of the findings has remainedconstant. The findings in regard to the distribution offunctional grading are shown in Table 1.

The 12 yearlings for which no grade wasassigned included 7 afflicted with the fourthbranchial arch defect syndrome and an additional5 with malfunction on the right side and where nophysical explanation was discovered.

TABLE 1: Laryngeal function grading of 3,497yearlings

RLN 1 2 3 4 5 Notgrading graded

784 2006 617 69 9 12% 22.4 57.4 17.6 2.0 0.026 0.34

25


All horses showing Grade 5 were laterconfirmed to show severe obstructive dyspnoeaand that most of the Grade 4 horses were alsoclinically diseased. This is in line with previousfindings (Morris and Seeherman 1991) whichshowed that dynamic collapse of the left arytenoidcartilage (ACC) and vocal fold (VCC) developedin the overwhelming majority – 20 out of 27horses with Grade 4 (sic) motility at rest. Theprevalence of clinically significant recurrentlaryngeal neuropathy (RLN), ie Grades 4 and 5,was found to be 2.26% and this can be regarded asa base level for an unselected population ofThoroughbred horses. It compares with previousreports of selected groups (Table 1).

The greatest diversity of opinion hinges on thesignificance of Grade 3 motility and whether thisrepresents a performance-limiting malfunction, orwhether it should be viewed as a variant ofnormality. This grading does not discriminatebetween the abilities to achieve and to maintainfull abduction as these are subjective judgements.A large number of group, listed and stakes racewinners have come from the horses with thisgrading. The numbers of Grade 3 horses whichrequired, or were subjected to corrective surgerylater in life, is not known but from studies ofanimals examined by highspeed treadmillendoscopy (see page 47) it is safe to conclude thatthe majority are ‘normal’, showing sustainedsymmetrical abduction of the arytenoid cartilagesand vocal folds throughout exercise. However,horses with Grade 3 RLN are at a significantlygreater risk of sustaining ACC and/or VCC atexercise than horses with Grades 1 and 2 RLN.

Although the designation of a Grade 1 or 2score during quiet breathing does not conveyabsolute protection against ACC or VCC duringexercise, susceptible horses invariably show otherfeatures such as palpable atrophy of the crico-arytenoideus dorsalis muscle and a progressiveinspiratory noise at exercise.

In conclusion, the 5-point grading scheme forRLN has proved to be a practicable means toassess laryngeal function in Thoroughbreds thathas a useful predictive value with regard to thelikelihood of clinical disease, provided it is usedin conjunction with such techniques as palpationand an exercise test. Assessments of upperrespiratory tract function that rely on endoscopyduring quiet breathing alone should be regarded

as inadequate.REFERENCES

Baker, G.J. (1983) Laryngeal asynchrony in the horse:definition and significance. In: Equine ExercisePhysiology, Eds: D.H. Snow, S.G.B. Persson andR.J. Rose. Granta Editions, Cambridge, 46-50.

Kannegeiter, N.J. and Dore, M.L. (1995) Endoscopy ofthe upper respiratory tract during treadmill exercise:a clinical study of 100 horses. Aust. vet. J. 72, 101-107.

Lane, J.G., Ellis, D.E. and Greet, T.R.C. (1987)Observations on the examination of Thoroughbredyearlings for idiopathic laryngeal hemiplegia.Equine vet. J. 19, 531-536.

Lane, J.G. (1993) Equine recurrent laryngeal neuropathy(RLN): current attitudes to aetiology, diagnosis andtreatment. Proceedings of the 15th Bain-FallonMemorial Lectures, Aust. equine vet. Ass. 173-192.

Morris, E.A. and Seeherman, H.J. (1991) Clinicalevaluation of poor performance in the racehorse: theresults of 275 evaluations. Equine vet. J. 23, 169-174.

Pascoe, J.R., Ferraro, G.L., Cannon, J.H., Arthur, R.M.and Wheat, J.D. (1981) Exercise-inducedpulmonary haemorrhage in racing Thoroughbreds: apreliminary survey. Am. J. vet Res. 42, 703-707.

Rakestraw, P.C., Hackett, R.P., Ducharme, N.G., Nielen,G.J. and Erb, H.N. (1991) Arytenoid cartilagemovement in resting and exercising horses. Vet.Surgery 20, 122-127.

Raphael, C.F. (1982) Endoscopic findings in the upperrespiratory tract of 479 horses. J. Am. vet. med. Ass.181, 470-473.

Sweeney, C.R., Maxson, A.D. and Soma, L.R. (1991)Endoscopic findings in the upper respiratory tract of678 Thoroughbred racehorses. J. Am. vet med. Ass.198, 1037-1038.

TABLE 2: Previous endoscopic surveys toassess laryngeal function in horses

Authors Group Population RLN size incidence

(sic. grades 4 and 5)

Pascoe et al. 235 Horses in 2.6%(1981) training

Raphael 479 " 3.3%(1982)

Baker 537 " 4.7%(1983)

Lane et al. 6860 Yearlings at 0.96%(1987) sale

Sweeney et al. 678 Horses in 4.0%(1991) training

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ENDOSCOPIC GRADING SYSTEMS FOR LARYNGEALPARALYSIS - 6 GRADE SYSTEM

P. M. Dixon

Division of Veterinary Clinical Studies, The University of Edinburgh, Easter Bush Veterinary Centre,Easter Bush, Midlothian, EH25 9RG, UK

There is general agreement that laryngealendoscopy is currently the gold standard fordiagnosing equine laryngeal paralysis. Endoscopicevaluation during high-speed treadmill exercise iseven more accurate in the rare cases that shownormal laryngeal function (including laryngealasynchrony and arytenoid shivering) at rest, buthave a significant deterioration during fastexercise. Treadmill endoscopy is also the optimaltechnique for assessing degree of laryngealabductor dysfunction, which is determined mostaccurately at fast work (Morris and Seeherman1990). However, facilities for treadmill endoscopyare limited and such procedures involve training ofhorses, delay in obtaining results, technicalexpertise and capital outlay. Therefore, for theforeseeable future, resting endoscopy remains thestandard method for diagnosis and assessing thedegree of equine laryngeal paralysis.

Resting laryngeal endoscopy using flexibleendoscopes has been practiced for 30 years andthere is widespread consensus that asynchrony andshivering (usually left sided) of a larynx that canobtain and maintain full abduction are generallyinsignificant. Such findings are now rarely viewedwith the same degree of suspicion as they wereprior to work such as that of Morris andSeeherman (1990) who showed conclusively thathorses with laryngeal asynchrony and flutter canmaintain normal laryngeal function during highspeed treadmill endoscopy.

In the author’s opinion, even permanent, lowdegrees of laryngeal asymmetry can be presentwith no or minimal functional effects. High-speedtreadmill endoscopy of such cases has shownnormal laryngeal function during strenuousexercise. The author also disagrees with anyclassification system, which rates normal functionas ‘Grade 1’ of that dysfunction. It must be more

rational to have normal as zero, with increasingdegrees of dysfunction classified numerically.

The widely used laryngeal paralysis gradingsystem of Ducharme et al. (1989) and Hackett et al.(1991) separated laryngeal function into 4 grades, ietotally synchronous; asynchrony/flutter;asymmetry; and total hemiplegia. However, themajor disadvantage of that system is that itclassifies all asymmetry (incomplete abduction) ofthe larynx into a single category. Consequently,horses with very mild asymmetry (which may befunctionally normal) are classified in the samegroup as horses with almost total laryngealparalysis which, during treadmill exercise, willhave a grossly abnormal larynx. The sub-division ofthis category into 3 subgroups provides a 6-gradesystem, which allows a better assessment oflaryngeal function, as illustrated in Table 1 (Dixonet al. 2004). The 5-grade system of Lane (1993)partially addressed this issue but it is believed thatthe proposed 6-grade system is more advantageous.Embertson (1997) also sub-divided the restingendoscopic grades of recurrent laryngealneuropathy (RLN) that describe asymmetricmovements into 2 grades, and Hammer et al. (1998)sub-divided this same grade, as assessed duringhigh speed treadmill exercise, into 3 grades.

For a resting endoscopic examination, theendoscope is inserted via the right ventral meatusand positioned midline in the nasopharynx. Thesymmetry and synchrony of arytenoids isobserved during quiet breathing, followingswallowing (induced by trans-endoscopicallyflushing water through the nasopharynx) andduring temporary nostril occlusion (to assess thedegree of maximal arytenoid abduction).

In a study where 2 independent observersendoscopically examined and graded 45 horsesusing the above 6-grade laryngeal endoscopic

27


technique, a highly significant (P<0.001) positivecorrelation (Spearman rank correlation coefficients;right = 0.817; left = 0.913) was obtained betweenobservers (Hawe et al. 2001). The paired leftendoscopic scores did not differ significantly(P<0.05) between observers. Additionally right andleft RLN grades allocated post exercise endoscopy(n = 16) by both assessors showed a highlysignificant (P<0.001) positive correlation (Hawe etal. 2001). As previously noted with endoscopicgrading of laryngeal function by Archer et al.(1989); Ducharme et al. (1989); Hackett et al.(1991); Christley et al. (1997), having pre-determined, clearly defined criteria for endoscopicgrading helps minimise subjectivity and inter-assessor variation in the above study.

These laryngeal endoscopic grading systemsare semi-quantitative and by increasing the numberof grades, it becomes theoretically more difficultfor different workers to use them. Notwithstanding,it is in reality easy for clinicians to recogniseresting laryngeal asymmetry and then todifferentiate between horses that have, mild,moderate or severe (but not total) laryngeal paresis.We believe by using such a 6-grade endoscopysystem, clinicians can document more accuratelythe degree of equine laryngeal paralysis presentand would advocate its use as the endoscopicstandard for laryngeal function evaluation.

REFERENCES

Archer, R.M., Lindsay, W.A., and Duncan, I.D. (1989)Equine laryngeal hemiplegia: an endoscopic surveyof 400 draught horses. Vet. Surg. 18, 62-63.

Christley, R.M., Hodgson, D.R., Evans, D.L. and Rose,

R.J. (1997) Cardiorespiratory responses to exercisesin horses with different grades of idiopathiclaryngeal hemiplegia. Equine vet. J. 29, 6-10.

Dixon, P.M., McGorum, B.C., Railton, D.I., Hawe, C.,Tremaine, W.H. Pickles, K. and McCann, J.L.(2004) Clinical and endoscopic evidence ofprogressive recurrent laryngeal neuropathy (RLN)in 52 horses. Equine vet. J. Submitted

Ducharme, N.G., Hackett, R.P., Fubini, S.L. and Erb,H.N. (1989) Influence of sedation, side ofendoscopy and time of evaluation on subjective andobjective evaluation of endoscopic examination inassessment of laryngeal function in racehorses. Vet.Surg. 18, 63-64.

Embertson, R. M. (1997) Evaluation of the upperrespiratory tract in the immature horse. In: Proc.Dubai Int. equine Symp. Eds: N.W. Rantanen andM.L. Hauser. Published by Matthew R RantanenDesign, Ca. USA. pp 399-345.

Hackett, R.P., Ducharme, N.G., Fubini, S.L., and Erb,H.N. (1991) The reliability of endoscopicexamination in assessment of arytenoid cartilagemovement in horses – Part I: subjective and objectivelaryngeal evaluation. Vet. Surg. 20, 174-179.

Hammer, E.J., Tulleners, E.P., Parente, E.J. and Martin,B.B. (1998) Videoendoscopic assessment ofdynamic laryngeal function during exercise inhorses with grade-III left laryngeal hemiparesis atrest: 26 cases (1992-1995). J. Am. vet. med. Ass.212, 399-403.

Hawe, C., Dixon, P.M. and Mayhew, I.G. (2001) A studyof an electrodiagnostic technique for the evaluationof equine recurrent laryngeal neuropathy. Equinevet. J. 33, 459-465.

Lane, J.G. (1993) Recurrent Laryngeal Neuropathy. In:Proceedings of the 15th Bain – Fallon MemorialLecture, Canberra, Australia: Aust. equine vet. Ass.pp 173-192.

Morris, E.A. and Seeherman, H.J. (1990) Evaluation ofupper respiratory tract function during strenuousexercise in racehorses. J. Am. vet. med. Ass. 196,431-438.

TABLE 1: Grading of RLN by resting endoscopic examination; Dixon et al. (2000)

Grade Endoscopic findings

0 (Normal) perfect synchrony of arytenoid movement, and symmetry of appearance,full bilateral arytenoid abduction achieved and maintained (eg during nasalocclusion on excitement).

1 (Normal) asynchronous arytenoid movements, ± presence of arytenoid or vocalshiver but full symmetrical arytenoid abduction achieved and maintained.

2 (Mild paresis) slight arytenoid asymmetry, incomplete arytenoid abduction orcomplete but transient abduction ie unable to maintain full abduction.

3 (Moderate paresis) obvious arytenoid abductory deficit and arytenoids asymmetry.

4 (Severe paresis) marked but not total arytenoid abductory deficit and asymmetry,very little arytenoid movement.

5 (Total paresis [hemiplegia]) no arytenoid movements detectable.

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29


SESSION 3:

Progression andendoscopic variation

Chairman: Paddy Dixon

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31


LONG-TERM LONGITUDINAL STUDY OF LARYNGEALFUNCTION IN 187 FOALS

J. G. Lane


The sale of foals to be retained to go into trainingor to be resold as yearlings – ‘pin-hooking’ –forms a major component in the marketplace forThoroughbred horses. Prospective purchasers seekto take precautions to ensure that the animalsconcerned will be suitable for resale, or can betrained effectively for racing. It has becomefashionable for foals to be subjected to endoscopicexaminations on behalf of prospective purchasersprior to sale. Some breeders also seek endoscopicexaminations of foals ahead of sales if only forpeace of mind. However, is endoscopy of foals aworthwhile procedure and are the resultsdependable?

A number of congenital structuralabnormalities of the upper respiratory tract (URT)can be diagnosed accurately by a combination ofpalpation and endoscopy (Embertson 1997).

These conditions include midline clefts and otherdefects of the palate, pharyngeal and sub-epiglottal cysts and fourth branchial arch defects.These abnormalities are collectively relativelyunusual and arise in no more than 0.5% ofThoroughbreds born (see page 49). A majorinterest for foal purchasers often centres onlaryngeal function and the identification ofrecurrent laryngeal neuropathy (RLN). To assessthe reliability of the interpretation of laryngealfunction, a group of 197 foals were examined byendoscopy and 187 were available for re-examination one year later. The video-endoscopicrecords were reviewed ‘blindly’ – the findings areshown in the Table 1 and the obvious conclusionis that there are inconsistencies in the 2 series ofresults. The laryngeal function of some foalsappeared to be within normal limits, but then to

TABLE 1: Comparison of laryngeal function of 197 foals with the same horses one year later

Yearling grades (187)

1 (32) 2 (112) 3 (37) 4 (6) 5 (0) NA1 (36) 12 14 4 0 0 62 (123) 17 86 16 1 0 3

Foal grades (197) 3 (29) 3 11 12 2 0 14 (9) 0 1 5 3 0 05 (0) 0 0 0 0 0 0

10 horses (NA) were not available to be examined as yearlings

TABLE 2: Comparison of the laryngeal function grading of 187 yearlings with their median winningsbetween 2 and 4 years of age

Laryngeal grade 1 2 3 4 5(32) (112) (37) (6) (0)

Median Winnings (£) 1933 5358 5367 724 0

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have ‘deteriorated’ over the following 12 months,while others, which would have been consideredunsuitable had they been examined prior to sale asfoals turned out to be totally normal. There wasno foal or yearling in the group studied which was afflicted with any of the congenitalabnormalities mentioned above. In summary,endoscopy of foals is not an absolutelydependable technique and decisions on whether tobuy or to reject should not be based upon thistechnique.

A review of subsequent racing performancesat 2, 3 and 4 years of age showed that the medianstakes winnings of the yearlings in this study weregreatest in the Grade 3 group (Table 2).

REFERENCES

Embertson, R.M. (1997) Weanling and yearling upperairway evaluation. In: Current Techniques in EquineSurgery and Lameness Eds: N.A. White and J.N. Moore. Philadelphia: W.B. Saunders Co. 122-127.

33


ENDOSCOPIC OBSERVATIONS ON LARYNGEALSYMMETRY AND MOVEMENTS IN YOUNG RACINGHORSES

B. H. Anderson, N. J. Kannegieter and B. E. Goulden

Institute of Veterinary, Animal, and Biomedical Sciences, Massey University, Palmerston North, New Zealand

Respiratory endoscopists have found arytenoidcartilage movement during quiet respiration inhorses to be remarkably variable. This variability,according to the findings of Baker (1983), doesnot progress in the individual animal tohemiplegia. About 87% of the horses Bakerstudied, however, were 3 years of age or over. Ithas been shown that the pathological changescharacteristic of denervation and re-innervation inthe intrinsic laryngeal muscles dramaticallyincrease in prevalence and severity inThoroughbred horses during the yearling to 2-year-old period (B.H. Anderson, unpublisheddata). Presumably, if asynchronous arytenoidmovements are related to these pathologicalchanges, then progression of asynchrony tohemiplegia is most likely to be found in animals ofthis age.

An endoscopic survey of young racehorseswas performed (Anderson et al. 1997) to examinethe prevalence and character of laryngealmovements during quiet respiration. The main aimwas to determine whether those arytenoidmovements that could possibly reflect theefficiency of left dorsal cricoarytenoid musclefunction changed over a period of time.

Of the 462 horses examined, 439 wereThoroughbreds and 23 were Standardbreds, 250were less than 2 years of age (6–21 months), and202 were 2 years old. One hundred and nine ofthese horses were examined again 16 months later.Arytenoid movements were given one of 4 grades.Grades 1 and 2 were considered normal andunlikely to be the result of abnormal left dorsalcricoarytenoid muscle function, whilst Grades 3and 4 were considered likely, or almost certainlythe result of abnormal left dorsal cricoarytenoidmuscle function (a grading system similar to thatused by many endoscopists for laryngeal

examinations). The percutaneous prominence ofthe muscular process of left and right arytenoidcartilages, endoscopic arytenoid movement on leftand right sides, age, sex and breed were recorded.Chi-squared analysis was used to determine theassociation between age, breed, sex and the otherrecorded variables, and the presence or absence ofabnormal laryngeal movements.

At the first examination, 48% of the horseshad Grade 1, 37% grade 2, 15% Grade 3 and 0.2%Grade 4 left laryngeal movements. Of the horsesexamined 16 months later 52% had Grade 1, 33%Grade 2, 14% Grade 3 and 1% Grade 4 leftlaryngeal movements. Fifteen percent of horseswith Grade 1 and 8% with Grade 2 initially werefound to be Grade 3 at the subsequentexamination. Conversely, 53% of horses withGrade 3 initially were found to be Grade 1 and21% Grade 2 at the subsequent examination. Onehorse that was Grade 3 at the initial examinationwas Grade 4 at the subsequent examination.Overall, 43% of horses were graded the same,29% were given a ‘better’ grade and 28% weregiven a ‘worse’ grade.

Age and sex were not associated withabnormal left laryngeal movements. The presenceof abnormal arytenoid movements wassignificantly less in Standardbreds, butsignificantly higher, in those horses that had amore prominent muscular process of the leftarytenoid cartilage. The number of Grade 2 and 3laryngeal movements recorded on the left side wassignificantly higher than the right.

Why such a variation in grades occurred is notknown but one or some combination of thefollowing possibilities could have been involved:the repeatability of the endoscopic examinationtechnique used was unsatisfactory; the cut-offpoint between normal (Grade 1 and 2) and

34


abnormal (Grade 3 and 4) laryngeal movementgrades was inaccurate; the inter-relationshipbetween pathological changes in the left arytenoidmuscles and the arytenoid movements consideredto be indicative of these changes is unreliable orerroneous; in young Thoroughbred horses, changesin grade of arytenoid movements frequently occur.In the present study, 8 of 11 of the horses changingfrom what was considered normal laryngealmovements to abnormal, changed from Grade 1 toGrade 3. Similarly, of those horses changinglaryngeal grade from what was consideredabnormal to normal, 10 of 14 changed from Grade3 to Grade 1. Although the results of this study willbe affected by the repeatability of the endoscopicprocedure used it is unlikely that errors were madein differentiating Grade 3 laryngeal movementsfrom Grade 1. Not withstanding the other factorsmentioned, in this age group it appears that: a)asymmetrical laryngeal movements are common;b) laryngeal movements may interchange betweenwhat is considered normal and abnormal; c)development of more obvious degrees ofasynchrony is low (12%); and d) development oflaryngeal hemiplegia in horses that haveendoscopic evidence of deficient left abductormuscle function is also low (5%).

RECENT INVESTIGATIONS

More recently, Dixon et al. (2002) reported onendoscopic and/or clinical progression ofrecurrent laryngeal neuropathy (RLN) in oldernational hunt and sport horses (predominantlyThoroughbred). Fifty-two of the 351 horsesexamined (15%) showed evidence of progressionof the degree of laryngeal dysfunction over amedian period of 12 months (range 1.5–48months) with the onset of progression occurring atmedian age of 7 years.

The results of this study and the one reportedabove (involving predominantly Thoroughbreds)indicate that the progression of RLN oralternatively, clinically significant arytenoidabductor dysfunction, could vary between 5 and15%. The age of onset of the deterioration inarytenoid function is, however, markedly different.The reason for this is unknown. In addition, Dixonet al. (2002) have reported that the time or rate at

which progression can develop may be as short as6 weeks. In other cases deterioration can takemonths to years. This has important implicationsfor examination of horses for sale and supports theclinical impressions of veterinarians involved insales endoscopy.

In contrast to the above study, Dixon et al.(2002) found no evidence of improvement inlaryngeal function in the clinical cases examined.In another endoscopic study of the laryngealmovements of Thoroughbreds (Lane 2000)reported on the results of 2 examinationsconducted 12 months apart on 197 foals. At thetime of the second examination 187 yearlingswere available. Video-endoscopic records werereviewed ‘blindly’ on 3 occasions. The resultsshowed marked inconsistencies in the 2 series.The laryngeal function of some foals appeared tobe within normal limits, but appeared to havedeteriorated over the following 12 months.Conversely, 9 foals examined initially wereobserved with marked abductor deficiency (Grade4 of 5) but when examined 12 months later onewas considered normal (Grade 2 of 5), 5 wereconsidered equivocal (Grade 3 of 5) and 3remained Grade 4. While it was concluded thatendoscopy of foals is not reliable and decisions onwhether to buy or to reject horses should not bebased upon this technique, it is possible that someof the variation in laryngeal function could be theresult of successful re-innervation of de-innervated intrinsic laryngeal musculature.

REFERENCES

Anderson, B.H., Kannegieter, N.J., Goulden, B.E. (1997)Endoscopic observations on laryngeal symmetryand movements in young racing horses. N. Z. vet. J.45, 188-192.

Baker, G.J. (1983) Laryngeal asynchrony in the horse:Definition and significance. In: Equine ExercisePhysiology. Eds: D.H. Snow, S.G.B. Persson andR.J. Rose RJ., pp 46-50.

Dixon, P.M., McGorum, B.C., Railton, D.I., Hawe, C.,Tremaine, W.H., Pickles, K. and McCann, J. (2002)Clinical and endoscopic evidence of progression of152 cases of equine recurrent laryngeal neuropathy(RLN). Equine vet. J. 34, 29-34.

Lane, J.G. (2000) Limitations of assessment of laryngealfunction in the young Thoroughbred. Proc.Racehorse Pract. Conf. Newmarket, England 22nd-24th June.

35


VARIATION IN LARYNGEAL FUNCTION IN MATUREHORSES AND PROGRESSIVE CASES OF RECURRENTLARYNGEAL NEUROPATHY (RLN)

P. M. Dixon

Division of Veterinary Clinical Studies, The University of Edinburgh, Easter Bush Veterinary Centre,Easter Bush, Midlothian, Scotland EH25 9RG, UK

The literature on ‘roaring’ in the 17th and 18thcenturies cites many reports of cases of recurrentlaryngeal neuropathy (RLN) that appear to beprogressive. However, due to lack of endoscopicverification of the precise cause of the upperairway stridor, it is possible that some of thesecases were non-RLN upper airway abnormalities.In contrast to this early literature, repeatedendoscopic examinations of National Huntracehorses over a number of years by Baker(1982) found no evidence of progression of RLN.However, more recent observations by Embertson(1997) in foals in the USA and Anderson et al.(1997) in 2–3-year-olds in New Zealand showedvariation (improvement and deterioration) inlaryngeal function between examinations. Theremay be physiological reasons why ‘normal’equine larynges (including those displayingarytenoid shivering or asynchrony, but can remainfully abducted) show such variation butendoscopic interpretation of laryngeal function isalso subject to both inter- and intra-observervariation at repeat examinations (Ducharme et al.1991; Hackett et al. 1991).

The histology (fibre-type grouping on ATP-ase histochemistry) of RLN affected musclesshows it to be a dynamic disease; affected musclesshow evidence of cyclical de-innervation and re-innervation (Gunn 1973; Duncan et al. 1974;Cahill and Goulden 1986). Based on the abovemuscle histochemistry, RLN affected laryngealfunction may improve or worsen, depending onthe balance between laryngeal muscle de-innervation or re-innervation at the examinations.

The main pathological features of therecurrent laryngeal nerve in horses suffering fromRLN suggest a chronic progressive disorder.Griffiths (1991) suggested that some horses with

sub-clinical RLN lesions would later developclinical disease. In view of the above notedpathological lesions of the laryngeal muscle andthe recurrent laryngeal nerve, it is perhaps notsurprising that some cases of RLN are in factprogressive.

Dixon et al. (2002) found that 52 out of 351horses (15%) with RLN showed progression in thedegree of the disease over periods ranging from 6weeks to over 4 years (mean 12 months). Themedian age at the onset of progression was 7years. In 30 cases there was both endoscopicevidence, with a median deterioration of 3endoscopic grades (range 1–5 grades), and clinicalevidence, with 97% of these horses concurrentlydeveloping sudden-onset of abnormal exercise-related respiratory noises and 43% concurrentlyreporting reduced exercise performance. In someof these cases the degree of dysfunction changedfrom normal function to total hemiparesis. Someof these cases were examined on treadmills on anumber of occasions, absolutely confirming thatthere are progressive and often major changes inlaryngeal function.

Of the remaining 22 horses, there was justclinical evidence of RLN progression, includingthe sudden onset of abnormal exercise respiratorysounds in 73% and the worsening of such sound in23%. These abnormal ‘noises’ were associatedwith reduced exercise in 59% of these cases.Although examined endoscopically on just asingle occasion, 59% of the 22 cases had marked(total or almost total hemiparesis) that did notappear compatible with the previous exerciseperformance history. Although 52 cases in thestudy had apparent deterioration of laryngealfunction, no improvement in laryngeal functionwas detected in any cases in the current study, in

36


contrast to the findings of Flemming (1889) andAnderson et al. (1997).

More recently, even more acute cases oflaryngeal function variation were recorded,including a case where 2 competent equineveterinarians clinically examined (includingduring exercise) a racehorse pre-purchase, andduring a sale, and neither found any detectableabnormality. Within 4 days of the sale the horsestarted to make a ‘noise’ and endoscopicexamination a week later showed markedlaryngeal dysfunction. The author’s referralpopulation includes very few young racehorses,but such deterioration in laryngeal function mayalso occur in this age group.

The main significance of the above findingsconcerns interpretation of differences in clinical orendoscopic findings between veterinarians,especially at sale times. Provided that the initialclinical and/or endoscopic examinations areperformed by competent veterinarians, and that astandard and identifiable endoscopic gradingsystem is used, any differences in clinical andendoscopic findings detected at a later stage mustbe considered as possibly being due to furtherdeterioration of laryngeal function during thisperiod. Some delegates at this HavemeyerWorkshop (Embertson 2004; Anderson 2004)presented further evidence of cases of short-termdeterioration in laryngeal function, furtherclarifying to the sales authorities and the litigationlawyers that not all such differences are due tonegligence.

Another practical aspect of recognition ofprogressive deterioration in laryngeal functionconcerns the treatment of such cases. Cases thatinitially have normal laryngeal function, and arelater found to have a mild to moderate degree oflaryngeal paralysis, may be treated byventriculectomy and/or vocalcordectomy (varyingon their work discipline). However, with furtherprogression of the laryngeal hemiparesis, affectedhorses may require laryngoplasty at a later date.Clinicians should consider whether cases of RLNare progressive by historical, endoscopic andclinical findings, and if progression is stronglysuspected, perhaps laryngoplasty should beperformed on the first occasion on such horses,even if severe degrees of laryngeal dysfunction arenot present at that time.

It is concluded there is now irrefutablehistorical, clinical and endoscopic evidence thatequine laryngeal function can deteriorate often

slowly but on occasions very rapidly (over weeks)in a proportion of RLN cases.

REFERENCES

Anderson, B. H. (2004) Sales: Problems in the diagnosisof RLN, an Australasian perspective. EquineRecurrent Laryngeal Neuropathy. HavemeyerFoundation Monograph Series No 11, Eds: P. Dixon,E. Robinson and J. F. Wade, R&W Publications(Newmarket) Ltd, pp 45-46.

Anderson, B.H., Kannegieter, N.J., and Goulden, B.E.(1997) Endoscopic observations on laryngealsymmetry and movements in young racing horses.N. Z. vet. J. 45, 188-192.

Baker, G.J. (1982) Laryngeal asynchrony in the horse:Definition and significance. In: Proc. 1st int. Conf.equine Exerc. Physiol, Eds: D.H. Snow, S.G.B.Persson and R.J. Rose, Granta Publications,Cambridge. pp 46-50.

Cahill, J.1. and Goulden, B.E. (1986) Equine laryngealhemiplegia. Part 4. Muscle Pathology. N. Z. vet. J.34, 186-190.

Dixon, P.M., McGorum, B.C., Railton, D.I., Hawe, C.,Tremaine, W.H., Pickles, K. and McCann, J.L.(2002). Laryngeal paralysis: A long term study of375 cases in a mixed breed population of horses.Equine vet. J. 33, 452-458.

Ducharme, N.G., Hackett, R.P., Fubini, S.L., and Erb,H.N. (1991) The reliability of endoscopicexamination in assessment of arytenoid cartilagemovement in horses. Part II. Influence of side ofexamination, re-examination and sedation. Vet. Surg.20, 180-184.

Duncan, I.D., Griffiths, I.R., McQueen, A.M., and Baker,G.J. (1974) The pathology of equine laryngealhemiplegia. Acta. Neuropath. 27, 337-348.

Embertson, R. M. (2004) Sales: Problems in diagnosis ofRLN–USA perspective. Equine RecurrentLaryngeal Neuropathy. Havemeyer FoundationMonograph Series No 11, Eds: P. Dixon, E.Robinson and J. F. Wade, R&W Publications(Newmarket) Ltd, pp 42-44.

Embertson, R. M. (1997) Evaluation of the upperrespiratory tract in the immature horse. In: Proc.Dubai int. equine Symp. - The Diagnosis andTreatment of Respiratory Disease. Eds: N.W.Rantanen and M.L. Hauser. Published by MatthewR Rantanen Design, Ca. USA. pp 399-345.

Fleming G. (1889) In: Roaring in Horses (laryngismusparalyticus) Balliere, Tindall, and Cox, London. pp1-160.

Griffiths, I.R. (1991) The pathogenesis of equinelaryngeal hemiplegia. Equine vet. J. 23, 75-78.

Gunn, H.M. (1973) Further observations on laryngealskeletal muscle in the horse. Equine vet. J. 5, 77-78.

Hackett, R.P., Ducharme, N.G., Fubini, S.L. and Erb,H.N. (1991) The reliability of endoscopicexamination in assessments of arytenoid cartilagemovement in horses. Part 1: Subjective objectivelaryngeal evaluation. Vet. Surg. 20, 174-179.

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SESSION 4:

Diagnosis of RLN andnon-RLN URT disorders

Chairman: Eric Parente

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39


SALES: PROBLEMS IN DIAGNOSIS OF RLN – UK PERSPECTIVE

D. R. Ellis, T. R. C. Greet† and J. G. Lane*

Greenwood, Ellis & Partners, Reynolds House, 166 High Street, Newmarket, Suffolk, †Rossdale & Partners,Beaufort Cottage Equine Hospital, Cotton End Road, Exning, Newmarket, Suffolk CB8 7NN and *Departmentof Clinical Veterinary Science, University of Bristol, Langford House, Langford, Bristol, BS40 5DU, UK

Tattersalls, Ltd Conditions of Sale re WindConditions in Thoroughbred Yearlings or Horsesin Training:

1978–1983 A horse is returnable if it can beheard to make a characteristicabnormal inspiratory sound whenexercised actively.

1984 As above but add and/or haslaryngeal hemiplegia whenexamined with the endoscope.

1985 Makes a characteristic abnormalinspiratory sound AND has laryngealhemiplegia (RLN).

After the horse is sold the purchaser appoints aveterinary surgeon to listen when the horse islunged and if it makes any abnormal inspiratorynoise it is endoscoped. If it is found to haverecurrent laryngeal neuropathy (RLN) thepurchaser returns the horse to Tattersalls foradjudication by their panel. The panel hasincluded the authors since 1984 with occasionalalternates. Yearlings are returnable within 24 h ofsale, and horses in training within 7 days. Thepanel examines the horse soon after its return,often later on the same day as the original test bythe purchaser’s veterinary surgeon. Each memberof the panel palpates the larynx for atrophy,cartilage symmetry and surgical scars. The larynxis also palpated immediately after exercise forfremitus and the right arytenoid depression test.These observations provide supportive evidenceand with the exception of surgical scars would notbe decisive. The yearling is then lunged on bothreins at the canter which may be repeated on aparticular rein but it is never lunged to exhaustionand the exercise lasts only a few minutes. Thelunging ring is well designed with good acoustics

and a fibresand surface. Horses in training areridden at a fast canter uphill on a polytrack surfacewith members of the panel standing close to theend of the canter to hear the animal pass by. Thisexercise can be repeated if necessary. The horse isthen allowed to settle down after the exercisebefore it is endoscoped. Originally the panelendoscoped horses before exercise but this policywas changed in order to mimic the examination bythe purchaser’s veterinary surgeon and eliminatebias in the exercise test. The horse is scopedwithout a twitch, if possible, and only sedated ifessential and with the agreement of the vendor andpurchaser. The larynx and pharynx are examinedvia the right nostril in order to reduce the parallaxeffect for left sided RLN. During the examinationthe nostrils are blocked and deglutition isstimulated. The panel does not employ a slap test.Until recently each member examined the larynxvia the same endoscope in sequence. A video-endoscope is now used but the examination is notrecorded on tape

Endoscopic criteria for RLN which mean thehorse will be returnable include gross restingasymmetry of the rima glottidis, failure to achievesymmetric or full abduction and failure tomaintain symmetric abduction during a completeinspiration, ie premature weakness. Each panelistforms his own view but sometimes members havediscussed certain aspects such as the character ofthe inspiratory noise or the endoscopic findings. Inmost cases the decision was unanimous but in 11.5% or 41 cases out of 356 between 1989 and 2002majority decisions were reached.

Problems with the system include incompleteexamination by a purchaser’s veterinary surgeonand some veterinarians have a higher percentageof passes among those they return to the panel.Judgement of noise can be difficult in yearlings

40


which are unfit or untrained and very ofteninspiratory noises will disappear with one or twolunging sessions. Panel members occasionallydiffer in their interpretation of the character of theinspiratory noise or on the grading of theendoscopic findings. For some years vendors wereable to insure against their yearling being returnedby the wind panel, either early in the year withouta preliminary test or one month before sellingfollowing a lunging test by their own veterinarysurgeon. The authors suspect that there were somedubious claims.

In the Horses in Training Sales the veterinarysurgeons of purchasers often lunge the horsebefore returning it to the panel. The horse withRLN may make a whistle or roar on the lunge butbe silent when galloped in a straight line.

Other upper airway conditions have includedpharyngeal lymphoid hyperplasia of varyingdegrees. The more severe cases often makeabnormal inspiratory sound, sometimesindistinguishable from the characteristic roar orwhistle required by the Conditions of Sale. Dorsaldisplacement of the soft palate was seen but nonewas permanent and no palatal deformities werefound. One horse with epiglottic entrapment didnot have RLN and was not returnable. Four casesof fourth branchial arch anomalies were identified.One of these showed no evidence of laryngealasymmetry or RLN and was passed. Two werefailed and returned to the purchaser and one wastaken back by the vendor before the panelcompleted its examination. Two cases of rightsided RLN, which did not have fourth branchialarch anomalies, were identified and returnable.Cases of thin, flimsy epiglottis were noted butwere not among those which were failed.

Three studies have been prepared forpublication on the findings of Tattersalls’ panel.

An interesting feature of the Table 1 findingsis that those which were returned on the basis ofsound only performed significantly less well thanthose which were returned with RLN. Figuresfrom Tables 2 and 3 confirmed that the horseswhich were adjudicated as returnable by the panel,raced and won significantly less often than theirsex matched controls sold in the same sale.

The panel periodically review the modusoperandi and diagnostic criteria. They haveconsidered including other congenital and incurable

TABLE 1: Summary of race records of yearlingsreturned for their wind under Tattersalls’Condition of Sale and Control 1978–1984

1978-198327 returned for whistling/roaring only(52% did not run; 22% won; 2.8 average starts per horse)

198428 returned for whistling/roaring and/or RLN.(39.3% did not run; 39% won; 5.9 average starts per horse)

1978-1984 controls – the 2 sold before and the 2 after thereturned lot (19.5% did not run; 37.9% won; 6.67average starts per horse)

Lane et al. (1987)

TABLE 2: Tattersalls Yearling Sales 1987–1995:Summary of matched control study of yearlingsreturned for their wind

1987–1995 (9,524 yearlings sold)78.8% examined by purchasers’ vets1.56% referred to panel0.65% failed0.91% passedAt least 3:1 colts: fillies

1987-1995 Racing PerformanceAged 2–4 yearsPasses 10.85 mean races 1.87 winsControls 9.09 mean races 1.41 wins+Failures 7.32 mean races 0.97 wins*Controls 10.69 mean races 1.42 wins+

S. White Thesis, University of London* Significant difference; + Controls – one soldbefore and one after the lot referred to the paneland of the same sex

TABLE 3: Tattersalls Yearling Sales 1987–1993:Summary of matched control study of yearlingsreturned for their wind

7,463 yearlings sold78.8 examined by purchasers’ vets1.65% referred to panel0.67% failed4: 1 colts: fillies(Sex ratio of all catalogued yearlings 1.27:1)

1987–1993 Racing PerformanceAged 2–4 yearsFailures

Ran 8.48 mean races Won mean 1.32 racesControls – (the 2 sold before and the 2 sold after the referred lot and of the same sex)

Ran 13.71 mean races Won mean 2.18 races

J. Griffiths Project (in preparation) 1987–1993

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disorders such as branchial arch anomaly or palataldefects. However, their low incidence and, in a fewcases of fourth branchial arch anomaly the difficultyof diagnosis, have persuaded them to leave theConditions of Sale unchanged. Also, if otherdiseases were included, endoscopic examination offoals would increase significantly. As the trade inbuying foals to sell on as yearlings is so important,widespread pre-sale scoping of foals would lead tomisleading advice which would not be in theinterests of the horse, purchasers or vendors (Lane etal. 1987). The panel also discussed the use of video-endoscopy but were dissuaded as it was believedthat a recording would have to be made, whichwould then be used for intense discussion bylawyers. More recently this view has been relaxedand the panel are now able to see the endoscopicfindings simultaneously and a better assessment ismade in a shorter period of time.

This task of adjudicating such a Condition ofSale is pragmatic at best and it is not in theinterests of the auctioneers to have too manyyearlings returned as was the case in 1984(2.75%). The percentage of returns has thus restedat less than 1% in the 20 years that the authorshave conducted this task. It has also reduced thenumber of unsound yearlings being submitted tothe sales as vendors have been more careful inchecking them beforehand. No major litigationhas ensued and analysis of our results reassure usthat we are diagnosing a performance-limitingdisease.

REFERENCES

Lane, J.G., Ellis, D.R. and Greet, T.R.C. (1987)Observation on the examination of Thorooughbredyearlings for idiopathic laryngeal hemiplegia.Equine vet. J. 19, 531–536.

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SALES: PROBLEMS IN DIAGNOSIS OF RLN-USAPERSPECTIVE

R. M. Embertson

Rood and Riddle Equine Hospital, P.O. Box 12070, Lexington, Kentucky 40580 USA

INTRODUCTION

Examination of the upper airway (UA) hasbecome an important part of the purchaseexamination performed on horses intended forathletic endeavours. The examination is obviouslydone to avoid purchasing a horse with anabnormality that will adversely affect the ability ofthe horse to train or race. The focus of this paperis the problems encountered evaluating the UA ofthe immature racehorse (weanling, yearling, 2-year-old), particularly in reference to arytenoidfunction.

The Thoroughbred (TB) sales are where mostveterinarians have gained experience in evaluationof the UA of the immature horse. The UAexamination of the yearling at the sales ground inthe USA essentially consists of a quick visualexamination of the head, an endoscopicexamination of the UA (usually through one nasalpassage), and infrequently external palpation ofthe larynx. The TB sales companies have placedconditions of sale in the sales catalogue that allowfor the return of a horse to the seller if specificabnormalities of the UA are found immediatelypost sale. This provides the buyer with reasonableassurance that the UA is normal and theoreticallylessens the need for pre-sale UA endoscopy.However, even though the UA of an individualmay pass the conditions of sale, it may not pass thecriteria the examining veterinarian considersacceptable. This has resulted in pre-sale UAexamination of most horses at the yearling sales.

The UA conditions of sale found in the salescatalogue, in addition to the pre-sale UAexamination has led most vendors to have the UAof their horses evaluated prior to the sale. Thisavoids unwelcome surprises at the sale. The

process has evolved to the point that relatively fewhorses arrive at the sale with one of theabnormalities listed in the conditions of sale. Withthe addition of pre sale scrutiny, it is now rare toencounter a post-sale dispute regarding the UA.The UA abnormalities listed in the conditions ofsale are laryngeal hemiplegia, rostral displacementof the palatopharyngeal arch, epiglotticentrapment, permanent dorsal displacement of thesoft palate, severe arytenoid chondritis orchondroma, sub-epiglottic cyst, and cleft palate.

The definition of laryngeal hemiplegia in theKeeneland catalogue is ‘consistent immobility orinability to fully abduct the arytenoid cartilage’. Inthe Fasig-Tipton catalog the definition is the sameexcept the word ‘consistent’ is replaced by‘complete’. Arytenoid movement is probably thearea of most concern during the UA purchaseexamination.

PERFORMING THE UPPER AIRWAYEXAMINATION

Problems encountered in performing anexamination of the UA can make diagnosis ofrecurrent laryngeal neuropathy (RLN) a difficulttask. The vendor can be uncooperative and allowfew or no UA examinations pre-sale. There hasbeen some concern from vendors regarding theendoscopic procedure physically harming thehorse, especially with popular yearlings that maybe subjected to numerous UA exams. Thepossibility of physical damage to the UA is verylow, but not zero. There has also been someconcern about harm to the sales value of theyearling if a negative opinion of the UA is not keptconfidential.

A few yearlings are intolerant of theendoscopic procedure, making the examination

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itself difficult. This creates a small risk of injury tothe horse or the people involved with theprocedure. Sedation is usually not an option. Thus,experienced handlers become very important.

To address the above concerns, some vendorswill allow only a few experienced veterinarians toexamine endoscopically certain yearlings. Theymay ask other veterinarians wanting to examinethe UA to contact the few veterinarians who didexamine the horse, for their opinion. However, ingeneral, most vendors allow as many UAexaminations as requested. There is a directrelationship between the number of veterinaryexaminations of the UA and the number ofpotential buyers.

INTERPRETING UPPER AIRWAY FINDINGS

Accurate interpretation of the findings from UAexamination is not difficult for most horses as theyare well within normal limits. However, for somehorses this can be challenging. A veterinarian isexpected to determine suitability of the UA forracing during a brief single examination. Thepharynx/larynx is observed at rest, afterswallowing, and usually during nasal occlusion.

In most immature horses the arytenoids arewell abducted throughout much of the UAexamination, or easily maximally abduct followingswallowing, or when the UA is stressed duringnasal occlusion. Rarely is complete paralysis of anarytenoid found in a yearling. In the experience ofthe author’s practice this occurs in less than 0.2%of the general population of thoroughbredyearlings examined during the first three-quartersof their yearling year. The arytenoid function ofyearlings that fall between complete paralysis andrelatively easily achieved maximal abduction canbe difficult to interpret and requires good judgmentto determine suitability for purchase.

It is recognised that many normally functioningarytenoids that are neither perfectly symmetricalnor synchronous, do not become dysfunctional. It isalso generally believed that complete arytenoidparalysis is usually preceded by progressive,deterioration of arytenoid function of variableduration. Thus, when evaluating the UA of a salesyearling the arytenoids that do not function in anideal fashion do raise the level of concern.

It has been noted that arytenoid movement insome yearlings can change mildly over a few toseveral months, over a few days, or even frommorning to afternoon. This may change the

opinion of the examining veterinarian of whetherthe UA is acceptable. Some yearlings areuncooperative and cannot be induced to fullyabduct the left and right arytenoids even with nasalocclusion. The author considers this within normallimits for this age if they are relativelysymmetrical and synchronous. In some yearlingsone arytenoid (usually the left) does not fullyabduct, even with nasal occlusion. The authorconsiders this normal if the arytenoid abducts to atleast 95% of what would be considered maximalabduction.

Is a yearling within normal limits if anarytenoid can fully abduct briefly after swallowingand fully abduct briefly with nasal occlusion, butnot maintain abduction? This becomes a judgmentcall on whether the abduction was maintained longenough to be considered acceptable by theexamining veterinarian.

RECORDING FINDINGS (GRADINGSYSTEMS)

Being able to record endoscopic findings in aconsistent manner is important. This allowssubsequent review of notes to determineaccurately the status of the UA during thatexamination. The veterinarian can then explain toa client or another veterinarian what was seen atthat time. This also provides a comparativereference for a subsequent examination of thesame horse and for UA findings of other horses.

Different grading systems for arytenoidmovement have been used. This can makecommunication between veterinarians difficultunless the actual description of the arytenoidmovement is used. Some of the grading systemsproposed and used have had from 4 to 10 differentcategories for arytenoid movement. Someveterinarians have abandoned these gradingsystems and just describe what was seen. Someveterinarians combine all the findings of the UAendoscopic examination and give the entirepharynx/larynx a letter grade.

A relatively simple grading scale that is easyto use and widely accepted is needed. The problemwith having too few categories is the broad rangeof arytenoid movements that fit in a singlecategory. A system with too many categoriesbecomes too complicated to use easily.

Regardless of the grading system used, somearytenoids will not fit precisely into a specificcategory. However, a widely accepted grading

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system used by veterinarians all over the world,will provide consistent and more accuratecommunication between veterinarians.

PREDICTING FUTURE FUNCTION OF THEARYTENOID

It is now well recognised that arytenoid movementwithin an individual can change over variableperiods of time, both for the better and for theworse. Thus, making accurate predictions inimmature horses for future function can bedifficult. In general the younger the horse, themore difficult this becomes.

It is important for buyers and sellers tounderstand that regarding arytenoid movement,

opinions on suitability for athletic function arebased on the examination performed that day. Thismay result (has resulted) in horses that appearnormal having subsequent problems, and in horsesthat do not quite appear normal, having nosubsequent problems.

There is less risk for the veterinarian and thebuyer to purchase a horse with what is considereda normal UA and avoid purchasing a horse with aquestionable UA, than to take a chance on a horsewith a questionable UA.

In summary, although the knowledgeregarding arytenoid movements in young horseshas improved, there will continue to be very goodracehorses that had less than ideal arytenoidfunction as a young horse.

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SALES: PROBLEMS IN THE DIAGNOSIS OF RLN – AUSTRALASIAN PERSPECTIVE

B. H. Anderson

Ballarat Veterinary Practice, 1410 Sturt Street, Ballarat, Victoria 3350, Australia

In an ideal world treadmill video-endoscopywould be used to determine the clinicalsignificance of varying degrees of recurrentlaryngeal neuropathy (RLN) identified during postsale endoscopic examinations. This is not practicaland so the less perfect procedure of restingendoscopy must be relied on. Unfortunately, thistechnique will not predict with 100% accuracywhich horses will make a ‘whistling’ or ‘roaring’noise at fast exercise.

In New Zealand and Australia a 5-pointgrading system is used to help endoscopistsdetermine the clinical significance of RLN. Grade1 and 2 laryngeal movements are consideredwithin normal limits. Grade 3 laryngealmovements are equivocal. Grade 4 and 5 laryngealmovements are due to clinically significant RLN(supported by a number of treadmill studiesshowing respiratory impairment during fastexercise in these animals). Grade 4 and 5 horsesfail the post sale endoscopic examination.

Horses with Grade 3 laryngeal function passthe post sale endoscopic examination. Endoscopyin these horses reveals slight laryngeal asymmetryat rest but full abduction can be achieved by thearytenoid cartilage. However, activity is generallyreduced on one side (usually the left). Fullbilateral abduction can be stimulated either bypartial asphyxiation (nasal occlusion manoeuvre)or by inducing swallowing, but is frequently notsustained. Although some of these horses mayhave impaired athletic performance, recenttreadmill studies (Lane 2000) indicate that in atleast 75% full bilateral arytenoid abduction ismaintained during fast exercise. Fortunately forendoscopists at sales within the United Kingdom adynamic component is added to the testingprocedure by using ‘wind testing’ and this aidhelps improve accuracy in determining clinically

significant RLN. Under this system horses withGrade 3 laryngeal movements that also make acharacteristic ‘whistle or roaring noise’ whenlunged at the canter, fail post sales examinations.Without the benefit of an exercise test and becausethe majority of Grade 3 horses have normal upperrespiratory tract function at fast exercise, failingsuch horses in New Zealand and Australia wouldbe very problematic. This is an area of caveatemptor and would seem to be fair to both vendorsand purchasers.

Using a static method to describe a dynamicprocess has limitations. A wide range of defectivelaryngeal movements exist and cut off points cannever be as precise as one would wish. Problemcases are likely. In addition, even apparentlynormal horses (Grade 1 or 2 laryngeal movementsat rest) have been found to have abnormallaryngeal movements (Grade 3–5 or dynamicarytenoid collapse) (Kannegieter and Dore 1995;Lane 2000) and respiratory noise when gallopedon the treadmill. Furthermore, it is sobering toappreciate that the progression of RLN inThoroughbred horses to degrees which may beclinically important is estimated as 5–15%,(Anderson et al. 1997; Dixon et al. 2002). Morealarming for endoscopists however is that thisprogression may occur quickly, over some fewweeks or months.

The challenge in the sales environment is to beconfident that a horse can fully abduct thearytenoid cartilages. As a matter of qualitycontrol, all horses with Grade 3 laryngealmovements are examined by a secondveterinarian. In horses in which laryngeal abductorfunction is questionable, video-endoscopicexamination is made and reviewed carefully todetermine that full symmetrical abduction of bothcartilages is present.

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Recently, it has come to the attention ofexamining veterinarians that some of the horsesthey are examining appear sedated. On entrance tothe stall, such horses are quiet, often have a lowerhead carriage, droopy lips and may have slightprotrusion of the third eyelid. The use of suchdrugs as acetylpromazine and valium by vendorsmay be the cause. It is clear from experience anddocumented literature that some sedative agents,notably xylazine, can reduce the range andfrequency of laryngeal movements. Often horseswhich had normal movements (Grade 1 and 2) willdevelop Grade 3 laryngeal movements followingsedation. While it is unlikely that Grade 4laryngeal movements will be induced followingsedation it is possible that horses with Grade 3movements which may be borderline (ie havedifficulty in achieving full arytenoid abduction)could be altered to such a degree that determiningaccurately if full arytenoid abduction is attainedcould be difficult. Veterinarians are advised that iftheir clients are using such agents to ‘calm’ horsesin the sales environment, this may jeopardise the

interpretation of laryngeal function byendoscopists. Certainly the horses most at risk arethose with some degree of neuromusculardysfunction. Presumably sedative agents work ondepression of neuromuscular function.

REFERENCES

Anderson, B.H., Kannegieter, N.J., Goulden, B.E. (1997)Endoscopic observations on laryngeal symmetryand movements in young racing horses. N. Z. vet. J.45, 188-192.

Dixon, P.M., McGorum, B.C., Railton, D.I., Hawe, C.,Tremaine, W.H., Pickles, K. and McCann, J. (2002)Clinical and endoscopic evidence of progression of152 cases of equine recurrent laryngeal neuropathy(RLN). Equine vet. J. 34, 29-34.

Kannegieter, N.J., Dore, M.L. (1995) Endoscopy of theupper respiratory tract during treadmill exercise: aclinical study of 100 horses. Aust. vet. J. 72, 101-107.

Lane, J.G. (2000) Assessment of upper airwayobstruction and high-speed treadmill endoscopy.Proc. Racehorse Practice Conf. Newmarket,England, 22nd –24th June.

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DIFFERENCES BETWEEN RESTING AND TREADMILLENDOSCOPIC FINDINGS IN REGARD TO RLN

J. G. Lane


Earlier in this workshop presentations were maderegarding a series of schemes by which to gradeequine laryngeal motility during quiet breathing,ie when the patient is standing in the stable or hasrecently returned from exercise. In fact, for themajority of equine clinicians such endoscopicexaminations form the lynch-pin for diagnosis inhorses showing signs suggestive of dynamic upperrespiratory tract (URT) obstruction, but howdependable are the findings.

The acid test for any grading scheme forrecurrent laryngeal neuropathy (RLN) must behow well the findings at rest translate into thelaryngeal function during maximal exercise. Themost common cause of disquiet or dispute inregard to the interpretation of endoscopic findingsin horses arises with those horses showing Grade3 RLN motility, ie the 18% of the total populationwhich show asymmetry during quiet breathing butwhich are capable of full symmetrical abductionafter swallowing or during the nostril occlusionmanoeuvre. Prospective purchasers at sales areadvised frequently not to bid for such animals,either because it is perceived that Grade 3represents a performance-limiting malfunction asit stands, or that horses showing such laryngealmotility are likely to deteriorate to become Grade4 or 5 later. What evidence is there that either ofthese perceptions are true?

Dixon et al. (2002) have shown that isolatedindividual horses from all RLN grading groupsmay show progression of malfunction and thathorses with Grades 1 and 2 (sic) scores are no lesslikely to sustain deterioration of laryngeal functionthan those showing Grades 3 and 4 (sic) motility.Earlier Baker (1983) had suggested that for theoverwhelming majority of horses laryngealfunction, as perceived endoscopically, remainsunchanged throughout life.

In a study of 459 Thoroughbred horsesreferred to the University of Bristol's EquineSports Medicine Centre the RLN gradings ofhorses examined at rest on arrival were comparedwith the diagnosis achieved by endoscopy duringhighspeed treadmill endoscopy (HSTME) seeTable 1 (Franklin 2002).

Thus, in a selected population of horses thatwere referred for the investigation of poorperformance, often with a history of abnormalrespiratory noise, only 29/82 (35%) animals withGrade 3 RLN at rest were confirmed to showdynamic collapse of the left arytenoid cartilageand/or vocal fold during treadmill exercise. Theseresults also show that there were isolated cases(19/338–5.6%) where horses showing ‘normal’laryngeal motility – Grades 1 and 2 - during quietbreathing showed dynamic arytenoid or cordcollapse under exercise conditions. Also, 4/23(17%) of horses with Grade 4 RLN failed to showdynamic collapse of the vocal fold or arytenoid

TABLE 1: Comparison between laryngealfunction at rest and findings during highspeedtreadmill endoscopy in 459 Thoroughbredhorses

82 Grade 1 at rest yielded 1 ACC ontreadmill

3 VCC

256 Grade 2 at rest yielded 11 ACC4 VCC



6 Grade 5 at rest yielded 6 ACC

Others 10

ACC = arytenoid cartilage collapseVCC = vocal cord collapse

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cartilage although the rima glottidis was slightlyasymmetric at all stages of the exercise test. Theseobservations are at odds with a previous reportwhich came to the more simplified conclusion thatall horses with Grade 1 and 2 RLN showed fullsustained abduction during treadmill exercise(Morris and Seeherman 1990), and the same authorsreported that 20 out of 27 horses with Grade 4 RLN(sic) showed ACC or VCC during treadmill exercise(Morris and Seeherman, 1991). Kannegeiter andDore (1995) also used the 1–5 grading scheme andshowed that while resting scores provide a usefuloverall guide, exceptional horses appear ‘normal’ atrest but sustain dynamic collapse during treadmillexercise and, vice-versa, that a small number of‘abnormal’ horses become 'normal' under exerciseconditions. In all instances where dynamic collapseof the vocal cord and/or arytenoid cartilage occurredin the Bristol cases there was an obvious inspiratorynoise, and in most instances, palpable atrophy of theintrinsic musculature on the left side of the larynxwas detected.

To the unaided human ear the inspiratory noisesproduced by horses afflicted with axial deviation ofthe ary-epiglottal folds (ADAEF) is notdistinguishable from the ‘roaring’ or ‘whistling’associated with RLN. In this series of 459 horsesthere were 10 horses with ADAEF and no otherconcurrent form of dynamic collapse in the URT, 40where it was associated with palatal malfunction,and 7 where there was concurrent dynamic collapseof the arytenoid or vocal fold. These findings arecomparable with those reported elsewhere (Parenteet al. 1994; Kannegeiter and Dore 1995; King et al.2001). The overall conclusion is that URTobstructions are commonly complex with thedynamic collapse of multiple structures which canonly be established by HSTME.

Clearly, not all clinicians have access to thefacilities for endoscopy during highspeedtreadmill exercise. The observations aboveconfirm that endoscopy at rest should never beused in isolation from other diagnostic techniques,and that the possibility of erroneous diagnosis isreduced considerably when endoscopy is used inconjunction with palpation findings andattendance at an exercise test to listen foruntoward respiratory noises.

REFERENCES

Baker, G.J. (1983) Laryngeal asynchrony in the horse:definition and significance. In: Equine ExercisePhysiology, Eds: D.H.Snow, S.G.B.Persson andR.J.Rose. Granta Editions, Cambridge, 46-55

Dixon, P.M., McGorum, B.C., Railton, D.I., Hawe, C.,Tremaine, W.H., Pickles, K. and McCann, J. (2002)Clinical and endoscopic evidence of progression in152 cases of equine recurrent laryngeal neuropathy(RLN). Equine vet. J. 34, 29-34.

Kannegeiter, N.J. and Dore, M.L. (1995) Endoscopy ofthe upper respiratory tract during treadmill exercise:a clinical study of 100 horses. Aust. vet. J. 72, 101-107.

King, D.S., Tulleners, E.P., Martin, B.B., Parente, E.J.and Boston, R. (2001) Clinical experiences withaxial deviation of the aryepiglottal folds in 52racehorses. Vet. Surg. 30, 151-160.

Morris, E.A. and Seeherman, H.J. (1990) Evaluation ofupper respiratory tract function during strenuousexercise in racehorses. J. Am. vet. med. Ass. 196,431-438.

Morris, E.A. and Seeherman, H.J. (1991) Clinicalevaluation of poor performance in the racehorse: theresults of 275 evaluations. Equine vet. J. 23, 169-174.

Parente, E.J., Martin, B.B., Tulleners, E.P. and Ross,M.W. (1994) Upper respiratory dysfunctions in thehorse during high-speed exercise. Proc. Am. Ass.Equine Pract. 40, 81-82.

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NON-RLN UPPER RESPIRATORY TRACT DISORDERSFOUND IN A SURVEY OF 3,497 THOROUGHBREDYEARLINGS

J. G. Lane


Surveys of structural and functional abnormalitiesof the upper respiratory tract of the horse havepreviously been based upon selected populations,for example, those submitted to public sales (Laneet al. 1987) or in training (Pascoe et al. 1981;Raphael 1982; Baker 1983; Sweeney et al. 1991),where unsaleable or untrainable individuals willhave been excluded earlier. In addition, no surveyof dynamic dysfunctional conditions, occurringonly under exercise, has been attempted to date.Thus, it is generally held that dorsal displacementof the soft palate (DDSP) and recurrent laryngealneuropathy (RLN) are the 2 most frequentlyencountered disorders of the region. Theprevalence of non-RLN upper respiratory tract(URT) disorders found during the video-endoscopic study of 3,497 yearlings was asfollows:

Fourth branchialarch defects (4-BAD) 7 cases 0.20%

Sub-epiglottal cyst (SEC) 5 cases 0.14%

Epiglottal entrapment (EE) 2 cases 0.06%

Right laryngealmalfunction 5 cases 0.14%

Hast (1972) has described the development of thelarynx in the early human embryo and showed thatthe extrinsic structures are derived from the fourthbranchial arch and the intrinsic structures from thesixth arch. 4-BAD is a syndrome of irreparablecongenital defects resulting from a failure ofdevelopment of some or all of the derivatives of thefourth branchial arch (Lane 1993). The structuresinvolved are the wings of the thyroid cartilage, thecricothyroid articulation, the cricothyroideusmuscles and the cricopharyngeal sphinctermuscles. Any permutation of aplasia or hypoplasiaof these structures may arise uni- or bilaterally.

The condition has been identified in otherbreeds such as the Hanovarian, warmbloods,Welsh Section A ponies and the Haflinger (Cook1974; Goulden et al. 1976; Wilson et al. 1986;Deegan and Klein et al. 1987; Klein et al. 1989;Dixon et al. 1993). Generally, has been reportedunder titles such as rostral displacement of thepalato-pharyngeal arch (RDPA) orcricopharyngeal-laryngeal dysplasia.

The author has reviewed the findings in 60 4-BAD-afflicted Thoroughbred horses and theresults are summarised here. The presenting signsof horses with 4-BAD are variable and reflect theseverity of the absence of the structures involved.However, in order of frequency, the signs areabnormal respiratory sounds at exercise (50 out ofthe 60 horses), belching (13), nasal discharge (10),coughing (10) and recurrent colic (5). Theinvoluntary aerophagia and eructation sometimesmay be confused with the noises produced by‘wind-suckers’.

There is no current evidence that the syndromeis genetically transmitted. A complete evaluationof the extent of 4-BAD can only be made atexploratory surgery or autopsy but the combinedfindings of palpation, endoscopy and radiographyare generally sufficient to justify a diagnosis.When the cartilage components are defective, anunusually wide gap can be palpated between thecaudal margin of the thyroid and the rostral edgeof the cricoid, whereas in the normal larynx the 2structures overlap. The 2 endoscopic features toalert the clinician to the possibility of 4-BAD areRDPA (33 cases) where the caudal pillars of thesoft palate form a cowl, which partly obscures thecorniculate processes dorsally and defectivearytenoid motility (45 cases). 4-BAD is the mostcommon explanation for apparent right sided RLN(Tulleners et al. 1996) and there is a marked over-

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representation of right sided cases. In the 60 cases15 were bilateral, 39 were right unilateral and in 6the defects were confined to the left side. In oneinstance 4-BAD was only detected as dynamicRDPA during treadmill exercise. RDPA itself issimply an endoscopic symptom of a majorunderlying laryngeal disorder and should not beregarded as a disease in its own right. It ariseswhen the upper oesophageal sphincter muscles arenot present to provide an anchor for the palatalarch caudal to the apices of the corniculateprocesses of the arytenoid cartilages. When thecrico- and thyro-pharyngeus muscles are absent,there is a failure to close the upper oesophagus sothat lateral radiographs will reveal a continuouscolumn of air extending from the pharynx into theoesophagus. The RDPA is seen as a ‘dew drop’intruding into this air column from the dorsal wall.Repeated aerophagia leaves those animals withoutan upper oesophageal sphincter susceptible toepisodes of colic which may be life threatening.Three horses have died or been destroyed throughtympanitic and one other has required surgicaldecompression.

The performance records of 51 of the horseshave been traced: 22 were unnamed; 29 werenamed but unraced; 11 raced but were unplaced; 4were placed and 7 won, albeit all in minorcompetitions. Thus, horses afflicted with 4-BADare generally ineffective athletes.

Five cases of right laryngeal malfunction,other than the 7 cases of 4-BAD, were identified inthe stud survey of yearlings. Three of these werelater subjected to surgery with a view to prostheticlaryngoplasty, but were found to be inoperable byvirtue of hypoplasia of the muscular process of theright arytenoid cartilage. Given that the arytenoidcartilages develop from the sixth branchial archshould a 6-BAD syndrome be added to the clinicalvocabulary?

It is generally believed that sub-epiglottalcysts are congenital and if this is so the incidenceof 0.14% demonstrates that the disorder is indeedrare. In contrast the aetiopathogenesis of epiglottalentrapment is not known and the results ofrepeated endoscopic examinations confirm that atleast some cases are acquired. Thus, theidentification of only 2 cases in 3,497 yearlingsdoes not reflect the overall incidence. Similarly,

arytenoid chondropathy is known to be anacquired disorder and a failure to record a singlecase even in quite a large population of younghorses is not significant.

REFERENCES

Baker, G.J. (1983) Laryngeal asynchrony in the horse:definition and significance. In: Equine ExercisePhysiology, Eds: D.H.Snow, S.G.B.Persson andR.J.Rose. Granta Editions, Cambridge, 46-50.

Cook, W.R. (1974) Some observations on diseases of theear, nose and throat in the horse, and endoscopy usinga flexible fibreoptic endoscope. Vet. Rec. 94, 533-541.

Deegen, E, and Klein, H.J. (1987) Rostrale verlagerungdes arcus palatopharyngicus beim pferd.Pferdeheilkunde 3, 303-308.

Dixon, P.M., McGorum, B.C. and Else, R.W. (1993)Cricopharyngeal-laryngeal dysplasia in a horse withsudden clinical onset of idiopathic laryngealhemiparesis. N.Z. vet. J. 41, 134-138.

Hast, M.H. (1972) Early development of the humanlaryngeal muscles. Ann. Otol. Rhino. Laryngol. 81,524.

Goulden, B.E., Anderson, L.J., Davies, A.S. and Barnes,G.R.G. (1976) Rostral displacement of thepalatopharyngeal arch: a case report. Equine vet. J.8, 95-98.

Klein, H.J., Deegen, E., Stockhofe, N. and Wissdorf, H.(1989) Rostral displacement of the palatopharyngealarch in a seven-month-old Hanovarian colt. Equinevet. J. 21, 382-383.

Lane, J.G., Ellis, D.E. and Greet, T.R.C. (1987)Observations on the examination of Thoroughbredyearlings for idiopathic laryngeal hemiplegia.Equine vet. J. 19, 531-536.

Lane, J.G. (1993) Fourth branchial arch defects in thehorse. Proceedings of the 15th Bain-FallonMemorial Lectures Aust. equine vet. Ass., 209-212.

Pascoe, J.R., Ferraro, G.L., Cannon, J.H., Arthur, R.M.and Wheat, J.D. (1981) Exercise-inducedpulmonary haemorrhage in racing Thoroughbreds: apreliminary survey. Am. J. vet. Res. 42, 703-707.

Raphael, C.F. (1982) Endoscopic findings in the upperrespiratory tract of 479 horses. J. Am. vet. med. Ass.181, 470-473.

Sweeney, C.R., Maxson, A.D. and Soma, L.R. (1991)Endoscopic findings in the upper respiratory tract of678 Thoroughbred racehorses. J. Am. vet. med. Ass.198, 1037-1038.

Tulleners, E.P., Ross, M.W. and Hawkins, J. (1996)Management of right laryngeal hemiplegia inhorses: 28 cases. Vet.. Surg. 25, 439.

Wilson, R.G., Sutton, R.H. and Groenendyk, S. (1986)Rostral displacement of the palatopharyngeal archin a Thoroughbred yearling. Aust. vet. J. 99-100.

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NON-RLN URT DISORDERS IDENTIFIED DURING POSTSALE ENDOSCOPIC EXAMINATION OF 5,559 TBYEARLINGS (1997-2002) IN NEW ZEALAND

B. H. Anderson

Ballarat Veterinary Practice, 1410 Sturt Street, Ballarat, Victoria 3350, Australia

At the 1995 National Thoroughbred Yearling salesin New Zealand, post sale endoscopicexaminations of the larynx and pharynx wereintroduced. Following the fall of the hammer, thepurchaser is given the opportunity to have his/herhorse endoscoped by a veterinarian – approved bythe auctioneer – who then examines the larynx andpharynx of the presented horse for the presence of,and only of, one or more of the following 6conditions: a) Laryngeal hemiplegia; b)Subepiglottic cyst(s); c) Persistent dorsaldisplacement of the soft palate; d) Epiglotticentrapment; e) Rostral displacement of thepalatopharyngeal arch; and f) Arytenoid chondritisor chondroma. The examination is of a pass or failnature and the endoscopist is under no obligationto reveal the findings of the examination to thepurchaser or vendor and merely records the result.

Of the 5,559 horses examined between1997–2002 (Tables 1 and 2), 41 failed theconditions of sales, a failure rate of 0.74%. Eightof these horses had left sided recurrent laryngealneuropathy (RLN) and will not be discussedfurther. A further 3 horses had markedly deficientright sided arytenoid cartilage abduction,presumably due to RLN.

Of the other 30 horses 19 failed due toinflammatory conditions, including 12 due toarytenoid chondritis, 6 because of mechanicalinterference with arytenoid abductor function(principally pharyngeal/guttural pouch masses orsevere epiglottic inflammation) and one withepiglottic chondritis. A further 11 horses failedbecause of non-inflammatory lesions including 2horses with persistent dorsal displacement of thesoft palate, 5 horses with epiglottic entrapment, 3horses with rostral displacement of thepalatopharyngeal arch and one horse withhypoplasia of the soft palate.

These results indicate that less than 1% ofhorses presented for post sale endoscopy fail theexamination and that inflammatory conditionsaccounted for 46% (19/41) of all failures witharytenoid chondritis the most common (30% or12/41). Follow up showed that in a significantnumber of horses (42% or 17/41), which failed theconditions of sale on the day of examinationtreatment, either surgical or medical, resulted in asaleable horse.

It is interesting to note the high number ofhorses affected with arytenoid chondritis.Compared to results from other endoscopic

TABLE 1: Number of endoscopic examinations at the National Yearling Sales (1997–2002) and failurerate

Year No. endoscopic No. horses failing Percent of horses failing examinations conditions of sale conditions of sale

1997 691 4 0.581998 928 8 0.861999 698 3 0.422000 1,028 12 1.22001 1,161 5 0.432002 1,053 9 0.86Total 5,559 41 0.7

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examinations at sales around the world, theproblem is unusually common in New Zealand.The exact reasons for this are unknown.

In addition, a number of horses have beenrecognised that have arytenoid mucosal injury(Anderson 2000). These mucosal injuries manifestas small erosions/ulcers, or alternatively, raisedareas of epithelial injury. They are found on themedial surface of each arytenoid just above wherethe vocal cords join onto the arytenoid cartilages(the vocal processes) and may also be found on thevocal cords themselves. They may be hyperaemicor even have small, slightly purulent centres andcan vary in colour from red to white. Althoughoccasionally unilateral most often there are 2lesions, one on either cartilage and they arereferred to as ‘kissing lesions’. Even if thereappears to be only one lesion, close scrutiny of theopposite arytenoid cartilage usually reveals asmall area of accompanying injury. The exactcause of these lesions is not known. Reports in the

literature regarding such lesions in horses aresparse but they have been reported in yearlingThoroughbreds at horse sales in Australia (Kelly etal. 2003). Review of laryngeal diseases andinjuries in man, cattle and other species indicatesthat the cause(s) of these injuries is likelymultifactorial with infectious causes having amajor role (Fig 1). Mucosal inflammation ormucositis occurs and is followed by mucosalulceration when the superficial epthelium isdenuded. Because there is no submucosa, themucosal epithelial layer is tightly adhered to theunderlying perichondrium of the arytenoidcartilage. Pressure, the result of both intrinsic andextrinsic trauma over the thin, relatively immobile,mucosal layer results in erosion and ulceration.Once the mucosal barrier is breeched bacterialinfection of the underlying structures is possible.If the infection remains localised a relatively quickhealing response occurs with or without the use ofantibitotic/anti-inflammatory treatment. Healing

TABLE 2: Reasons for and number of horses failing conditions of sale at the National Yearling Sales(1997– 2002)

Condition Number Comments

Arytenoid chondritis 12 Some horses with focal lesions have beentreated by debridement and have been sold or are racing

Epiglottic entrapment 5 All treated and sold

Persistent dorsal displacement of 2 Both resolved with antibiotic/anti-soft palate inflammatory treatment

Right side Grade 4 or 5 3 Aetiology unknownlaryngeal movements 1 horse had grade 4 laryngeal

movements and rostral displacement of the palatopharyngeal arch

Right side Grade 4 or 5 4 3 dorsopharyngeal massesmovements due to mechanical 1 severe epiglottic inflammation obstruction All resolved with treatment

Left side Grade 4 or 5 laryngeal movements (ILH) 8 1 horse had what appeared to be a

unilateral rostral displacement of the pharyngeal arch as well as ILH7 horses ILH

Left side Grade 4 or 5 laryngeal 2 1 dorso pharyngeal mass movements due to mechanical 1 severe epiglottic inflammationobstruction All resolved with treatment

Rostral displacement 3palatopharyngeal arch

Chondritis left side of epiglottis 1 Failed because the chondritisresulted in an obstruction of the rima glottidis

Hypoplasia ofsoft palate 1 Broken in, trialled but retired

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Infectious Agents

- Viruses

- Bacteria

- Fungi

ArytenoidMucosal

Inflammation andOedema

Respiratory Irritants

- Ammonia

- Feed and barn dust

Extrinsic Trauma

- Naso/orotracheal intubation

- Course feed stuffs

Allergic and Immune

Mediated Processes

Intrinsic Trauma

- Vocalisation

- Coughing

- Throat clearing

- Endoscopy +Pressure over

immobile

epithelium/mucosa

MucosalUlceration

Uncommon Common• Deep infection in

submucosa and

perichondrium

• Cartilage infection and

proliferative granulation

tissue production

Cartilage swelling and

distortion

• Perilaryngeal tissues

affected

• Cricoarytenoid joint

affected

• Incomplete abduction

ArytenoidChondritis

Laser

Focal Curettage

Arytenoidectomy

• Superficial

mucosal/submucosal

infection

• Minimal granulation

tissue production

• Cartilage not affected

Arytenoid MucosalInjury

Topical and/or systemic

antibiotics and anti-

inflammatories

Wound Healing 7-21 d

Fig 1: Suggested pathogenesis and outcome of arytenoid mucosal injury.

occurs by epithelialisation, mild fibroplasia(granulation tissue production) and somecontraction. Typically, the underlying arytenoidcartilage is not affected. The potential for suchinjuries to progress to the more serious arytenoidchondritis (discussed below) is thought to be low(Smith 2000; Kelly et al. 2003; B.H. Anderson,unpublished data) but happens occasionally. Kellyet al. (2003) reported idiopathic mucosal lesionsof the arytenoids cartilages in 21 Thoroughbred

yearlings (0.63% of 3,312 horses having post saleupper respiratory tract examinations over a 5 yearperiod). In 2 horses (10%) granulomas developedat the site of ulceration and in one horse (5%)chondropathy developed.

Strictly defined, arytenoid chondritis meansinflammation of the arytenoid cartilage. However,the condition usually referred to as arytenoidchondritis is an inflammatory swelling involvingthe arytenoid cartilage, peri-arytenoid tissue,

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laryngeal mucosal surface and dorsal muscularstructures. Endoscopically this condition isrecognised as a medially displaced, swollen, mis-shapen, arytenoid cartilage. In most cases thecartilage is reddened or hyperaemic. There may bereduced or absent cartilage movement in moresevere cases. Discharging pus-filled lesions on themedial border of the arytenoid cartilage may bepresent as well as ulcers or epithelial swellings(‘kissing lesions’) on either cartilage. Intra-luminal projections of granulation tissue may alsobe present.

It is not clear what factors or conditions areimportant in determining if infection becomesestablished within the arytenoid cartilage ratherthan remaining in superficial tissues. What hasbecome difficult in the sales environment isdetermining if infection or inflammation isconfined only to the mucosa or if cartilage isinvolved. Differentiating generalised mucosaloedema from cartilage enlargement, and

determining if luminal projections of granulationtissue involve the underlying cartilage or not isnot always easy. Experience gained from surgicaltreatment has revealed that if luminal projectionsof granulation tissue are marked, invariably theunderlying cartilage is affected. However, eachcase is considered ‘on the day’ and a decision onthe absence or presence of chondritis is aided bycareful examination of video-endoscopicpictures.

REFERENCES

Anderson, B.H. (2000) Post sale endoscopicexamination of horses in New Zealand. Proc.EquineSeminar, Wairakei, 71-76.

Kelly, G., Lumsden, J.M., Dunkerly, G. (2003)Idiopathic mucosal lesions of the arytenoidcartilages of 21 Thoroughbred yearlings: 1997-2001. Equine vet. J. 35 (3), 276-281.

Smith, R.L. (2000) Arytenoid Chondritis in Horses andOther Species. Thesis, Massey University,Palmerston North, New Zealand.

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NON-RECURRENT LARYNGEAL NEUROPATHY (RLN)CAUSES OF EQUINE LARYNGEAL PARALYSIS

B. McGorum and P. M. Dixon

Department of Veterinary Clinical Studies, Easter Bush Veterinary Centre, University of Edinburgh,Roslin, Midlothian EH25 9RG, UK

Non-recurrent laryngeal neuropathy (non-RLN)accounts for the small proportion (6% Gouldenand Anderson 1981; 11% Dixon et al. 2001) ofhorses with laryngeal paralysis in which aprobable cause can be identified. Conversely, RLNcases have no such detectable underlying cause.

Non-RLN laryngeal paralysis may be a sequelto localised injury to the vagus or recurrentlaryngeal nerves at any site along their circuitouscourses. Such injury may occur in disorders of theguttural pouch (mycosis, rupture of the rectuscapitis ventralis muscles, temporohyoid fracture,trauma), pharynx (trauma, abscessation,neoplasia), neck (perivascular/perineural irritantinjection reactions, trauma, iatrogenic nervedamage during oesophageal and thyroid surgery)or mediastinum (neoplasia, abscessation). Non-RLN paralysis may also be a manifestation of ageneralised disorder, eg a polyneuropathy ormyopathy. Bilateral laryngeal paralysis, which isconsiderably less common (2–6%) than unilateralparalysis, almost invariably results fromgeneralised neuromuscular disorders.

Liver disease is a common cause of bilaterallaryngeal paralysis (Mayhew 1989; Pearson 1991;McGorum et al. 1999). McGorum et al. (1999)recorded bilateral laryngeal paralysis in 7 of 50horses with primary hepatic disease, all of whichhad hepatic encephalopathy and hyper-ammonaemia. All cases presented with loudinspiratory stridor and many were referred forinvestigation of suspected primary upperrespiratory tract obstruction. In all cases,endoscopy revealed total bilateral paralysis, withboth arytenoids passively adducted to the midlineduring inspiration. Ponies were affected moreoften than horses, but this probably reflects anincreased frequency of liver failure in poniesrather than increased susceptibility. The laryngeal

paralysis was often temporary, worsening duringexacerbations of encephalopathy and resolvingwith restoration of hepatic function. No gross orhistopathological abnormalities were identified inthe laryngeal muscles, the recurrent laryngealnerve or other peripheral nerves of affected horses.

The pathogenesis of this complication remainsunclear. Most reported cases are in horses withliver failure and hepatic encephalopathy, but it isunknown whether it occurs with compensatedliver disease. Similarly, while it is reported inhorses with pyrrolizidine alkaloid induced liverdisease (Pearson 1991; McGorum et al. 1999), therole of this substance, which may be neurotoxic(Cooper and Huxtable 1999), is unclear. As thelaryngeal paralysis may be temporary, and nohisto-pathological lesions have been identified, itmay reflect neuromuscular dysfunction rather thanpathology. Such dysfunction could occur bymechanisms akin to those that cause hepaticencephalopathy. Alternatively, it may represent aform of peripheral neuropathy, a common sequelto human hepatic disease. The pathogenesis ofperipheral neuropathy in human liver diseasepatients is unknown, but may involve metabolicinhibition of axonal membrane function,metabolic damage to Schwann cells and/ordisordered insulin metabolism akin to diabeticneuropathy.

Interestingly, all 3 ponies with liver diseaseinduced bilateral laryngeal paralysis that had post-mortem examinations, also had pituitaryadenomas, but no overt clinical hyperadreno-corticism (McGorum et al. 1999). While pituitaryadenomas are relatively common in older ponies,and may not relate to the laryngeal dysfunction,increased production of pituitary derived peptidesmay contribute to the pathogenesis of thiscomplication. However, Pearson (1991) made no

56


reference to pituitary adenomas in 2 ponies withliver failure and inspiratory dyspnoea, which weresubjected to detailed post mortem examination.

Rarely, horses may develop post operativelaryngeal paralysis, sometimes complicated bysecondary severe pulmonary oedema and/orhaemorrhage (Abrahamsen et al. 1990; Dixon etal. 1993, 2001). These cases had variable recoveryof laryngeal function, with one horse showingcomplete resolution within 24 h, while another hadresidual laryngeal dysfunction after one year.Post-operative laryngeal paralysis was most likelyto have resulted from excessive head/neckextension, which could induce neural stretchinjury or cause neural hypoxia via occlusion of thevasa nervorum. Alternatively, laryngeal paralysismay have resulted from compression of therecurrent laryngeal nerve against a rigid structurein the neck. Myopathy, persistent hypoxia and pre-existing laryngeal dysfunction are additionalfactors that may contribute to development of thiscomplication. Temporary post operative laryngealparalysis has also been reported in a dog.

A variety of toxic peripheral neuropathies maycause equine laryngeal paralysis including delayedorganophosphate induced toxicity, Australianstringhalt, lead poisoning and plant poisoning.However in all such cases, laryngeal paralysis isclearly part of generalised disorder that affectsmultiple nerves, and so presents little diagnosticproblem. Delayed organophosphate inducedtoxicity leads predominantly to degeneration oflong axons in peripheral nerves and spinal cord, andresults from covalent binding of organophosphatesto ‘neuropathy target esterase’. Organophosphateinduced laryngeal paralysis may be permanent(Rose et al. 1981; Duncan and Brook 1985).Ingestion of 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 causesneuropathy with distal axonal degeneration.Feeding experiments with Lathyrus sativus (Indianvetch) indicated that, even with prolonged feeding,only a minority of horses were affected. Leadtoxicosis primarily targets peripheral nerves, andapproximately 13% of horses with lead toxicosisdevelop laryngeal dysfunction (Sojka et al. 1996),which may or may not recover with time. Thepathogenesis of lead neurotoxicosis is multi-factorial and includes inactivation of thiol andcysteine-containing enzymes, and Zn-, Cu-, Fe-

dependent enzymes, resulting in neural oxidativestress, and toxicity of cell membranes resulting inincreased membrane permeability.

Hyperkalaemic periodic paresis, a generalisedmyasthenic disorder, commonly presents withepisodic upper airway obstruction. While airwayobstruction in this disorder is multi-factorial,laryngeal spasm or paralysis occurs inapproximately half of affected horses. The severityand incidence of upper airway dysfunction may bereduced 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 afterinhalation anaesthesia in a horse. J. Am. vet. med.Ass. 197, 1363-1365.

Carr, E.A., Spier, S.J., Kortz, G.D., and Hoffman, E.P.(1996) Laryngeal and pharyngeal dysfunction inhorses homozygous for hyperkalemic periodicparalysis. J. Am. vet. med. Ass. 209, 798-803.

Cooper, R.A. and Huxtable, R.J. (1999) The relationshipbetween reactivity of metabolites of pyrrolizidinealkaloids and extrahepatic toxicity. Proc. WestPharmacol. Soc. 42, 13-16.

Dixon, P.M., Railton, D.I., and McGorum, B.C. (1993)Temporary bilateral laryngeal paralysis in a horseassociated with general-anaesthesia and postanesthetic 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 of 375 cases in amixed-breed population of horses. Equine vet. J. 33,452-458.

Duncan, I.D. and Brook, D. (1985) Bilateral laryngealparalysis in the horse. Equine vet. J. 17, 228-233.

Goulden, B.E. and Anderson, L.J. (1981) Equinelaryngeal hemiplegia part II: some clinicalobservations. N. Z. vet. J, 29, 194-198.

Mayhew, I.G. (1989) Large Animal Neurology. Lea andFebiger, London.

McGorum, B.C., Murphy, D., Love, S., and Milne, E.M.(1999) Clinicopathological features of equineprimary hepatic disease: a review of 50 cases. Vet.Rec. 145, 134-139.

Pearson, E.G. (1991) Liver failure attributable topyrrolizidine alkaloid toxicity and associated withinspiratory 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 withoral haloxon administration. Equine vet. J. 13, 171-176.

Sojka, J.E., Hope, W., and Pearson, D. (1996) Leadtoxicosis in 2 horses: similarity to equinedegenerative lower motor neuron disease. JVIM 10,420-423.

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SESSION 5:

Treatment of equinelaryngeal paralysis

Chairman: Geoff Lane

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59


DECISION MAKING IN PRACTICE FOR TREATMENTOF RECURRENT LARYNGEAL NEUROPATHY

T. R. C. Greet

Rossdale & Partners, Beaufort Cottage Equine Hospital, Cotton End Road, Exning, Newmarket, SuffolkCB8 7NN, UK

Recurrent laryngeal neuropathy is one of thecommonest respiratory conditions encountered inequine practice. Nowadays endoscopy is availableand used routinely in the vast majority ofpractices, and confirmation of the diagnosis in atleast the more advanced case is relativelystraightforward. It is the interpretation in the lessseverely affected horse that represents a far greaterchallenge to the less experienced clinician and onethat can lead to difficulty when treatment optionsare to be considered.

The author has used a 10 grade assessment ofthe disease based upon the endoscopic appearanceof laryngeal function and at least 3 other systemswill be discussed at this meeting. The key factor indeciding what, if any, surgical therapy is appropriatefor an individual horse, is the degree of its disability,which can be extremely difficult to assess.

Having briefly and unsuccessfully usedneuromuscular pedicle grafting, the author’ssurgical treatments are based upon moretraditional approaches. In the UK, surgicalablation of the vocal cord and ventricle are stillaccepted as valid procedures in the ‘noisy’ horsewith satisfactory performance. In the author’shospital this is performed this using a diode orNd:YAG laser in the standing patient. This hasproved an attractive option for clients, although nomore effective than using the traditional approach.The author believes that it is of benefit whencombined with laryngoplasty in reducing theincidence of wound problems significantly.

Laryngoplasty is reserved for horses which are‘short of air’ and performance is clearlysuboptimal. The author uses 2 implants (a braidedelastic and a coated braided polyester suture) asthis technique seems to produce the most reliableresults. Owners are counselled carefully regardingpost operative management in particular. Timespent at this stage in communication is wellworthwhile in reducing misunderstandings andclient dissatisfaction in the post operative period.The prognosis for the combined operation is hardto assess. In a survey undertaken by the authorinvolving over 100 horses, a detailed response was obtained in 66 cases. Of these 49 (ie nearly 75%) were deemed to be performing with a major improvement after surgery (ie with littleor no evidence of laryngeal obstruction). Ten additional cases had significantperformance improvement despite evidence of persistent laryngeal obstruction. Chronic sepsis necessitated the removal of implants in 3horses but only one was removed because ofdysphagia.

The implications of the survey were thatcareful patient selection is vital. Three of theunimproved group had undergone previouslaryngeal surgery, which might be considered abad prognostic sign. Clearly good results areeasier to achieve in horses which have lowerrespiratory demands at exercise and in patientswith a proven athletic record, as these animalstend to respond better to surgical procedures.

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LARYNGEAL RE-INNERVATION IN THE HORSE

I. Fulton

1410 Sturt Street, Ballarat, 3350, Victoria, Australia

Laryngeal re-innervation has been welldocumented in the human literature as a successfultreatment for a range of laryngeal dysfunctions(Tucker and Rusnov 1981; Tucker 1978).Investigation into the potential use of laryngeal re-innervation in horses with laryngeal hemiplegiahas occurred due to the complications that canoccur with prosthetic laryngoplasty.

EQUINE LARYNGEAL RE-INNERVATION

The first studies into laryngeal re-innervation inhorses were reported in 1989 (Ducharme et al.1989a,b,c). The nerve muscle pedicle graft, nerveimplantation and nerve anastomosis techniqueswere all investigated in ponies. In theseexperimental ponies, the recurrent laryngeal nervewas transected at the time of re-innervationsurgery. While the first 2 techniques demonstratedhistological evidence of re-innervation, theauthors concluded that laryngeal function wasinsufficient to allow for maximal exercise.Importantly this study identified the omohyoideusmuscle as an accessory muscle of respiration and,therefore, suitable for use as a donor muscle alongwith its nerve supply – the first or second cervicalnerves.

In 1990, the nerve muscle pedicle grafttechnique, using the first cervical nerve andomohyoideus muscle, was evaluated onexperimentally induced cases of left laryngealhemiplegia in Standardbred horses (Fulton et al.1991). In that study histologic evidence of re-innervation was demonstrated (Fulton et al. 1992)as was a return of laryngeal function, verified byupper airway flow mechanics studies (Fulton et al.1991). This study demonstrated that the paralysedcricoarytenoideus dorsalis muscle could be re-innervated and that in vigorously exercising

horses, upper airway function could return tobaseline levels between 6 and 12 months aftersurgery.

Re-innervation has also been attempted usinga muscle pedicle graft created from the right CADmuscle. It was hoped that muscle-to-muscleneurotisation would result in return of function tothe paralysed left CAD muscle; however thisattempt was unsuccessful (Harrison et al. 1992).

Since 1991 the nerve muscle pedicle grafttechnique has been used in selected clinical casesof laryngeal hemiplegia and hemi paresis in 129Thoroughbred, 10 Standardbred and 7 Warmbloodhorses. The following is a brief description of thesurgical technique, post operative care,complications, and follow-up results in thesecases.

SURGICAL TECHNIQUE

The nerve muscle pedicle graft is performed withthe horse under general anaesthesia. An incisionis made along the ventral border of the linguo-facial vein followed by accurate dissection of theleft first cervical nerve as it passes over the lateralaspect of the larynx to where it meets theomohyoideus muscle, an accessory muscle ofrespiration (Ducharme et al. 1989a) The firstcervical nerve branches are followed to their pointof insertion into the omohyoideus muscle. A smallblock of muscle is removed from theomohyoideus muscle with the fine branch of thefirst cervical nerve attached – up to 5 branchescan be isolated.

Exposure of the recipient muscle, thecricoarytenoideus dorsalis (CAD) muscle isachieved by rotating the larynx laterally. Thepedicle grafts are inserted into individual pocketsin the CAD muscle fibres of the CAD muscle. A

61


single 4-0 polydioxanone suture is used to hold thepedicle graft into the CAD muscle. A stentbandage is usually sutured over the skin incisionand an elastic bandage is used to apply pressureover the incision area, minimising the opportunityfor seroma formation.

Since September 2000 left cordectomy using adiode laser in combination with the nerve musclepedicle graft has been used. The cordectomy isroutinely performed the day following the nervemuscle pedicle graft procedure in the standingsedated horse.

Horses are routinely kept confined to a stallfor 2 weeks following surgery. After stallconfinement, a further 2 weeks in a day yardfollowed by paddock turnout for 12 weeks isnormally recommended. At this stage it is advisedthat the horse should go into training – 16 weekspost operatively. When the horses are returned toexercise it is advised that episodes of fast exerciseare introduced as early and as frequently aspossible. As the omohyoideus muscle is anaccessory muscle of respiration, considerablerespiratory effort must be undertaken to activatethe first cervical nerve.

After 6 weeks of training, trainers/owners arerequested to present the horse for endoscopicassessment of the larynx. At rest, the left arytenoidcartilage most commonly looks exactly as it didprior to surgery. Two diagnostic reflexes have beendeveloped to stimulate contraction of theomohyoideus muscle and therefore the newlyinnervated CAD. The first involves stretching thehead and neck upward as high as possible whileobserving the larynx closely through theendoscope. If re-innervation has occurred, there isoften a spontaneous flicker or single abduction ofthe left arytenoid cartilage. The second reflexinvolves pulling back rapidly with a finger orthumb on the commissure of the lips. Again asudden abduction of the left arytenoid cartilageoccurs if re-innervation has been successful. Thisreflex can be stimulated from the left or right sideof the head.

COMPLICATIONS

Complications associated with laryngeal re-innervation have been few when compared toprosthetic laryngoplasty. The most frequentcomplication has been seroma formation 3–5 daysfollowing surgery. The use of a compressive neckbandage that encircles the neck rostral and caudal

to the poll and maintained for 4–6 days postoperatively has reduced this to some extent. Someseromas have become infected, and these havebeen treated with antibiotics selected from cultureand sensitivity results. One horse developed alarge hematoma immediately post operatively thatrequired the incision to be re-opened and thevessel ligated.

RESULTS

ThoroughbredsRaced Thoroughbreds – 63 horses were includedin this group, 24 were Grade 4 horses, while 39horses had Grade 3 laryngeal hemiplegia. Of the59 horses available for follow up, 95% went on tostart in one or more races. The average length oftime from surgery to race one was 7.5 months forGrade 3 horses and 8.6 months for Grade 4 horses.The earliest that re-innervation was identified wasat 4 months, and the latest at 9 months. Followingsurgery, the horses raced an average of 12.5 timeseach. Of the 59 horses, 32 (54%) won one or moreraces after surgery.

To analyse the effectiveness of the nervemuscle pedicle graft, the following 4 variables,before and after surgery, were calculated for eachhorse: total performance ranking, total prizemoney, performance ranking per start, and prizemoney per start.

1. Total performance rankingThirty-four of the 59 (58%) horses had animproved total performance rank after surgery.

2. Total prize money Thirty-one of 59 horses (53%) earned moreprize money after surgery.

3. Performance ranking per startThirty-four of the 59 horses (58%) hadimproved performance ranking per start aftersurgery.

4. Prize money per start Thirty-four of the 59 horses (58%) earnedmore money per start after surgery thanbefore.

Unraced Thoroughbreds – 66 horses wereincluded in this group, 19 were Grade 3 leftlaryngeal hemiplegia (LLH) while 47 had Grade 4laryngeal function. Of the 66 horses, 39 (60%)went on to start in at least one race, 15 horses wereconsidered to be failures, 2 died, 3 were retired for

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reasons unrelated to the surgery, 4 were lost tofollow up, and 3 are still convalescing. Theaverage age at their first race was 3.1 years. The 39unraced Thoroughbreds that raced followingsurgery had an average of 10.6 starts each.

For the unraced horses that raced after surgery,money earned per start after surgery wascompared with the Australian average - Table 1demonstrates that each year, LLH-affected horsestreated with a nerve muscle pedicle graftperformed about the same as the national average.

StandardbredsTen horses underwent nerve muscle pedicle graft.Three horses were retired for reasons unrelated tosurgery prior to resuming racing and one horsewas considered a failure and did not race. Sixhorses returned to the race track. Of these 5 wonraces and 3 earned more money than beforesurgery.

WarmbloodsSeven horses were operated on. The oldest horse attime of surgery was 8-years-old and had beenhemiplegic for 2 years prior to surgery. Five of the7 horses went on to compete at a higher level thanbefore surgery.

CONCLUSIONS

The biggest disadvantage of the nerve graftsurgery is the time from surgery to the first race.

Time to first race for Group 1 horses was 7.5 and8.6 months for Grade 3 and Grade 4 laryngealfunction respectively, while following prostheticlaryngoplasty time to first race is 5.8 months(Hawkins et al. 1997).

In yearlings or early unraced 2-year-olds, thenerve muscle pedicle graft is a reasonable surgeryto offer owners. In the case of a 5-year-oldThoroughbred gelding, prosthetic laryngoplastycould be the logical choice

REFERENCES

Ducharme, N.G., Horney, F.D., Partlow, G.D. (1989a)Attempts to restore abduction of the paralysedequine arytenoid cartilage I. Nerve-muscle pedicletransplants. Can. J. vet. Res. 53, 202-220.

Ducharme, N.G., Horney, F.D., Hulland, T.J. Partlow,G.D., Schnurr, D. and Zutrauen, K. (1989b)Attempts to restore abduction of the paralysedequine arytenoid cartilage II. Nerve implantation(Pilot study) Can. J. vet. Res. 53, 210-215.

Ducharme, N.G., Viel, L., Partlow, G.D. Hulland, T.G.and Horney, F.D. (1989c) Attempts to restoreabduction of the paralysed equine arytenoidcartilage III. Nerve anastomosis. Can. J. vet. Res.53, 216-223.

Fulton, I.C., Derksen, F.J., Stick, J.A., Robinson, N.E.and Walshaw, R. (1991) Treatment of left laryngealhemiplegia in standardbreds using a nerve musclepedicle graft. Am. J. vet. Res. 52, 1461-1467.

Fulton, I.C., Derksen, F.J., Stick, J.A., Robinson, N.E.and Duncan, I.D. (1992) Histologic evaluation ofnerve muscle pedicle graft as a treatment for leftlaryngeal hemiplegia in Standardbreds. Am. J. vetRes. 53, 592-595.

Harrison, I.W., Speirs, V.C., Braund, K.G. and Steiss,J.E. (1992) Attempted re-innervation of the equinelarynx using a muscle pedicle graft. Cornell Vet 82,59-68.

Hawkins, J.F., Tulleners, E.P., Ross, M.W., Evans, L.H.and Raker, C.W. (1997) Laryngoplasty with orwithout ventriculo-cordectomy for treatment of leftlaryngeal hemiplegia in 230 racehorses. Vet. Surg.26, 484-491.

Tucker, H.M. (1978) Human laryngeal re-innervation:Long term experience with the nerve muscle pedicletechnique. Laryngoscope 88, 598-604.

Tucker, H.M., Rusnov, M. (1981) Laryngeal re-innervation for unilateral vocal cord paralysis: Longterm results. Ann. Otolaryngol. 90, 457-45.

TABLE 1: Prize money per start for each year ofracing of LLH-affected horses treated with anerve muscle pedicle graft compared with thenational average (1996-2001) for Australianhorses

Year of racing NMP graft National averagehorses $/start $/start

2-year-olds (n=2) $1895.00 $2038.003-year-olds (n=34) $2822.00 $1425.004-year-olds (n=18) $1227.00 $1289.005-year-olds (n=6) $1054.00 $1167.006-year-olds (n=1) $1050.00 $1114.00

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EVALUATION OF RLN TREATMENT EFFICIENCY –LARYNGOPLASTY

P. M. Dixon


The first recorded attempt at laryngoplasty (LP)appears to have been by Moeller, who some 200years ago, transcutaneously sutured the affectedarytenoid to the thyroid cartilage in ‘roarers’ toprevent it collapsing into the airway (Cadoit1893). However, this form of laryngoplasty neverbecame popular and ventriculectomy was thestandard surgical procedure for laryngeal paralysisin the late 19th and the 20th century until theintroduction of the current laryngoplasty treatmentby Marks et al. (1970). Recent surveys haveshown in Britain (Bathe 1993) and in the UnitedStates (Hawkins et al. 1997; Hammer et al. 1998;Strand et al. 2000) that laryngoplasty is currentlythe most widely used treatment for equinelaryngeal paralysis.

At least 11 studies have shown laryngoplastyto be of value, as assessed by absence of orreduction in abnormal exercise related respiratory‘noises’ post operatively; or reported improvementin exercise performance, as reviewed by Dixon etal. (2003a). Some of their surveys also comparedrace times, or race earnings pre- and post surgery.A number of physiological studies including theearly work of Bayly et al. (1984) and of Tetens etal. (1996) and those of Weishaupt (Weishaupt etal. 2003) have shown improvements in airflowmechanics or in arterial blood gases following LPsurgery. However some of these studies wereperformed in experimental ponies underlaboratory conditions. Despite the above volumeof evidence of its efficacy, laryngoplasty is notalways successful in clinical cases and somehorses suffer significant post operative problems.

Obtaining and even more importantly,maintaining the required degree of arytenoidabduction is the key to success of laryngoplasty.Maximum levels of abduction are not required toallow maximal exercise performance. The degree

of LP abduction obtained can be assessed semi-qualitatively using a number of grading systems.A recent study has shown a very strong statisticalcorrelation between maximal abduction (ie Grade1 abduction – where the arytenoids are at 90degrees to the vertical, or even in some occasionsbeyond that level and maximal Grade 2 iearytenoids close to 90 degrees to the vertical) withaspiration and coughing (Dixon et al. 2003a). Theabsence of noise at 12 months plus postoperatively correlated significantly with thedegree of laryngeal abduction present at 6 weeks.

There is progressive loss of arytenoidabduction post operatively in most cases,especially in the first few weeks following surgery(Dixon et al. 2003b). The reasons for thisabductory loss are not understood fully. Mostcases of recurrent laryngeal neuropathy (RLN)have preferential atrophy of their adductormuscles (Duncan et al. 1991) and so laryngealadductor deficits are usually worse than abductordeficits - in contrast to Semon’s law.Consequently, arytenoid adductory tension on theprosthesis is unlikely to be the main cause ofabductory loss. A more likely explanation is thatduring swallowing, full adduction of thearytenoids occurs as the pharyngeal muscles(including the caudal constrictors) constrictsequentially in a peristaltic fashion to push thefood bolus from the pharynx into the oesophagus.Consequently a surgically abducted arytenoid thatis protruding laterally will be subjected to repeatedadductory pressures during swallowing. This maydecrease the degree of abduction progressively, insome cases totally.

Very many surgeons also perform concurrentventriculectomy or ventriculo-cordectomy withlaryngoplasty - an insurance perhaps, in case oflaryngloplasty failure? Some clinicians question if

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these procedures should be performed concurrently.A pertinent question posed recently by JimSchumacher is whether a ventriculectomy isnecessary if an ipsilateral vocalcordedctomy isperformed? Does ventriculectomy just cause morescarring of the lateral ventricular wall and alsoprevent effective suturing of the vocalcordectomywound that could limit intra-laryngeal scarring atthe site of vocalcordectomy?

There is little doubt that the fibroelastic tissuesof the vocal fold are tensed by laryngoplasty (asdigitally assessed at laryngotomy) and will thenplace permanent tension on the prosthesis.Therefore, performing a concurrent vocal-cordectomy can remove some of that adductorypressure on the prosthesis and so help mainlaryngoplasty abduction. Recent work has shownthat ventriculo-cordectomy can decrease abnormalnoises in horses with laryngeal hemiplegia to evena greater degree than laryngoplasty (Brown et al.2003). This is a further reason for performingconcurrent ipsilateral ventriculo-cordectomyalong with laryngoplasty. It can also be an‘insurance’ because if the laryngoplasty losesmuch of its abduction, the affected arytenoidshould at least be fixed in a position where itcannot obstruct the contralateral side of the larynx.At the same time the concurrentvocalcordectomy/ventriculectomy will hopefullyincrease the ventral laryngeal airway to help withairflow during exercise.

The prevention of sutures cutting into thecartilages at their anchor points would seemimportant in preventing excessive loss ofabduction. A variety of suture materials have beenused for laryngoplasty and all have differentmerits. Thicker braided prostheses may place lessfocal pressure on the cartilages and therefore less‘pull through’ may occur with these. However, ifbraided non-absorbable sutures become infected, apersistent external sinus tract may well occur.Although monofilament stainless steel wires havethe advantage of allowing adjustment oflaryngoplasty abduction (either loosening ortightening) at surgery or during further surgery, itis possible that their fine calibre may promote‘pull through’ the cartilage. The use of elasticatedsutures has the advantage that they may allowcontinued tension to occur even with ‘pullthrough’. Nemeth (1987) used an absorbablesuture and later reported satisfactory results in a

high proportion of cases, which is difficult toexplain scientifically. Further studies intoimproving laryngoplasty suture retention aredescribed by Parente (2004).

The success of treating equine laryngealparalysis varies on how a successful outcome isdefined (Ducharme and Hackett 1991). If thepresence of an abnormal ‘noise’ was the primarycomplaint of the owner, then elimination of thisnoise constitutes a surgical success. In contrastHawkins et al. (1997) suggested that eliminationof exercise intolerance, and not necessarily ofnoises, should be the main criterion to consider forLP success in horses. The latter may be difficult toquantify for many reasons. A review of publishedclinical case studies by Dixon et al. 2003a showsa reported reduction, with circa 75% of horsesreported to have total absence of noises followinglaryngoplasty. This is similar to the 73% recordedby Dixon et al. (2003a) in a study on 200 oldermixed-work horses.

A draw back of using noise elimination as thesole criterion to identify success of LP may be thathorses may make ‘noises’ and yet have nosignificant upper airflow obstruction. Converselythe elimination of noises does not necessarilyindicate the presence of optimal laryngeal airflow(Brown et al. 2003). In addition, some owners arepoor at detecting abnormal noises as noted bySpiers et al. (1983) who detected abnormal noisesin horses where the owner could not detect them.This is also a common finding by the author whenless experienced owners present cases of RLN forexamination. The assessment of the effects of LPon exercise performance can be subjective andmany studies including those of Ducharme andHackett (1995), Kidd and Slone (2002) and Dixonet al. (2003a) have shown that laryngoplasty ismost likely to improve performance in non-racehorses. Such cases are likely to have severe ortotal laryngeal paralysis prior to presentation.

Despite the amount of evidence on the value oflaryngloplasty, this procedure needs to beevaluated further by larger physiological studies inclinical cases, pre- and post surgery. Such studiesmay be difficult to conduct, bearing in mind thereluctance of owners and trainers to bring horsesback for further treadmill evaluations, even moreso when they perceive their horse to be nowperforming satisfactorily.

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REFERENCES

Bathe, A.P. (1993) Left laryngeal hemiplegia in thehorse: A survey of diagnostic criteria andmanagement practices employed by 20 veterinarysurgeons in Europe. Equine vet. Educ. 5, 84-85.

Bayly, W.M., Grant, B.D., and Modransky, P.D. (1984)Arterial blood gas tensions during exercise in ahorse with laryngeal hemiplegia, before and aftercorrective surgery. Res. vet. Sci. 36, 256-258.

Brown, J.A., Derksen, F.J., Hartman, W.M., Robinson,N.E., and Stick, J.A. (2003) Ventriculo-cordectomyreduces respiratory noise in horses with laryngealhemiplegia. Equine vet. J. 35, (6) 570-574.

Cadoit, P.J. (1893) Roaring in Horses: Its Pathology andTreatment. Translated by T.J.W. Dollar, SwanSommnenschein & Co. London. pp 15-78.

Dixon, P.M., McGorum, B.C., Railton, D.I., Tremaine,W.H., Dacre, K. and McCann J. (2003a) Long-termsurvey of laryngoplasty and ventriculo-cordectomyin an older, mixed-breed population of 200 horses.Part 2: Owners’ assessment of the value of surgery.Equine. vet. J. 35, 397-401.

Dixon, P.M., McGorum, B.C., Railton, D.I., Tremaine,W.H., Dacre, K. and McCann J. (2003b) Long-termsurvey of laryngoplasty and ventriculo-cordectomyin an older, mixed-breed population of 200 horses.Part 1: Maintainence of surgical arytenoidsabduction and complication of surgery. Equine. vet.J. 35, 389-396.

Ducharme, N.G. and Hackett, R.P. (1991) The value ofsurgical treatment of laryngeal hemiplegia in horses.Comp. cont. Educ. pract. Vet. 13, 472-475.

Ducharme, N.G. and Hackett, R.P. (1995) Surgicalalternatives in the treatment of laryngeal hemiplegiain horses. Proceedings of Geneva Congress ofEquine Medicine and Surgery. Swiss Vet. 11-5, pp59-61.

Duncan, I.D., Amundson, J., Cuddon, P.A., Sufit, R.,Jackson, K.F. and Lindsay, W.A. (1991) Preferentialdenervation of the adductor muscles of the equinelarynx 1: muscle pathology. Equine vet. J. 23, 94-98.

Hammer, E.J, Tulleners, E.P., Parente, E.J. and Martin,B.B. (1998) Videoendoscopic assessment ofdynamic laryngeal function during exercise in

horses with grade-3 left laryngeal hemiparesis atrest: 26 cases (1992-1995). J. Am. vet. med. Ass.212, 399-403.

Hawkins, J.F., Tulleners, E.P., Ross, M.W., Evans, L.H.,and Raker, C.W. (1997) Laryngoplasty with orwithout ventriculectomy for treatment of leftlaryngeal hemiplegia in 230 racehorses. Vet. Surg.26, 484-491.

Kidd, J.A. and Slone, D.E. (2002) Treatment oflaryngeal hemiplegia in horses by prostheticlaryngoplasty, ventriculectomy and vocalcordectomy. Vet. Rec. 150, 481-484.

Marks, D., Mackay-Smith, M.P., Cushing, L.S., andLeslie, J.A. (1970) Observations on laryngealhemiplegia in the horse and treatment by abductormuscle prosthesis. Equine vet. J. 2, 159-166.

Nemeth, F. (1987) Techniques and results of the surgicaltreatment of roaring in 398 horses, using a modifiedMackay-Smith method. Pferdeheilkunde 3, 27-31.

Parente, E.J. (2004) Improvements in laryngoplasty.Havemeyer Foundation Monograph Series No 11,Eds: P. Dixon, E. Robinson and J.F.Wade, R&WPublications (Newmarket) Ltd, pp 66-67.

Speirs, V.G., Bourke, J.M., and Anderson, G.A. (1983)Assessment of the efficiency of an abductor muscleprosthesis for the treatment of laryngeal hemiplegiain horses. Aust. vet. J. 60, 294-299.

Strand, E., Martin, S.G., Haynes, P.F., McLure, J.R. andVice, J.D. (2000) Career racing performance inThoroughbreds treated with prosthetic laryngoplastyfor laryngeal neuropathy: 52 cases. (1981-1989). J.Am. vet. med. Ass. 217, 1689-1696.

Tetens, J., Derksen, F.J., Stick, J.A., Lloyd, J.W. andRobinson, N.E. (1996) Efficacy of prostheticlaryngoplasty with and without bilateral ventriculo-cordectomy as treatments for laryngeal hemiplegiain horses. Am. J. vet. Res. 57, 1668-1673.

Weishaupt, M.A., Vogt, R., Fürst, A. and Auer, J.A.(2003) Spirometric and endoscopic assessment ofsurgical treatment in horses with laryngealhemiplegia. Equine Recurrent LaryngealNeuropathy. Havemeyer Foundation MonographSeries No 11, Eds: P. Dixon, E. Robinson andJ.F.Wade, R&W Publications (Newmarket) Ltd, pp81-82.

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IMPROVEMENTS IN LARYNGOPLASTY

E. J. Parente

University of Pennsylvania, New Bolton Centre, 382 West Street Road, Kennet Square, PA 19348, USA

Despite recognition of laryngeal hemiplegia forover 100 years and development of thelaryngoplasty procedure over 30 years ago, therehave been no major changes to treatment oflaryngeal hemiplegia since its description byMarks et al. (1970). There is still reluctance bytrainers to have the procedure performed as it doesnot return the horse to ‘normal’, and has potentialcomplications. Furthermore, failure to maintainabduction of the arytenoid, both short-term andlong-term, is a documented problem. This has ledto interest in modifications of the standardlaryngoplasty and alternative procedures.Unfortunately, alternative procedures such as re-innervation have had limited success and require alonger return to return to training.

A minor but significant improvement inlaryngoplasty is removal of the vocal cord. Whileearly research did not detect a significantimprovement in airway mechanics with aventriculectomy, most surgeons now believe thatremoval of the vocal cord is beneficial based onboth clinical and experimental evidence. Treadmillendoscopy clearly demonstrates the deviation ofthe vocal cord during inspiration if it is notremoved as an adjunctive procedure withlaryngoplasty. While the sacculectomy may nottruly stabilise the cord, there is some questionwhether a sacculectomy is beneficial by creatingfibrous support for the abducted arytenoid.

The majority of efforts to improvelaryngoplasty deal with maintenance of arytenoidabduction and thus suture retention (Dixon et al.2003). Causes of failure are thought to beassociated with suture pull out, assumed throughthe muscular process based on experimentalmodels (Dean et al. 2001). Yet, more often itappears to be ‘loosening’ in clinical cases thatresults in decreased abduction. One technique

developed to minimise loosening was concurrentrecurrent laryngeal neurectomy while performinglaryngoplasty for horses with remaining laryngealmotion (Davenport et al. 2001). The hypothesiswas that cycling from remaining muscular pullresulted in suture loosening. Performing theneurectomy was ineffective in improving theprognosis relative to standard laryngoplasty.

Other methods to maintain arytenoidabduction include techniques to place sutures anddifferent suture materials. Mechanical testing of invitro models has been promising but thesemethods do not yet have long-term clinical follow-up and may present greater difficulty in placementin vivo than present standard procedures.

We have pursued 2 other methods. We nowoften approach the muscular process from behindthe cricopharyngeus muscle. This can beperformed with appropriate positioning of thehorse under general anaesthesia. Dissection isperformed easily just above a branch of the cranialthyroid vein and just caudal to thecricopharyngeus muscle through dense fascia toaccess the muscular process of the arytenoid. Thisapproach should minimise any slack of the suturematerial by fascial interference and preventcrossing of suture that could occur when passingmultiple strands under the cricopharyngeusmuscle belly.

An approach to improve stability of the larynxwith laryngoplasty has also been developed bycreating an arthrosis of the cricoarytenoid (CA)joint. The hypotheses for the experimental modelwere: 1) that surgical destruction of the CA jointcould be performed using a motorised burr via aroutine laryngoplasty surgical approach; 2) thatsurgical destruction of the CA joint with amotorised burr in conjunction with laryngoplastywould result in joint fusion and improved stability

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of the arytenoid cartilage; and 3) that surgicaldestruction of the CA joint using a motorised burrwould not result in any complications in relation tolaryngeal/pharyngeal tissues or laryngeal function.

Eight horses with normal laryngeal functionwere prepared for aseptic surgery and a standardlaryngoplasty. Three horses were controls,receiving a standard laryngoplasty and 5 haddebridement of the CA joint as well as a standardlaryngoplasty. To access the CA joint, thetendinous insertion of the cricoarytenoideusdorsalis muscle was transected from the caudalborder of the muscular process. The muscularprocess was retracted cranially exposing thelateral CA joint capsule. The capsule was incisedexposing the articular cartilage which wasdebrided with a 2 mm motorised burr. Two #5polyester sutures were placed through the cricoidcartilage and muscular process in typical fashion.The video-endoscope was placed through thenostril to assess any penetration of laryngealmucosa with the prosthetic sutures and theposition of the arytenoid. The loops of suture weretied independently while observing the abductionof the arytenoid with the endoscope. Soft tissuesand skin were closed routinely. All horses weregiven antimicrobials and anti-inflammatories forone week with stall rest, then turned out on pasturefor another 83 days.

Endoscopy was performed and recorded themorning after surgery and at the conclusion of thestudy. Still images were captured and digitisedafter induced maximal abduction. The degree ofarytenoid cartilage abduction was calculated byusing an approach similar to one previouslydescribed. A line was drawn connecting the mostdorsal and ventral points of the glottis andextended dorsally for a distance one third of thedorsoventral height of the larynx. Tangential lineswere then drawn from that point to the edge ofeach corniculate. The angle between the 2 lineswas recorded as the angle of abduction, and theright to left quotient was determined by dividingthe right angle by the left angle.

All horses were subjected to euthanasia 90days from the time of surgery. The larynges of thehorses were removed intact with approximately 20cm of trachea immediately after euthanasia formechanical testing. The right arytenoid was fixedin maximal abduction with one #2 polyester suturebetween the muscular process and the cricoidcartilage. The specimens were secured to a wooden

board by needles placed through the epiglottis. A16 gallon vacuum cleaner was secured to thetrachea and adjusted to produce flows of 10, 20, 30,40, 50 l/s. Airflow was measured with a 5 cm-diameter ‘fleish-type’ pneumotachometer placedbetween the adaptor and the vacuum cleaner.Translaryngeal pressure difference, andtranslaryngeal impedence, were calculated at thedifferent airflows – with the suture intact and afterit was cut free from the cricoid cartilage withoutdisrupting any fibrous tissue around the muscularprocess. Digital photographs were obtained at thevarious airflows with and without the suture cutfrom the cricoid. From the photographs, the right toleft angle quotient were measured and calculated asdescribed.

The results indicate fusion of the CA jointprovides additional stability to a standardlaryngoplasty in this experimental model. No horsesexperienced any post operative complications.

REFERENCES

Davenport, C.L., Tulleners, E.P., Parente, E.J. (2001)The effect of recurrent laryngeal neurectomy inconjunction with laryngoplasty and unilateralventriculo-cordectomy in thoroughbred racehorses.Vet. Surg. 30, 417-421.

Dean, P.W., Nelson, J.K., Schumacher, J. (1990) Effectsof age and prosthesis material on in vitro cartilageretention of laryngoplasty prostheses in horses. Am.J. vet. Res. 51, 114-117.

Dixon, P.M., McGorum, B.C., Railton, D.I., Hawe, C.,Tremaine, W.H., Dacre, K. and McCann, J. (2003)Long-term survery of laryngoplasty and ventriculo-cordectomy in an older, mixed-breed population of200 horses. Part 1: Maintenance of surgicalarytenoid abduction and complications of surgery.Equine vet. J. 35, 389-396.

Herde, I., Boening, K.J., Sasse, H.L. (2001) Arytenoidcartilage retention of laryngoplasty in horses – invitro assessment of effect of age, placement site, andimplantation technique. In: Proc. Am. Ass. equinePract. 47, 115-119.

Jansson, N., Ducharme, N.G., Hackett, R.P. andMohammed, H.O. (2000) An in vitro comparison ofcordopexy, cordopexy and laryngoplasty, andlaryngoplasty for treatment of equine laryngealhemiplegia. Vet. Surg. 29, 326-334.

Marks, D., Mackay-Smith, M.P., Cushing, L.S. andLeslie, J.A. (1970) Use of a prosthetic device forsurgical correction of laryngeal hemiplegia inhorses. J. Am. vet. med. Ass. 157, 167-163.

Schumacher, J., Wilson, A. M., Pardoe, C. and Easter,J.L. (2000) In vitro evaluation of a novel prosthesisfor laryngoplasty of horses with recurrent laryngealneuropathy. Equine vet. J. 32, 43-46.

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VENTRICULECTOMY/CORDECTOMY

N. Ducharme

Department of Veterinary Surgery, Cornell University, Ithaca, New York, USA

The vocal cords (folds or plica vocalis) form theventrolateral limits of the rima glottidis. Whenhorses with laryngeal hemiplegia are examined byvideo-endoscopy while exercising on a high speedtreadmill, one can observe the left vocal fold to becollapsing in the airway and therefore, restricting(Derksen et al. 1986; Shappel et al. 1988; Tetenset al. 1996) the ventral diameter of the larynx (Fig1). In some cases there is also an associated

ipsilateral arytenoepiglottic fold collapse. Finally,in a small percentage of horses, there is alsobilateral vocal fold collapse. Because it wasrecognised early in the study of this disease thatthe vocal fold and ventricle contributes to theupper respiratory noise and poor performance,ventriculectomy with or without cordectomy wereintroduced. Indeed, ventriculectomy, cordectomyand arytenoidectomy were introduced and thenabandoned in the 19th century by Gunther. At thebeginning of the 20th century, ventriculectomywas re-introduced by Professor William L.Williams and popularised by Sir FrederickHobday. The procedure was extended to aventriculo-cordectomy late in the 20th century.This modification was supported by treadmillobservation that indicated that a ventriculectomydid not always prevent collapse of the ipsilateralvocal fold, the source of the upper airwayobstruction of the ventral aspect of the rimaglottidis. Over the last decade, some surgeonshave begun to remove only the vocal cord.

The value of unilateral or bilateral ventriculo-cordectomy/cordectomy (VC/C) in horses withGrade IV recurrent laryngeal neuropathy (RLN) iscontroversial. This is partially because theventriculectomy alone (without vocal foldremoval) is of little value. The ventriculectomywas initially thought to induce adhesions betweenthe left arytenoid and thyroid cartilages that wouldlimit axial displacement of the arytenoid cartilageduring exercise. However, Shappel et al. (1988),determined impedance during exercise at up to 7.2m/s on a 6.38° incline and found no measurableevidence that ventriculectomy alone yields anyimprovement in the size of the rima glottidis.Although this study has been criticised forassessing performance in submaximal stress, it ishard to conceive that a procedure that shows no

Fig 1: Schematic of Grade IV laryngeal hemiplegiaexperiencing dynamic collapse of left vocal folds (whitearrow) during exercise. Note associated collapse of theleft arytenoepiglottic folds (black arrow).

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mechanical advantage at low speed would be ofsome benefit at a higher speed. The value ofventriculectomy as an added procedure to thelaryngoplasty was evaluated in 3 studies (Derksenet al. 1986, Shappel et al. 1988, and Tetens et al.1996) and revealed the same finding ieventriculectomy is not needed so laryngoplastyalone is the treatment of choice for restoration ofupper airway mechanics, both at maximal andsubmaximal exercise. Despite these findings, mostsurgeons continue to perform a VC/C withlaryngoplasty in horses with RLN.

There are multiple reasons for the belief thatventriculo-cordectomy or cordectomy are usefulprocedures. Firstly, it is felt that the upper airwaymechanic data is not sufficiently sensitive ashorses with a laryngoplasty do not have, on visualinspection, a normal airway yet they have normalupper airway mechanics. Perhaps other indicessuch as arterial blood gases should be used toassess the effect of laryngoplasty on ventilation. Inone such study, Edwards (1996), found that alaryngoplasty did not normalise blood gases inhorses exercising at 14 m/s on a high speedtreadmill indicating that after laryngoplasty,airway size is not restored to normal. This latterfinding is consistent with the video-endoscopicevidence of the larynx at exercise that the airwayis not restored to normal after laryngoplasty. In thesame study, unilateral ventriculo-cordectomy didimprove airway mechanics (using impedance flowof 24 l/s) over a laryngoplasty alone, but still didnot normalise blood gases or airway mechanics,indicating the airway is not restored to normal inhorses exercising at 14 m/s. On the contrary,bilateral ventriculo-cordectomy did not have anyadvantage over only a laryngoplasty based onairway mechanics data in horses exercising atspeeds up to 13 m/s (Tetens et al. 1996). Thedifference in the findings may be due to thesensitivity of the different indices of upper airwaymechanics used in both studies and differences inthe study design.

Should the use of ventriculo-cordectomy/cordectomy (VC/C) be considered as the soletreatment of horses affected with Grade IV RLN?Most recently (Derksen 2004a,b), unilateral lasercordectomy or bilateral ventriculo-cordectomywere shown to improve airway mechanics inexperimentally induced left laryngeal hemiplegia,although to a much lesser degree thanlaryngoplasty. This degree of improvement maybe sufficient in horses travelling at low speed, and

there is some data suggesting that in horses suchas draft horses, the airway mechanics areimproved with ventriculo-cordectomy. Airwaysounds should also be a concern when judgingthese surgical techniques. Objective data becameavailable when Brown et al. (2004) found, basedon sound analysis, that bilateral ventriculo-cordectomy can reduce the abnormal upper airwaysounds in horses with laryngeal hemiplegia.Further data (Derksen 2004a,b) indicated thatunilateral laser cordectomy or bilateral ventriculo-cordectomy alone restores normal upper airwaysounds in horses with experimentally created leftlaryngeal hemiplegia. Laryngoplasty alone wasinferior to VC/C in the improvement in upperairway sound that it yielded.

What about the use of ventriculo-cordectomy/cordectomy (VC/C) as the sole treatment of horsesaffected with Grade III B RLN? There is no dataat this time to answer this question. It is knownthat horses with partial arytenoid cartilagecollapse at exercise have vocal fold collapse. Inthose horses where the degree of collapse of thearytenoid cartilage is no less than the position ofthe arytenoid cartilage after a laryngoplasty, theauthor feels that removing the vocal fold would beof value and would not expose the horse to thepossibility of failed laryngoplasty and thus, aworsening of the situation.

SURGICAL PROCEDURE

The horse is placed in a stock for restraint and anintravenous jugular catheter placed under asepticconditions. A specially padded halter is used toelevate the head during the procedures; sedationresults in marked relaxation such that the buckleson the halter must be appropriately padded. Thehead elevation is facilitated by having a ring on thenose band of the halter and on the ceiling or frontof the stock. For sedation of the average 450 kghorse, the authors used a mixture of 5 mgdetomidine and 5 mg butorphanol followed withone or 2 repeated detomidine (2 mg) injections asneeded. To desensitise the upper airway and theright nasal cavity, a solution containing 50 cclidocaine hydrochloride and 10 cc 0.15% solutionof phenylephrine is applied through the biopsychannel of the video-endoscope.

The author performs the procedure using adiode laser fibre or ND: YAG laser. The video-endoscope is inserted in the right nostril and thelaser fibre passed through into the biopsy channel

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such that it is positioned over the axial surface ofthe left vocal fold. The incision must start at thecaudal and ventral aspect of the vocal fold andextend to the rostral aspect of the vocal cord.Care should be taken not to extend the incision tothe abaxial surface of the vocal cord at this timebecause there are significant blood vessels at thejunction of the rostral and abaxial edges of thevocal cord. The video-endoscope is then placedthrough the left nasal cavity to give a betterperspective of the next incision. A graspingbronchoesophagoscopic forceps (product no.8280.62, Richard Wolfe Medical InstrumentsCorporation, Vernon Hills, Ill.), bent with an arcof approximately 30° to conform to the curve ofthe nasal passage and pharynx, is inserted ontothe right nasal cavity until it becomes visible onthe dorsal aspect of the epiglottic cartilage.Elevation of the head at this point facilitates thegrasping of the vocal cord immediately dorsal tothe rostral incision. The vocal fold is then pulledaxially and rostrally such that the laser fibre doesnot inadvertently touch the right vocal fold. Thisforms a triangle of vocal fold (apex in theforceps). The base of this triangle of the vocalcord is incised vertically starting 3–4 mm distalto the vocal process of the arytenoid’s cartilage.The vertical incision is continued until theventral incision is reached and vocal cordexcised. Care must be taken not to lase thecontralateral vocal cord during the latter process.Post operatively, the horses are administeredsystemic antibiotics for 7 days andphenylbutazone for 5 days. The surgical site isusually healed in 2–3 weeks.

Currently, the author still performs ventriculo-cordectomy or cordectomy to treat exerciseintolerance in horses working at low velocity (likedraft horses), horses with partial collapse of theleft arytenoid cartilage and/or vocal fold atexercise, and in association to a laryngoplasty. It isalso used to reduce/normalise abnormal airwaysounds in horses with Grade III or IV RLN.

REFERENCES

Brown, J.A., Derksen, F.J., Stick, J.A., Hartmann, W.M.,Robinson, N.E. (2004) Ventriculo-cordectomyreduces respiratory noise in horses with laryngealhemiplegia. Equine vet. J. In press.

Cadiot, P.J. (1892) Roaring in Horses: Its Pathology andTreatment. Ed: T.J.W. Dollar, London,Sonnenschein and Co., pp 6-78.

Derksen, J.F. (2004) Treatment of recurrent laryngealneuropathy: Physiological and performanceevaluation. Equine Recurrent Laryngeal NeuropathyHavemeyer Foundation Monograph Series 11, Eds:P. Dixon, E. Robinson and J.F. Wade, R&WPublications (Newmarket) Ltd, pp 77-78.

Derksen, J.F. (2004) Treatment of recurrent laryngealneuropathy: Evaluation by respiratory soundanalysis. Equine Recurrent Laryngeal NeuropathyHavemeyer Foundation Monograph Series 11, Eds:P. Dixon, E. Robinson and J.F. Wade, R&WPublications (Newmarket) Ltd, pp 79-80.

Derksen, J.F., Stick, J.A., Scott, E.A., Robinson, N.E.,and Slocombe, R.F. (1986) Effects of laryngealhemiplegia and laryngoplasty on airway flowmechanics in exercising horses. Am. J. vet. Res. 47,16-26.

Dixon, P.M., Railton, D.I. and McGorum, B.C. (1994)Ventral glottic stenosis in 3 horses. Equine vet. J. 26,166-170.

Ducharme, N.G., Goodrich, L. and Woodie, B. (2002)Vocal cordectomy as an aid in the management ofhorses with laryngeal hemiparesis/hemiplegia.Clinical Technique in equine Practice 1, 17-21.

Hobday, F. (1936) The surgical treatment of roaring inhorses. Vet. clinics North Am. 17, 17-21.

Edwards, R.E., Ducharme, N.G., Hackett, R.P.,Ainsworth, D.A., Shannon, K., Mitchell, L.M.(1996) The Value of Respiratory Mechanics forDetection of Partial Laryngeal Obstruction inExercising Horses. MS thesis. Cornell University.

Shappel, K.K., Derksen, F.J., Stick, J.A. and Robinson,N.E. (1988) Effects of ventriculectomy, prostheticlaryngoplasty, and exercise on upper airwayfunction in horses with induced left laryngealhemiplegia. Am. J. vet. Res. 49, 1760-1766.

Tetens, J., Derksen, F.J., Stick, J.A., Lloyd, J.W. andRobinson, N.E. (1996) Efficacy of bilateral prostheticlaryngoplasty with and without bilateral ventriculo-cordectomy as treatments for laryngeal hemiplegia inhorses. Am. J. vet. Res. 57, 1668-1673.

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VENTRICULO-CORDECTOMY FOR TREATMENT OFRECURRENT LARYNGEAL NEUROPATHY: 75 CASES INA MIXED POPULATION OF HORSES

S. Z. Barakzai and P M. Dixon


INTRODUCTION

There are few reports in the literature of theefficacy of ventriculectomy, cordectomy orventriculo-cordectomy (VC) for the treatment ofequine recurrent laryngeal neuropathy (RLN).Laryngoplasty (LP) with or withoutventriculectomy or vocal cordectomy are currentlythe techniques of choice for the treatment of RLNfor most equine surgeons. Recent experimentalstudies have shown that VC significantly reducesabnormal respiratory noises in horses withexperimentally induced laryngeal hemiplegia(Brown et al. 2003), and this technique has beenrecommended if reduction of respiratory noise isthe primary objective of surgery. VC has also beenshown to improve upper airway function in horseswith experimentally induced laryngealhemiplegia, but not to baseline levels (Brown et al.2003). Kidd and Slone (2003) suggested thatinclusion of a vocalcordectomy along with the LPprocedure was important in terms of eliminatingrespiratory noise in clinical cases. Vocal cordcollapse has been reported to occur withoutsignificant arytenoid cartilage collapse in horseswith lower grades of RLN undergoing high-speedtreadmill endoscopy (Hammer et al. 1998; Lane2003; Dixon and Barakzai, unpublishedobservations), and it is possible that for such cases,VC would provide a good alternative to LP. To theauthors’ knowledge, there has been no large studyof the clinical use of VC published to date.

AIMS

This study proposed that for performance horses(ie racehorses) with low grades of RLN (Grade 2or 3, using a 6-grade system, Dixon et al. 2001), or

for non-performance horses with any grade ofRLN, VC alone would reduce clinical signs ofRLN. The study also aimed to determine the rateof post operative complications and owner’sassessment of the value of surgery and comparethese to LP + VC surgery (Dixon et al. 2003a,b).

MATERIALS AND METHODS

Seventy-five horses which underwent unilateralventriculectomy and vocalcordectomy at theRoyal (Dick) School of Veterinary Studies(R(D)SVS) for treatment of idiopathic RLN wereselected for subjective restrospective analysis.Surgery was performed via a ventral laryngotomyincision, and after sharp excision of the laryngealventricle and vocal fold, the crico-thyroidmembrane was closed with 3.5 metric polyglactin910 (Vicryl, Ethicon). Cases were endoscoped atone day, 6 days and 6 weeks post operatively. Apostal questionnaire was sent to all owners/trainersafter the horses had been back in work for at leastone year following surgery, which was followedup by a telephone questionnaire if there was noresponse within 2 months.

RESULTS

The breeds included 50 Thoroughbreds, 21Thoroughbred crosses, 1 Clydesdale and 3 ponies.The work of horses in this study included 40National Hunt racehorses, one flat racehorse, 12hunters, 7 eventers, 3 showjumpers, and 12miscellaneous work loads. The median age was 6years (range 3–15 years), and median height was16.2 hh (range 12.0–18.2 hh). Presenting signsincluded abnormal exercise related respiratory‘noises’ detected by the owner/trainer (53%), poorexercise performance (11%), abnormal noises and

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poor performance (33%), and abnormalrespiratory noises detected at a pre-purchaseveterinary examination (3%). The median pre-operative endoscopic grade of RLN was 2 (range2–5), with 74 horses afflicted with left sided RLNand one afflicted with right sided RLN. Twenty-nine percent of horses had endoscopic evidence oflower airway disease on resting endoscopy.

Complications of surgery: Sixty-two percentof horses had no discharge from the laryngotomywound when the horse returned home, one weekpost operatively. In 20% of horses, the dischargehad resolved by 2 weeks post operatively, and in3% of horses the laryngotomy discharge persistedfor more than 4 weeks. Twenty-two percent ofhorses coughed after surgery (Fig 1), of which

27% coughed whilst eating and the remaindercoughed at times unassociated with eating. Sixty-six percent of horses did not make abnormalnoises post operatively (Fig 2). Nine percentcontinued to make abnormal noise at the canter,21% made noises at the gallop, and 4% of ownerswere unsure if abnormal noises were present. Ofthe 23 horses which made abnormal noises atexercise post operatively, 19 returned to full workregardless, and 6 were diagnosed with otherdisorders in the year post-operatively including 3with dorsal displacement of the soft palate, onewith facial paralysis, one with pulmonary diseaseand one false nostril atheroma.

Post operative performance: Ninety-threepercent of horses returned to full work after

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Fig 2: Bar chart showing % horses making abnormalrespiratory noises post operatively for both ventriculo-cordectomy (VC) and laryngoplasty with ventriculo-cordectomy (LP) procedures (Dixon et al. 2003a).

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Fig 4: Bar chart showing the owner/trainers’ overallopinion of surgery for both ventriculo-cordectomy (VC)and laryngoplasty with ventriculo-cordectomy (LP)procedures (Dixon et al. 2003b).

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surgery, 6% were able to perform reduced work,and one horse was retired. Fify-nine percent ofowners reported that the horse’s performance hadincreased as compared to pre-operativeperformance, 16% reported no change, and theremaining owners were unsure of any such change(Fig 3). Overall, 86% of owners considered thesurgery to be worthwhile, 3% did not consider it tobe worthwhile, and 11% were unsure of its value(Fig 4).

DISCUSSION AND CONCLUSIONS

When compared to LP procedures, VC had alower rate of post operative complications.Unsurprisingly, healing of the laryngotomy woundwas very similar to healing in horses thatunderwent LP with VC (Dixon et al. 2003a), withthe vast majority of horses having no dischargefrom the surgical site at 2 weeks post operatively.However, in horses which underwent LP plus VC,an additional 19% had wound complications(seromas, suture abcesses etc) associated with theLP wound. Although 22% of horses coughed postVC, this is considerably fewer than the 43% ofhorses which coughed after LP, and this isunsurprising because after VC the arytenoidcartilages are not fixed in an abducted position andshould be able to adduct and protect the airwayduring deglutition. Additionally, in the majority ofhorses which did cough post VC, coughing wasnot associated with eating and may therefore beattributable in some cases to pre-existing lowerairway disease (present in 29% of horses) ratherthan dysphagia due to surgical interference.

A larger percentage of horses were reported tomake abnormal respiratory noises post VC (34%)as compared to LP combined with VC (27%)(Dixon et al. 2003a) even though the group whichunderwent VC alone had a lower pre-operativemedian grade of RLN than those undergoing VCcombined with LP. This is surprising given that themajority of noise is thought to arise from vibrationof the vocal cord in horses afflicted with RLN

(Hammer et al. 1998; Kidd and Slone 2002).Similarly, slightly fewer horses were consideredsubjectively to have increased exerciseperformance post operatively as compared tohorses which underwent LP, but the overall rate ofowner satisfaction was very similar for the 2procedures.

This study shows that ventriculo-cordectomyis a useful alternative to laryngoplasty for selectedcases of RLN and is associated with a low postoperative complication rate and a high rate ofowner satisfaction.

REFERENCES

Brown, J.A., Derksen, F.J., Stick, J.A., Hartmann, W.M.,Robinson, N.E. (2003) Ventriculo-cordectomyreduces respiratory noise in horses with laryngealhemiplegia. Equine vet. J. 35, 570-774.

Dixon, P.M., McGorum, B.C., Railton, D.I., Hawe, C.,Tremaine, W.H., Pickles, K. and McCann, J. (2001)Laryngeal paralysis: a study of 375 cases in amixed-breed population. Equine vet. J. 33, 452-458.

Dixon, P.M., McGorum, B.C., Railton, D.I., Hawe, C.,Tremaine, W.H., Dacre, K. and McCann, J. (2003a)Long-term survey of laryngoplasty and Ventriculo-cordectomy in an older, mixed-breed population of200 horses. Part 1: Maintenance of surgicalarytenoid abduction and complications of surgery.Equine vet. J. 35, 389-396.

Dixon, P.M., McGorum, B.C., Railton, D.I., Hawe, C.,Tremaine, W.H., Dacre, K. and McCann, J. (2003b)Long-term survey of laryngoplasty and Ventriculo-cordectomy in an older, mixed-breed population of200 horses. Part 2: Owners’ assessment of the valueof surgery. Equine vet. J. 35, 397-401.

Hammer, E.J., Tulleners, E.P., Parente, E.J. and Martin,B.B. (1998) Videoendoscopic assessment ofdynamic laryngeal function during exercise inhorses with grade III left laryngeal hemiparesis atrest: 26 cases (1992-1995).

Kidd, J.A. and Slone, D.E. (2002) Treatment oflaryngeal hemiplegia in horses by prostheticlaryngoplasty, ventriculectomy and vocalcordectomy. Vet. Record 150, 481-484.

Lane, J.G. (2003) Differences between resting andtreadmill endoscoipic findings in regard to RLN. In:Proc. Havemeyer Foundation Monograph Series No11, Eds: P. Dixon, E. Robinson and J. F. Wade,R&W Publications (Newmarket) Ltd, pp 47-48.

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SESSION 6:

Evaluation of RLNtreatment efficacy

Chairman: Norm Ducharme

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TREATMENT OF RECURRENT LARYNGEALNEUROPATHY: PHYSIOLOGICAL AND PERFORMANCE EVALUATION

F. J. Derksen

College of Veterinary Medicine, Michigan State University, East Lansing, Michigan 48824-1314, USA

In exercising horses with recurrent laryngealneuropathy (RLN) there is dynamic collapse of theaffected arytenoid cartilage during inspiration andan inspiratory upper airway obstruction. Severityof the collapse and obstruction depends on degreeof laryngeal paresis (Martin et al. 2000). Theobstruction is characterised by increasedinspiratory trans-upper airway pressure,inspiratory impedance and inspiratory time, anddecreased inspiratory flows, respiratory frequencyand minute ventilation. Hypoxemia and hyper-capnia are also observed. (Derksen et al. 1986).Treatments for laryngeal hemiplegia include:prosthetic laryngoplasty ventriculectomy,ventriculo-cordectomy, laser cordectomy, partial,total and subtotal arytenoidectomy and laryngealre-innervation.

PROSTHETIC LARYNGOPLASTY

The prosthetic laryngoplasty technique was firstdescribed by Marks et al. (1970). The goal of theprocedure is to produce mechanical abduction ofthe arytenoid cartilage midway between normalresting and full abduction. Laryngoplasty returnsupper airway flow mechanics to baseline levels by30 days after surgery (Derksen et al. 1986;Shappell et al. 1988). Stabilisation of the affectedarytenoid is more important than the degree ofabduction. Indeed, there is no correlation betweendegree of arytenoid abduction and residual airwayobstruction following surgery (Russell et al. 1994).Prosthetic laryngoplasty is the treatment of choicefor RLN in horses where airway obstruction andexercise intolerance are the primary concern(Russell and Slone 1994; Hawkins et al. 1997).However, post operative complications arecommon and include prosthetic failure, dysphagia,coughing and infection (Hawkins et al. 1997).

VENTRICULO-CORDECTOMY

Ventriculectomy or sacculectomy, refers to theremoval of the laryngeal saccule. Ventriculectomyaims to produce abduction of the affectedarytenoid cartilage by formation of adhesionsbetween the arytenoid and thyroid cartilages andto reduce filling of the ventricle with air duringinspiration. Vocal cordectomy is often performedalone or in conjunction with ventriculectomy(ventriculo-cordectomy). These procedures maybe performed unilaterally or bilaterally andremaining tissues are left to heal by secondintention or sutured. Variations in surgicaltechniques are likely to influence efficacy.Unilateral ventriculectomy alone does not improveupper airway function 30 days after surgery(Shappell et al. 1988). Both unilateral vocalcordectomy and bilateral ventriculo-cordectomyreduce, but do not eliminate, upper airwayobstruction in laryngeal hemiplegia affectedhorses. These effects are evident 30 daysfollowing surgery. The beneficial effects ofprosthetic laryngoplasty on upper airway flowmechanics are not enhanced with bilateralventriculo-cordectomy (Tetens et al. 1996).

ARYTENOIDECTOMY

Arytenoidectomy is rarely the first choice ofsurgery for RLN but it is indicated in cases offailed prosthetic laryngoplasty or arytenoidchondritis. The total arytenoid cartilage may beremoved, (total arytenoidectomy), the muscularprocess may be left in place (partialarytenoidectomy), or the corniculate process maybe spared (subtotal arytenoidectomy).

Partial arytenoidectomy combined withbilateral ventriculo-cordectomy improves upper

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airway flow mechanics in exercising horses withexperimentally induced laryngeal hemiplegia(Lumsden et al. 1994) but flow volume loopanalysis shows that some airway obstructionremains. Complications following arytenoidectomyare common and include dysphagia and coughing.In search of a technique with fewer complications,subtotal arytenoidectomy was proposed. However,this fails to improve upper airway function(Belknap et al. 1990). Endoscopic evaluationduring exercise following subtotal arytenoidectomydemonstrates that the unsupported corniculateprocess collapses into the airway during inhalation.

LARYNGEAL RE-INNERVATION

As RLN treatments are ineffective or associatedwith serious complications, there has been interestin finding a more physiological solution, eglaryngeal re-innervation. Branches of the firstcervical nerve and associated omohyoideus muscleare transplanted into the affected crico-arytenoideus dorsalis muscle. The nerve musclepedicle graft technique is effective in restoringupper airway flow mechanics in horses withexperimentally induced laryngeal hemiplegia(Fulton et al. 1991). As the first cervical nerve isan accessory muscle of respiration, and the nerveis activated only during exercise, surgical successcan only be assessed at exercise. It may take up toa year for upper airway flow mechanics to returnto normal. Associated complications are mild andrare. Fulton et al. (2003) reported that the nervemuscle pedicle graft technique is as effective asprosthetic laryngoplasty in returningThoroughbreds to competitive racing andtherefore it is recommended when complicationslinked with other techniques are unacceptable, orwhen time between surgery and return to athleticactivity is less important.

EFFECT ON RACING PERFORMANCE

How effectively can surgery restore athleticperformance in RLN-affected racehorses? Stick etal. (2001) showed that elite Thoroughbredyearlings with Grade 3 or 4 RLN had reducedperformance as adults. Assuming that theyreceived the best available care, this suggests thatcurrent surgical treatments cannot fully restoreathletic performance in an elite Thoroughbredwith RLN. This is supported by other studies(Strand et al. 2000).

REFERENCES

Belknap, J.K., Derksen, F.J., Nickels, F.A., Stick, J.A.and Robinson, N.E. (1990) Failure of subtotalarytenoidectomy to improve upper airway flowmechanics in exercising standardbreds with inducedlaryngeal hemiplegia. Am. J. vet. Res. 51, 1481-1487.

Derksen, F.J., Stick, J.A., Scott, E.A., Robinson, N.E.and Slocombe, R.F. (1986) Effect of laryngealhemiplegia and laryngoplasty on airway flowmechanics in exercising horses. Am. J. vet. Res. 47,16-20.

Fulton, I.C., Derksen, F.J., Stick, J.A., Robinson, N.E.and Walshaw, R. (1991) Treatment of left laryngealhemiplegia in standardbreds, using a nerve musclepedicle graft. Am. J. vet. Res. 52, 1461-1467.

Fulton, I.C., Stick, J.A. and Derksen, F.J. (2003)Laryngeal re-innervation in the horse. Vet. Clin.North Am. equine Pract. 19, 189-208, viii.

Hawkins, J.F., Tulleners, E.P., Ross, M.W., Evans, L.H.and Raker, C.W. (1997) Laryngoplasty with orwithout ventriculectomy for treatment of leftlaryngeal hemiplegia in 230 racehorses. Vet. Surg.26, 484-491.

Lumsden, J.M., Derksen, F.J., Stick, J.A., Robinson,N.E. and Nickels, F.A. (1994) Evaluation of partialarytenoidectomy as a treatment for equine laryngealhemiplegia. Equine vet. J. 26, 125-129.

Marks, D., Mackay-Smith, M.P., Cushing, L.S. andLeslie, J.A. (1970) Use of a prosthetic device forsurgical correction of laryngeal hemiplegia inhorses. J. Am. vet. med. Ass. 157, 157-163.

Martin, B.B., Jr., Reef, V.B., Parente, E.J. and Sage, A.D.(2000) Causes of poor performance of horses duringtraining, racing, or showing: 348 cases (1992-1996).J. Am. vet. med. Ass. 216, 554-558.

Russell, A.P. and Slone, D.E. (1994) Performanceanalysis after prosthetic laryngoplasty and bilateralventriculectomy for laryngeal hemiplegia in horses:70 cases (1986-1991). J. Am. vet. med. Ass. 204,1235-1241.

Shappell, K.K., Derksen, F.J., Stick, J.A. and Robinson,N.E. (1988) Effects of ventriculectomy, prostheticlaryngoplasty, and exercise on upper airwayfunction in horses with induced left laryngealhemiplegia. Am. J. vet. Res. 49, 1760-1765.

Stick, J.A., Peloso, J.G., Morehead, J.P., Lloyd, J.,Eberhart, S., Padungtod, P. and Derksen, F.J. (2001)Endoscopic assessment of airway function as apredictor of racing performance in Thoroughbredyearlings: 427 cases (1997-2000). J. Am. vet. med.Ass. 219, 962-967.

Strand, E., Martin, G.S., Haynes, P.F., McClure, J.R. andVice, J.D. (2000) Career racing performance inThoroughbreds treated with prosthetic laryngoplastyfor laryngeal neuropathy: 52 cases (1981-1989). J.Am. vet. med. Ass. 217, 1689-1696.


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TREATMENT OF RECURRENT LARYNGEALNEUROPATHY: EVALUATION BY RESPIRATORYSOUND ANALYSIS

F. J. Derksen

College of Veterinary Medicine, Michigan State University, 200 Westborough Road, North Grafton,Michigan 48824-1314, USA

Upper respiratory disease is suspected in anexercising horse when an abnormal respiratorynoise is heard and when the horse’s performance isreduced. While performance reduction can becaused by dysfunction in many systems,respiratory noise during exercise is specific for anupper airway problem.

For sport horses, respiratory noise caused byconditions such as recurrent laryngeal neuropathy(RLN) can be more important than the obstructionitself. There is information in the literaturedescribing the efficacy of surgical procedures inimproving upper airway flow mechanics inexercising horses with RLN, (Derksen et al. 1986;Shappell et al. 1988; Tetens et al. 1996) but thereis little information about noise reduction. Thisinformation is also important for racehorses, asresidual respiratory noise after surgery is ofteninterpreted as failure to improve upper airway flowmechanics (Russell and Slone 1994; Hawkins etal. 1997; Kidd and Slone 2002). However, therelationship between noise and upper airwayobstruction has not been evaluated critically(Derksen 2003).

RECORDING AND ANALYSING RESPIRATORYSOUNDS IN EXERCISING HORSES

The first challenge associated with the quantitativeevaluation of respiratory sound in exercisinghorses is the squelching of extraneous noises. Toaccomplish this, a dynamic unidirectionalmicrophone is placed in such a way that therecording microphone is directed towards thenostrils and rests approximately 4 cm from thehorse’s nose. The microphone is connected to acassette recorder containing an automatic gaincontrol and a compression circuit. The combinedfeatures of this system reduce extraneous noises.

The recorded sounds are evaluated usingcomputer-based spectrum analysis (Derksen et al.2001).

RLN AND RESPIRATORY NOISE

Exercising horses with RLN make a distinctiveinspiratory noise. In affected horses, high-intensity sounds are present throughout inhalation(Cable et al. 2002; Franklin et al. 2003). Thissound is characterised by 3 frequency bands calledformants which are centred at approximately 400,1700, and 3700 Hz. Quantitative indicesdescribing the loudness and character of the soundinclude inspiratory sound level and the soundintensity of the 3 inspiratory formants (Derksen etal. 2001). The sound intensity of the formant 2,centred at about 1700 Hz, is most important,because this formant is in a frequency range wherehuman hearing is most acute.

EFFICACY OF SURGICAL PROCEDURES INREDUCING NOISE CAUSED BY RLN

Surgical techniques recommended for thetreatment of RLN include prostheticlaryngoplasty, the nerve muscle pedicle grafttechnique, ventriculectomy, ventriculo-cordectomy, laser cordectomy, and total, partial,and subtotal arytenoidectomy. Thus far, we haveonly studied the effect of prosthetic laryngoplastyand bilateral ventriculo-cordectomy on respiratorynoise caused by experimentally induced laryngealhemiplegia. Thirty days after surgery, bilateralventriculo-cordectomy has no effect on inspiratorynoise. However, at 90 and 120 days after surgerymost indices of inspiratory noise, including thesound intensity of formant 2, return to baselinelevels. Inspiratory sound level remains slightly but

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significantly elevated. Thus, bilateral ventriculo-cordectomy effectively reduces inspiratory noiseassociated with laryngeal hemiplegia.

The effects of prosthetic laryngoplasty onupper airway noise in laryngeal hemiplegiaaffected horses are already evident 30 days aftersurgery. However, key indices of sound intensity,including the sound intensity of formant 2, remainelevated relative to baseline levels. This indicatesthat prosthetic laryngoplasty is less effective thanventriculo-cordectomy in reducing laryngealhemiplegia associated noise. The efficacy ofprosthetic laryngoplasty in reducing airwayobstruction and noise is variable in individualhorses. The degree of remaining airwayobstruction following surgery and the amount ofresidual respiratory noise are not correlated.Therefore residual respiratory noise followingprosthetic laryngoplasty cannot be used todetermine the degree of remaining airwayobstruction in individual horses.

Interestingly, there is a significant positivecorrelation between the degree of arytenoidabduction and inspiratory noise following surgery.That is, the more arytenoid abduction achieved,the greater the residual noise. The degree ofarytenoid abduction following surgery does notcorrelate with residual airway obstruction.

REFERENCES

Cable, C.S., Ducharme, N.G., Hackett, R.P., Erb, H.N.,Mitchell, L.M. and Soderholm, L.V. (2002) Soundsignature for identification and quantification ofupper airway disease in horses. Am. J. vet. Res. 63,1707-1713.

Derksen, F.J. (2003) Practice is alive with the sounds ofhorses. Equine vet. J. 35, 224-225.

Derksen, F.J., Holcombe, S.J., Hartmann, W., Robinson,N.E. and Stick, J.A. (2001) Spectrum analysis ofrespiratory sounds in exercising horses withexperimentally induced laryngeal hemiplegia ordorsal displacement of the soft palate. Am. J. vet.Res. 62, 659-664.

Derksen, F.J., Stick, J.A., Scott, E.A., Robinson, N.E.and Slocombe, R.F. (1986) Effect of laryngealhemiplegia and laryngoplasty on airway flowmechanics in exercising horses. Am. J. vet. Res. 47,16-20.

Franklin, S.H., Usmar, S.G., Lane, J.G., Shuttleworth, J.and Burn, J.F. (2003) Spectral analysis ofrespiratory noise in horses with upper airwaydisorders. Equine vet. J. 35, 264-268.

Hawkins, J.F., Tulleners, E.P., Ross, M.W., Evans, L.H.and Raker, C.W. (1997) Laryngoplasty with orwithout ventriculectomy for treatment of leftlaryngeal hemiplegia in 230 racehorses. Vet. Surg.26, 484-491.





81


SPIROMETRIC AND ENDOSCOPIC ASSESSMENT OFSURGICAL TREATMENT IN HORSES WITHLARYNGEAL HEMIPLEGIA

M. A. Weishaupt, R. Vogt, A. Fürst and J. A. Auer

Equine Hospital, Faculty of Veterinary Medicine, University of Zurich, Switzerland

INTRODUCTION

The outcome of a ‘tie back’ operation is routinelyjudged, based on the endoscopic re-evaluation, thechanges in the quality and volume of the respiratorynoise and the performance history of the equineathlete. Exercise spirometry is a valuable method toquantify airflow limitation of upper airway diseases(Shappell et al. 1988; Belknap et al. 1990;Lumsden et al. 1993, 1994; Tetens et al. 1996;Weishaupt et al. 1998) and is therefore used in theauthors’ clinic to assess the functional improvementafter this surgical intervention.

The relationship between the degree ofabduction by laryngoplasty and the extent offunctional improvement is poorly investigated. Asover-abduction of the paralysed arytenoid mayresult in coughing and/or dysphagia, an optimallateralisation aims at correcting each athleteindividually in relation to its future athletic career.

The aim of this study was to quantify thefunctional improvement of a combinedlaryngoplasty-ventriculectomy procedure throughspirometric assessment and to correlate functionwith the arytenoid abduction angle determinedendoscopically before and after surgery.

MATERIAL AND METHODS

Horses were trained to canter on a high-speedtreadmill. Time and flow parameters weremeasured with an ultrasonic flowmeter (SpirosonScientific®, Isler Bioengeneering AG, Dürnten,Switzerland). The levels of exercise intensity wereadjusted to the horse's individual capabilities. Theleft abduction angle was surveyed on endoscopicpictures using the method described by Reutter(Reutter et al. 1994). A combined laryngoplasty-

ventriculectomy procedure was performed tocorrect the laryngeal hemiplegia. After arehabilitation and retraining period of 5 months,the horses were reassessed using the identicalexercise protocol. With the owner’s consent, 19Warmblood horses with left laryngeal hemiplegiaGrade 4/4 (Rakestraw et al. 1991) were assessedin this way.

RESULTS

Before surgery, beginning airflow limitation couldbe observed already at the trot; the conclusiveinspiratory flow limitation occurred usually onlyat canter intensities of 6.0-7.5 m/s at 6% incline(heart rates 158-209/min). The inspiratory flowcurve was characterised by a plateau phase andpeak values were limited at 48 ± 9.9 l/s (mean ±SD; range 26–63 l/s). At expiration no limitationwas obvious and peak flow reached 69 ± 9.8 l/s(range 49–94 l/s). Inspiratory time was alwaysprolonged. Horses with severe inspiratory,dynamic collapse of the paralysed arytenoid,showed an initial flow peak with a subsequentcharacteristic drop of flow. At the canter, 7 of the19 horses changed their 1:1 locomotion-to-respiration coupling (LRC) intermittently orpermanently to 2:1.

Differences in the degree of abduction and offunctional parameters after surgery are listed(Table 1).

Independent of the LRC strategy, peakinspiratory flow (PIF) increased over all horses by46.2% and thus proportional to the abductionangle. Minute ventilation (VE) increased inaverage by 30.9%.

Comparing the increase of PIF and VE withthe changes of the left abduction angle nosignificant correlation could be found (Pearson,

82


P<0.05). However, looking at the plots, 2 groupscould be discerned: In two thirds of the patients,PIF increased linearly with increasing abductionangle so that an increase of one degree improvedPIF by 1.2 l/s (R2 = 0.815). In the other horsesrespiratory function improved although thesurgical correction was inadequate but enough toprevent dynamic collapse of the paralysedarytenoid.

DISCUSSION

Based on geometric considerations, the area of theleft half of the rima glottidis, outlined by thearytenoid cartilage, the vocal cord and the midline,increased proportionally up to an abduction angleof 45°. In this range, PIF increased byapproximately one litre per second with everyfurther degree of abduction. Inappropriate surgicalcorrections (0–10° abduction) improvedrespiratory function disproportionately bypreventing dynamic collapse. For abductionangles above 45°, the geometric calculationsindicate that the laryngeal aperture does notfurther increase substantially, as the area isestimated to be a function of the sinus of the angle.The functional benefit of abduction angles >50° –which are usually aimed at in racehorses – has stillto be investigated.

In conclusion, sole endoscopic assessment may notreflect in all cases the functional improvement of alaryngoplasty-ventriculectomy procedure.

REFERENCES

Belknap, J.K., Derksen, F.J., Nickels, F.A., Stick, J.A.and Robinson, N.E. (1990) Failure of subtotalarytenoidectomy to improve upper airway flowmechanics in exercising standardbreds with inducedlaryngeal hemiplegia. Am. J. vet. Res. 51, 1481-1487.

Lumsden, J.M., Derksen, F.J., Stick, J.A., and Robinson,N.E. (1993) Use of flow-volume loops to evaluateupper airway obstruction in exercisingstandardbreds. Am. J. vet. Res. 54, 766-775.

Lumsden, J.M., Derksen, F.J., Stick, J.A., Robinson,N.E. and Nickels, F.A. (1994) Evaluation of partialarytenoidectomy as a treatment for equine laryngealhemiplegia. Equine vet. J. 26, 125-129.

Rakestraw, P.C., Hackett, R.P., Ducharme, N.G., Nielan,G.J. and Erb, H.N. (1991) Arytenoid cartilagemovement in resting and exercising horses. Vet.Surg. 20, 122-127.

Reutter, H., Straub, R. and Gerber, H. (1994) Diagnosisof idiopathic laryngeal hemiplegia in the horse:videoendoscopic examination with and withoutstimulation of respiration. Pferdeheilk 10, 397-405.


Tetens, J., Derksen, F.J., Stick, J.A., Lloyd, J.W. andRobinson, N.E. (1996) The efficacy of prostheticlaryngoplasty with and without bilateral ventriculo-cordectomy as treatments for laryngeal hemiplegiain horses. Am. J. vet. Res. 57, 1668-1673.

Weishaupt, M.A., Kästner, S.B.R., Grieshaber, K. and K.V.P. (1998) Airflow limitations in laryngealhemiplegia: chemical versus exercise inducedhyperventilation. Proc. WEAS, 1:9.

TABLE 1: Mean difference ± SD (percentage difference)

Aabd 7.1 ± 7.7 (+42.3%)*LRC 1:1 LRC 2:1

fR 0.3 ± 1.3 (+0.3%) 32 ± 14.5 (+50.1%)*tinsp -3.5 ± 3.2 (-6.1%)* -10.8 ± 4.5 (-16.9%)*VT 2.5 ± 1.2 (+18.1%)* -0.4 ± 4.5 (-1.7%)VE 269 ± 108 (+18.4%)* 593 ± 265 (+54.9%)*PIF 16.4 ± 7.0 (+31.5%)* 28.9 ± 9.5 (+73%)*PEF 3.5 ± 4.7 (+5.6%) 7.5 ± 6.1 (+11.2%)*

Aabd, abduction angle [degree]; fR, respiratory rate [1/min]; tinsp, inspiratory time fraction [%]; VT, tidal volume[l]; VE, minute ventilation [l/min]; PIF, peak inspiratory flow [l/s]; PEF, peak expiratory flow [l/s]* significant difference (paired t-test, P<0.05)

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MANAGEMENT OF CANINE LARYNGEAL PARALYSIS

J. G. Lane


In the horse recurrent laryngeal neuropathy hasbeen recognised as a clinical disorder forcenturies, but in the dog laryngeal paralysis wasfirst documented only 30 years ago (O’Brien et al.1973). It is likely that the condition is not new butnewly recognised and in former times it may havebeen confused with cardio-pulmonary failure ornon-responsive idiopathic millophyllinedeficiency (Table 1).

The major differences between the canine andequine presentations of the neurogenic failure ofthe intrinsic laryngeal musculature are that in dogsthe disease is typically bilateral by the time thatclinical signs appear, and older animals are likelyto be involved. A congenital and inherited versionof the disorder is recognised in the Bouvier deFlandres (van Haagen 1978) and the husky(Hendricks and O’Brien 1985), but the majority ofcanine patients are over 10 years of age atpresentation. Two thirds of afflicted dogs are maleor neutered male and those weighing 25–35 kg aremost susceptible. The best recognised predisposedbreeds include the Labrador retriever, Afghanhound, Irish setter, and English and Germanpointers (Lane 1986; see Table 2). Giant breedsare rarely involved probably because of theirlimited longevity.

The presenting signs for canine laryngealparalysis (Table 1) include stridorous breathingeven at rest, reduced exercise tolerance, a moistretching cough and loss of bark. Ownerexpectations of older dogs often lead to delayedpresentation.

Ventriculo-cordectomy has never beenproposed as a means to manage canine laryngealparalysis (Table 3) but initially a radical partiallaryngectomy was used (O’Brien et al. 1973). Thiscomprised the excision of the true and false vocalfolds as well as the ventral projections of thearytenoid cartilages. An unacceptable complicationrate was achieved (Ross et al. 1991).

Laryngoplasty (‘tie-back’) surgery representsone of the few instances where an equinetechnique has been transferred to canine surgery.The technique first proposed a lateralisation of thedisarticulated arytenoid on each side of the larynxto the wing of the thyroid cartilage using a ventralapproach (Harvey and van Haagen 1975). Thetechnique most widely used today comprises acombined prosthetic abductor implantation with alateralising suture on the left side of the larynxonly (Lane 1982; LaHue 1989). The left lateralapproach is similar to that used in the horse but thesmall muscular process of the dog is insufficientlyrobust to hold fixation sutures. Thus, the arytenoidis disarticulated to access the thicker body of thecartilage. Although the canine version of thedisease is invariably bilateral a unilateral solutionis sufficient for the demands of the sedentary lifeof an elderly dog. Only working dogs such asHuntaways are subjected routinely to bilateralsurgery (Burbidge et al. 1993).

The results of ‘tie-back’ surgery in dogs areexcellent in experienced hands and the incidenceof complication is much lower than for theequivalent procedure in horses (White 1989).

TABLE 1: Major presenting signs reported byowners of 750 dogs with acquired laryngealparalysis presented at UBVS

Stridor 656

Gagging/retching cough 434

Changed bark 327

Reduced exercise tolerance 317

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TABLE 2: Breed prevalence in 750 dogs with acquired laryngeal paralysis presented at UBVS

Breed UBVS Cases UK control population(Thrusfield, 1989)

No % %Labrador* 307 40.9 10.7Afghan hound* 84 11.2 NR < 3Irish setter* 61 8.1 NR < 3Golden retriever* 43 5.7 3.8English springer spaniel 20 2.7 2.9Border collie 16 2.1 4.5Flat coat retriever 14 1.9 NR < 3English setter 13 1.7 NR < 3Standard poodle 13 1.7 NR < 3St Bernard 10 1.3 NR < 3Finnish spitz 10 1.3 NR < 3Rhodesian ridgeback 9 1.2 NR < 3Weimaraner 7 0.9 NR < 3Airedale 6 0.8 NR < 3English cocker spaniel ‡ 6 0.8 4.3Greyhound 6 0.8 NR < 3Other + crosses 125 - -German SD ‡ 0 - 8.4Yorkshire terrier ‡ 0 - 6.0Jack Russell terrier ‡ 0 - 5.2West Highland terrier ‡ 0 - 3.9

* Significantly over-presented breeds‡ Significantly under-presented breedNR Insufficient numbers recorded but less than 3 percent

TABLE 3: The development of surgical treatments for acquired laryngeal paralysis of dogs

Date Technique Authors

1973 Partial laryngectomy O'Brien et al.

1975 Unilateral arytenoid lateralisation by ventral Harvey and Venker-van approach, using routine tracheotomy intubation Haagen

1982 Unilateral arytenoid lateralisation by lateral Lane

approach without routine tracheotomy

intubation

1982 Bilateral arytenoid lateralisation by ventral Rosen and Greenwood

approach

1983 Castellated laryngofissure and vocal fold Gourley et al.

resection

1986 Modified castellated laryngofissure with Smith et al.

arytenoid lateralisation

1986 Abductor prosthesis Lane

(also cited by LaHue 1989)

1986 Composite laryngoplasty combining unilateral Lane

abductor prosthesis with lateralisation

1993 Bilateral arytenoid lateralisation using Burbidge et al.

bilateral lateral approaches

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Apart from follow-up data from owners attemptshave been made to measure the physiologicalimpact of the airway obstruction and its reliefusing arterial gas tensions (Love et al. 1987) andtidal breathing flow-volume analysis (Amis et al.1986). However, elderly dogs are not amenable tocontrolled exercise regimes on treadmills andtechniques to assess respiratory obstruction indogs are limited.

REFERENCES

Amis, T.C. and Kurpershoek, C. (1986) Tidal breathingflow-volume analysis for clinical assessment ofairway obstruction in conscious dogs. Am. J. vet.Res. 47, 1002-1006.

Burbidge, H.M., Goulden, B.E. and Jones, B.R. (1993)Laryngeal paralysis in dogs: an evaluation of thebilateral arytenoid lateralisation procedure. J. smallAnim. Pract. 34, 515-519.

Gourley, V.M., Paul, M. and Gregory, C. (1983)Castellated laryngofissure and vocal fold resectionfor the treatment of laryngeal paralysis in the dog. J.Am. vet. med. Ass. 182, 1084-1086

Harvey, C.E. and van Haagen, A.J. (1975) Surgicalmanagement of pharyngeal and laryngeal airwayobstruction in the dog. Vet. Clin. North Am. 5, 515-535.

Hendricks, J.C. and O'Brien, J.A. (1985) Inheritedlaryngeal paralysis in Siberian Husky crosses. ProcACVIM.

LaHue, T.R. (1989) Treatment of laryngeal paralysis indogs by unilateral crico-arytenoid laryngoplasty. J.

Am. Anim. Hosp. Ass. 25, 317-324Lane, J.G. (1982) In ENT and oral surgery of the dog and

cat. Bristol: Wright Scientifica 80-102.Lane, J.G. (1986) Diseases and surgery of the larynx.

Proc. Am. anim. Hosp. Ass. 620-623.Love, S., Waterman, A.E. and Lane, J.G. (1987) The

assessment of corrective surgery for caninelaryngeal paralysis: a review of 35 cases. J. smallAnim. Pract. 28, 597-604.

O'Brien, J.A., Harvey, C.E., Kelly, A.M. and Tucker, J.A.(1973) Neurogenic atrophy of the laryngeal musclesof the dog. J. small Anim. Pract. 15, 521-532.

Rosen, E. and Greenwood, C. (1982) Bilateral arytenoidlateralisation for laryngeal paralysis in the dog. J.Am. vet. med. Ass. 180, 515-518.

Ross, J.T., Mattiesen, D.T. and Noone, K.E. (1991)Complications and long-term results after partiallaryngectomy for the treatment of idiopathiclaryngeal paralysis in 45 dogs. Vet. Surg. 20, 169-173.

Smith, M.M., Gourley, I.M. and Kurpershoek, C. (1986)Evaluation of a modified castellated laryngofissurefor alleviation of upper airway obstruction in dogswith laryngeal paralysis. J. Am. vet. med. Ass. 188,1279-1283.

Thrusfield, M.V. (1989) Demographic characteristics of the canine and feline populations of the United Kingdom in 1986. J. small Anim. Pract. 30,76-80

van Haagen, A.J. (1978) Spontaneous laryngealparalysis in young Bouviers. J. Am. Anim. Hosp.Ass. 14, 714-720.

White, R.A.S. (1989) Unilateral arytenoid lateralisation:an assessment of technique and long term results in62 dogs with laryngeal paralysis. J. small Anim.Pract. 30, 543-549.

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87


SESSION 7:

The future

Chairman: Ed Robinson

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89


IS RLN INHERITED? NEWER TECHNIQUES TO HELPINVESTIGATE THIS QUESTION

M. Binns and J. Swinburne

Animal Health Trust, Centre for Preventive Medicine, Lanwades Park, Kentford, Newmarket, SuffolkCB8 7UU, UK

Several papers have been published which suggestthat laryngeal hemiplegia has a genetic basis. Inmany of these studies it has been observed that theoffspring of affected stallions are more likely to beaffected than the offspring of unaffected controlstallions. For example, in one recent studyexamining 47 offspring of an affected stallion, 11were affected with laryngeal hemiplegia andanother 11 were suspect whereas, in a controlgroup of 50 offspring, only one affected and 4suspect individuals were seen. The difference issignificant at the P<0.01 level. A significantdifference in the average height at the withers ofthe affected stallion’s affected offspring was notedcompared to his unaffected offspring. Someauthors have proposed that a dominant gene maybe responsible for the disease. One group lookedfor an association between particular equineleucocyte antigen (ELA) haplotypes and laryngealhemiplegia with negative results.

The development of a genetic linkage map forthe horse provides the molecular tools to attempt tomap diseases and traits with a genetic basis in thehorse. A map with 359 microsatellite markers, with

markers assigned to every chromosome, waspublished in 2000. Further work has doubled thenumber of markers mapped on the linkage map.The recent publication of the first radiation hybrid(RH) map of the horse enables the power ofcomparative genetics to be applied to geneticstudies in the horse. The horse RH map identifiesconserved evolutionary segments between thehorse and human genomes. These resources havebeen supplemented by the construction of a highquality bacterial artificial chromosome (BAC)library, containing 10-fold coverage of the horsegenome, which provides researchers with readyaccess to cloned genomic copies of nearly all horsegenes. Increasing numbers of horse expressedsequence tags (ESTs) from multiple tissues are alsonow being deposited in the sequence databases.

The availability of these molecular tools toundertake genetic characterisation of diseases andtraits in the horse presents many opportunities toimprove the health of horses. Combiningsophisticated clinical expertise and moleculargenetics in the area of recurrent laryngealneuropathy should prove fruitful.

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MULTICENTRE TRIALS FOR EFFICACY OFTREATMENT

N. Ducharme

College of Veterinary Medicine, Cornell University, Ithaca, New York, USA

Over the last 30 years, there have been manysurveys and reports from multiple centresdescribing treatment results for a large number ofhorses with recurrent laryngeal neuropathy (RLN)(Russel and Sloane 1994; Hawkins et al. 1997;Strand et al. 2000; Kidd et al. 2002; Dixon et al.2003a,b). In addition, there is reasonableexperimental data available for evaluating thepatency of the upper airway after the currentsurgical options: ventriculectomy, ventriculo-cordectomy, laryngoplasty, subtotal arytenoi-dectomy, partial arytenoidectomy, and laryngealinnervation (Derksen et al. 1986; Shappel et al.1988; Tetens et al. 1996). Recently, moreknowledge has been gained about methods toobjectively measure upper airway sounds afterthese various treatments.

Is there a need for multicentre trials, and whatbenefits would a centrally coordinated multicentretrial provide? Before we answer these questions,consider that the success rate in various surveys forracehorses treated for laryngeal hemiplegia (LH)ranges from 50 to 70%. Also, significantcomplications such as tracheal aspirations,persistence of upper respiratory noise, incisionalseromas, incisional infection, and chondritis are stillseen. It is necessary to know the optimal way tomanage these complications in addition to reducingtheir number and severity. It would be useful toknow: 1) the odds ratio that a horse will developchondritis or decreased abduction after an incisionalseroma; 2) the desirable degree of abduction to betargeted at surgery related to a horse’s specificactivity; 3) whether more horses return to work aftera partial arytenoidectomy than after a laryngoplasty;whether the Netherlands’ elimination of horses withlaryngeal hemiplegia and some degree of laryngealhemiparesis from breeding considerations decreasedthe incidence of the disease; and 4) whether

laryngeal re-innervation is useful for reducing upperrespiratory noise in horses performing atsubmaximal exercise levels. Clearly there are manyunanswered questions that remain.

WHAT CORE OBJECTIVES WOULD AMULTICENTRE TRIAL ACHIEVE?

1) Accumulation of significant data forevaluating treatment results stratified bysubtypes of horse and activity.

2) A group could be set up to developrecommended guidelines for treating andmanaging LH complications based uponreview of the data evidence. This group couldalso help set research guidelines or priorities.

HOW WOULD THIS WORK?

‘The Equine Recurrent Laryngeal Neuropathy(ERLN) group’ could oversee the study design (ieinclusion criteria). The data would be entered at thepoint of collection only by participatinginvestigators using a web-based program thatwould allow anyone to view the data beingaccumulated. For example, the treatment could bestratified by breed, age at the time of treatment, andactivity (jumper, hunter, racehorses [point to point,flat race, steeple chase, 3 day event, quarter horse,barrel racing, and endurance] and show horses).The type of treatment (laryngeal re-innervation,laryngoplasty, partial arytenoidectomy) andtechnical details such as type and number ofsutures, pattern of anchorage, and experience ofsurgeon would also be recorded. Criteria forevaluating results consistently would be agreedupon beforehand so success would be uniformlydefined.

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Treatment complications are a critical factor toevaluate in the author’s opinion. One of the firstbenefits of a multicentre trial could be theknowledge obtained about complications and theirmanagement, which have not been well addressedhistorically. For example, data collected couldshow whether immediate re-operation or patienceis best for handling acute dysphagia. The ERLNgroup could make recommendations such as thoseshown in Figure 1 based on their review of currentevidence. Aside from diagnosis and treatmentconsiderations, blood samples could be used forgenomic testing, histopathological samples couldbe sent to different laboratories with differentfocuses, etc, and the understanding of theheritability of RLN could be increased.

ADVANTAGES IN ESTABLISHING RESEARCHCRITERIA AND PRIORITIES

Most researchers use different exercise protocolsand testing criteria. The group should establishrecommended exercise protocols in order to obtainconsistent data. For example, they could discussthe pros and cons for: 1) using exercise protocols

at maximal heart rate on an incline at lower speedsvs maximal heart rate at maximal speed; 2)different research protocols for sprinters comparedto horses that perform at longer distances; 3) thebest indices of airway mechanics data (ie arterialblood gases, flow volume loops and their indices,pressure flow curves and their indices, pulseoximetry); 4) standardising sound collectionprocedures for sound analysis; and 5) settingpriorities in the treatment: method of anchoringthe prosthesis, degree of abduction targeted, bestpost operative feeding protocol, post operativediet, etc.

The ERLN group could help identify areasthat have been researched enough and those inneed of further investigation.

WHAT ARE THE HURDLES?

The needs for an agency to fund the establishmentof the ELH group, organise a meeting, set up data collection, and maintain a website. The organisational procedures of similarorganisations, such as the Cochrane Collaboration(www.cochraneconsumer.com), could be

Acute dysphagia post operatively

Can the horse drink without nasalregurgitation?

Yes

Feed small amount ofhay from ground

No

Scope the horse: isthe arytenoid

hyperabducted? NoNo

Sedate horse, NPO,administered IV fluids,

re-operated if noimprovement in 48 h

Pass stomachtube, check for

choke

Fig 1: Example of guidelines to be established by the ERLN group.

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followed. Distances to be travelled by aninternational group would be an issue.

It is not a trivial issue to establish criteria thattruly assess performance. There have beenmultiple studies of horses’ performance postlaryngoplasty, but even objective performanceindices are affected by subjective issues, such astrack surface, degree of fitness, race availability,etc. It is difficult to evaluate a 2-year-old racehorsethat has not raced or has only had one start or toapply objective criteria to non-racehorses. Perhapsonly horses that have measurable successparameters (racehorses, grand prix jumping, etc)would be evaluated, but this is a difficult issue thatmust be resolved. The methods for collecting datamust be established. It is perhaps easier withracehorses, but how are complications evaluated,who reports it, and who contacts the owners?

POTENTIAL BENEFITS

The establishment of an equine health group thatfocuses on the equine larynx and could coordinatemulticentre trials whose design and sample sizewould allow accumulation of a large data set soconfounding variables are more likely to becircumvented. This group could review andpromote the best evidence for effective treatmentsand management of their complications. Thegroup’s study would allow veterinarians and horseowners to make informed decisions in managingtheir horses based on evidence-based medicine.

REFERENCES

Dixon, P.M., McGorum, B.C., Railton, D.I., Hawe, C.,Tremaine, W.H., Pickles, K. and McCann, J. (2003a)Long term survey of laryngoplasty and ventriculo-cordectomy in an older mixed-breed population of

200 horses. Part 1: Maintenance of surgicalarytenoid abduction and complications of surgery.Equine vet. J. 35, 389-396.

Dixon, P.M., McGorum, B.C., Railton, D.I., Hawe, C.,Tremaine, W.H., Pickles, K. and McCann, J.(2003b) Long term survey of laryngoplasty andventriculo-cordectomy in an older mixed-breedpopulation of 200 horses. Part 2: Owners’assessment of the value of surgery. Equine vet. J. 35,397-401.

Derksen, F.J., Stick, J.A., Scott, E.A., Robinson, N.E.and Slocombe, R.F. (1986) Effects of laryngealhemiplegia and laryngoplasty on airway flowmechanics in exercising horses. Am. J. vet. Res. 47,16-26.

Hawkins, J.F., Tulleners, E.P., Ross, M.W., Evans, L.H.and Raker, C.W. (1997) Laryngoplasty with orwithout ventriculectomy for treatment of leftlaryngeal hemiplegia in 230 horses. Vet. Surg. 26,484-491.



Shappel, K.K., Derksen, F..J., Stick, J.A. and Robinson,N.E. (1988) Effects of ventriculectomy, prostheticlaryngoplasty, and exercise on upper airwayfunction in horses with induced left laryngealhemiplegia. Am. J. vet. Res. 49, 1760-1766.

Strand, E., Martin, G.S., Haynes, P.F., McClure, J.R. andVice, J. (2000) Career racing performance inThoroughbreds treated with prosthetic laryngoplastyfor laryngeal neuropathy: 52 cases (1981-1989). J.Am. vet. med. Ass. 217, 1689-1696.

Tetens, J., Derksen, F.J., Stick, J.A., Lloyd, J.W. andRobinson, N.E. (1996) Efficacy of bilateralprosthetic laryngoplasty with and without bilateralventriculo-cordectomy as treatments for laryngealhemiplegia in horses. Am. J. vet. Res. 57, 1668-1673.

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WORKSHOP SUMMARY

CONSENSUS STATEMENTS ON EQUINERECURRENT LARYNGEAL NEUROPATHY

General

1. The term recurrent laryngeal neuropathy(RLN) is preferable to idiopathic laryngealhemiplegia (ILH) to describe a disease thatcan manifest as laryngeal paresis or paralysis.

2. RLN is mainly a disease of the left side of thelarynx.

3. Clinically and endoscopically RLN occurswith higher frequency in larger horses thanponies, but the relationship between body sizeand presence of disease is unresolved.

4. Abnormal inspiratory sounds during exercise,commonly referred to as ‘roaring or whistling’are a principal clinical sign of RLN.

5. RLN can cause reduced exercise performance.

6. Other dynamic inspiratory obstructions of theupper airway such as axial deviation of thearyepiglottic folds, arytenoid chondritis, andnasopharyngeal collapse can cause similarclinical signs to RLN.

Anatomy of the recurrent laryngeal nerve

1. The recurrent laryngeal nerve provides themotor innervation of all the equine laryngealmuscles except the cricothyroid, which isinnervated by the cranial laryngeal nerve.

2. The cell bodies of the lower motor neurons ofthe recurrent laryngeal nerves are located inthe nucleus ambiguus.

3. The recurrent laryngeal nerve comprisesefferent and afferent nerves, principallymedium sized, myelinated axons that are notdiscretely clustered according to their targetmuscle.

4. The proportion of motor and sensory fibres inthe recurrent laryngeal nerves is unknown.

5. The right and left recurrent laryngeal nervesloop around the subclavian artery and aorticarch, respectively.

6. The left recurrent laryngeal nerve is thelongest nerve in the horse and is believed toadhere tightly to the fascia of the aorta.

Pathology and pathogenesis

1. Although the disease clinically presentsalmost exclusively as a consequence ofreduced abduction (see Table 1 for definitionof terminology) of the left arytenoid cartilagedue to dysfunction of the cricoarytenoideusdorsalis muscle, the ipsilateral adductormuscles are preferentially denervated in RLN.

2. The lesions of RLN, which includepreferential degeneration of large diameteraxons, more prominent distally, are indicativeof a distal axonopathy.

3. The presence of similar lesions in other longnerves (eg phrenic or peroneal) of affectedhorses needs more investigation to determineif RLN is a mono – or a polyneuropathy.

4. RLN is not simply a result of nerve length;although the recurrent laryngeal nerve of largehorses is about 3 m, other mammals have nervesup to 6 m long (eg giraffe’s recurrent laryngealnerve) without neuronal degeneration.

5. The neuromuscular pathological changespresent in RLN indicate ongoing, continual orintermittent injury of the recurrent laryngealnerve with repeated attempts at regeneration.

6. Horses with other recognised neuropathies,for example stringhalt or Swedish knucklingdisease, can undergo complete recovery but itis unclear if this can occur in RLN.

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7. Even though there is histological andhistochemical evidence of regeneration ofnerves and reinnervation of muscles, clinicaland endoscopically evident recovery isuncommon in RLN.

8. It is not known if chromatolyis of the motorneurons of the nucleus ambiguus occurs inRLN. This information is critical toclassification of the type of neuropathy presentin this disorder.

9. Nerve and muscle lesions potentiallyconsistent with RLN have been observed infetuses and neonatal foals. This topic needsmore investigation because the presence ofRLN in early life has major implications in thepathogenesis of the disease.

10. The relationship between endoscopic changesin laryngeal movement and neuromuscularpathology in RLN is incompletelyunderstood.

11. If RLN is a neuropathy that affects only onenerve, it would be a unique mammalianneuropathy.

12. There is a total absence of information on themolecular pathology of RLN.

13. Canine idiopathic recurrent laryngealneuropathy is similar to equine RLN in that itaffects larger breeds but differs in that thecanine disease is usually bilateral and affectsolder dogs clinically.

14. There is evidence to suggest a certain degreeof heritability of RLN. However, themechanisms involved (structural or functionalweakness) and mode of inheritance remainunclear.

Other causes of laryngeal paresis or paralysis

1. Dysfunction of the recurrent laryngeal nervecan also be caused by perivascular injections,guttural pouch mycosis, cranial thoracicmasses, as a consequence of generalanaesthesia (possibly due to hyperextension ofthe head and neck during surgery), or otheriatrogenic causes during cervical surgery.

2. Bilateral laryngeal paresis commonlyaccompanies lead poisoning and can alsooccur with liver disease, following generalanaesthesia and with organophosphate toxicityand some plant toxicities.

3. The most common cause of right side laryngealdysfunction is cricopharyngeal laryngealdysplasia (4th branchial arch defect [4-BAD]).

DIAGNOSIS

General

1. Examination of a horse suspected of havingRLN should include the following: a history todetermine the animal’s exercise performance,nature of possible abnormal exercise relatedrespiratory sounds and when they occur;palpation of the larynx for muscular atrophy,and endoscopic examination.

2. An evaluation of the respiratory tract thatdepends on endoscopy alone is incomplete.

3. When there is a mismatch between endoscopicand historical and clinical findings, high-speedtreadmill endoscopy is indicated to evaluatethe function of the larynx during strenuousexercise.

TABLE 1: Definitions of terminology used to describe endoscopic appearance of the larynx

Abduction Movement of the corniculate process of the arytenoid cartilage away from the midline of the rima glottis

Adduction Movement of the corniculate process of the arytenoid cartilage toward the midline of the rima glottis

Full abduction Most of the corniculate process of the arytenoid cartilage lies horizontally (90 degrees to the midline of the rima glottis)

Asymmetry A difference in position of the right and left corniculate processes relative to the midline of the rima glottis

Asynchrony Movement of the corniculate processes occurs at different times. This can include twitching, shivering and delayed or biphasic movement of one arytenoid

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Guidelines for endoscopic examination for thepurpose of laryngeal evaluation

1. Evaluation should be performed with as littlerestraint as needed for safety of horse andpersonnel.

2. The use of chemical restraint can alterlaryngeal function.

3. To achieve consistency in the endoscopicappearance of the larynx, it is recommendedthat the same nostril be used routinely forintroduction of the endoscope.

4. The initial endoscopic examination should beconducted before rather than after exercise.This allows observation of a wider range oflaryngeal movements.

5. During the endoscopic examination, laryngealfunction should be observed during quietbreathing, swallowing and nasal occlusion.

Clinical grading of RLN

1. Although a number of grading systems areavailable and validated, they consistentlyagree on the following:

a) Inability to achieve full abduction of theaffected arytenoid cartilage duringexamination is likely to be associated withcompromised respiratory function duringexercise.

b) Glottic asymmetry at end-exhalation andasynchronous arytenoid movement duringinhalation are not cause for concern as long assuch horses can attain and maintain fullbilateral abduction of their arytenoidcartilages.

2. The grading systems shown in Tables 2 and 3is recommend by participants in the workshop.

3. There was no consensus on the functionalsignificance of obtaining full arytenoidabduction that is not maintained symmetrically.

4. In the majority of horses, laryngeal functionremains constant over time, but in somehorses, laryngeal function can deteriorate overa few weeks to years regardless of initialendoscopic appearance.

5. Endoscopic evaluation of the larynx inweanlings for presence of RLN is an

unreliable predictor of their laryngealendoscopic appearance as yearlings.

Other diagnostic procedures

1. Other tests of recurrent laryngeal functioninclude palpatory and endoscopic assessmentof the thoraco-laryngeal reflex (‘slap test’) andmeasurement of nerve conduction velocity, ieelectrolaryngeogram. Currently, none of theseprocedures is believed to be as effective asendoscopic examination for diagnosing RLN.

TREATMENT OF CLINICAL SIGNSASSOCIATED WITH RLN

1. Surgical treatments used for relief of theclinical signs of RLN include ventriculectomywith or without vocalcordectomy, prostheticlaryngoplasty, various degrees ofarytenoidectomy, and nerve muscle pediclegrafts (reinnervation surgery).

2. These procedures vary in their efficacy in thereduction of abnormal exercise related soundsand the relief of airway obstruction.

3. Most of the following conclusions are basedon studies in experimentally induced laryngealhemiplegia. In the following section ‘RLN’signifies the naturally occurring condition.

Abnormal upper respiratory sounds

1. Prosthetic laryngoplasty alone significantlyreduces the abnormal upper airway noise inRLN afflicted horses.

2. Following prosthetic laryngoplasty, there is noclear correlation between the degree ofresidual upper respiratory noise and themagnitude of surgical arytenoid abduction.

3. The degree of noise reduction afterlaryngoplasty may be more a factor of stabilityof the arytenoid cartilage rather than thedegree of arytenoid abduction.

4. Bilateral ventriculo-cordectomy can reduceabnormal upper airway sounds in horses withexperimentally induced left laryngealhemiplegia.

5. Unilateral ventriculo-cordectomy can reduceabnormal upper airway sounds in RLNafflicted horses.

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TABLE 2: Grading system of laryngeal function performed in the standing unsedated horse†

Grade Description Sub-grade

I All arytenoid cartilage movements are synchronous and symmetrical and full arytenoid cartilage abduction can be achieved and maintained

II Arytenoid cartilage movements are .1 Transient asynchrony, flutter or delayed asynchronous and/or larynx asymmetric movements are seenat times but full arytenoid cartilage .2 There is asymmetry of the rima glottidisabduction can be achieved and much of the time due to reduced mobilitymaintained of the affected arytenoid and vocal fold but

there are occasions, typically after swallowing or nasal occlusion when full symmetrical abduction is achieved and maintained

III Arytenoid cartilage movements are .1 There is asymmetry of the rima glottidis asynchronous and/or asymmetric. much of the time due to reduced mobility ofFull arytenoid cartilage abduction the arytenoid and vocal fold but there are cannot be achieved and occasions, typically after swallowing or nasalmaintained occlusion when full symmetrical abduction is

achieved but not maintained.2 Obvious arytenoid abductor deficit and arytenoid asymmetry. Full abduction is neverachieved.3 Marked but not total arytenoid abductor deficit and asymmetry with little arytenoid movement. Full abduction is never achieved

IV Complete immobility of the arytenoid cartilage and vocal fold

† Description generally refers to the left arytenoid cartilage in reference to the right. However this gradingsystem can apply to the right side (ie right Grade III-1)

6. Following ventriculo-cordectomy abnormalupper airway sounds can continue to decreasefor up to 90 days after surgery.

7. Bilateral ventriculo-cordectomy is superior tolaryngoplasty alone in reduction of abnormalsounds in horses with experimentally inducedleft laryngeal hemiplegia.

Exercise intolerance

1. Unilateral ventriculectomy is ineffective inrestoring normal airflow in horses withexperimentally induced left laryngealhemiplegia.

2. Prosthetic laryngoplasty can restore normalairflow in horses with experimentally inducedleft laryngeal hemiplegia.

3. Prosthetic laryngoplasty combined withbilateral ventriculectomy can restore normalairflow in sport horses with RLN.

4. In most horses subjected to prostheticlaryngoplasty, the degree of abduction of thearytenoid cartilage will decrease by varyingdegrees in the post operative period.

5. Evidence from studies of sport horses withRLN and horses with experimentally inducedlaryngeal hemiplegia indicates that the postoperative degrees of residual airwayobstruction and the degree of abduction of thearytenoid cartilage are poorly correlated.

6. Maximal abduction of the arytenoid cartilageduring prosthetic laryngoplasty may beunnecessary to restore laryngeal airwayfunction and is probably undesirable by causingincreased risk of aspiration and coughing.

7. Subtotal arytenoidectomy combined withipsilateral ventriculectomy is ineffective inrestoring airflow in horses withexperimentally induced left laryngealhemiplegia.

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TABLE 3: Grading system of laryngeal function‡ as assessed in the horse during exercise†


A Full abduction of the arytenoid cartilages during inspiration

B Partial abduction of the left arytenoid cartilages (between full abduction and the resting position)

C Abduction less than resting position including collapse into the contralateral half of the rima glottidis during inspiration

‡Description generally refers to the left arytenoid cartilage in reference to the right. However this gradingsystem can apply to the right side (ie right Grade III.1-B)†Update from Rakestraw, P.C., Hackett, R.P., Ducharme, N.G., Nielan, G.J., Erb, H.N. (1991) A comparisonof arytenoid cartilage movement in resting and exercising horses. Vet. Surg. 20, 122-127

8. Bilateral ventriculo-cordectomy and unilaterallaser cordectomy modestly improve upperairway function following experimentallyinduced laryngeal hemiplegia.

9. Partial arytenoidectomy combined withbilateral ventriculectomy improves airflow inhorses with experimentally induced leftlaryngeal hemiplegia.

10. Laryngeal reinnervation surgery can beequally as effective in the restoration of ahorse’s racing performance as prostheticlaryngoplasty.

EXERCISE INTOLERANCE AND ABNORMALUPPER RESPIRATORY SOUNDS

1. The implications of the above data are thatprosthetic laryngoplasty combined withventriculo-cordectomy/cordectomy comprisean effective surgical remedy for the treatmentof both the abnormal sound and exerciseintolerance present in horses with RLN.

2. Reinnervation surgery by use of the nervemuscle pedicle graft is an effective alternativeto the above.

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LIST OF PARTICIPANTS

BRIAN ANDERSON

Ballarat Veterinary Practice1410 Sturt StreetBallaratVictoria [email protected]

SAFIA BARAKZAI

Division of Veterinary Clinical StudiesUniversity of EdinburghEaster Bush Veterinary CentreEaster BushRoslinMidlothian, EH25 9RG, [email protected]

MATTHEW BINNS

Animal Health TrustLanwades ParkKentfordNewmarketSuffolk, CB8 7UU, [email protected]

FRED DERKSEN

College of Veterinary MedicineMichigan State UniversityEast LansingMichigan48824-1314, [email protected]

PADDY DIXON


NORM DUCHARME

Department of Veterinary SurgeryCornell UniversityIthacaNew York, [email protected]

DAVID ELLIS

Greenwood, Ellis & PartnersReynolds House166 High StreetNewmarketSuffolk, CB8 9WS, UK

ROLF EMBERTSON

Rood and Riddle Equine HospitalPO Box 12070LexingtonKY 40580, [email protected]

IAN FULTON

Ballarat Veterinary Practice1410 Sturt StreetBallaratVictoria [email protected]

TIM GREET

Rossdale & PartnersBeaufort Cottage Equine HospitalCotton End RoadExningNewmarketSuffolkCB8 7NN, [email protected]

CAROLINE HAHN


GEOFF LANE

Department of Clinical Veterinary ScienceDivision of Companion AnimalsLangford HouseLangfordBristol, BS40 5DU, [email protected]

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JOE MAYHEW

Division of Veterinary Clinical StudiesUniversity of EdinburghEaster Bush Veterinary CentreEaster Bush, Roslin, MidlothianEH25 9RG, [email protected]

BRUCE MCGORUM

Division of Veterinary Clinical StudiesUniversity of EdinburghEaster Bush Veterinary CentreEaster Bush, Roslin, MidlothianEH25 9RG, [email protected]

ERIC PARENTE

University of PennsylvaniaNew Bolton Centre382 West Street RoadKennet SquarePA 19348, [email protected]

RACHEL PEPPER

R & W Publications LimitedSuites 3 & 48 Kings CourtWillie Snaith RoadNewmarketSuffolk, CB8 7SG, [email protected]

GENE PRANZO

Dorothy Russell Havemeyer FoundationNew YorkUSA

ED ROBINSON

College of Veterinary MedicineMichigan State UniversityG-321 Veterinary Medical CentreEast [email protected]

JAN WADE

R & W Publications LimitedSuites 3 & 48 Kings CourtWillie Snaith RoadNewmarketSuffolkCB8 [email protected]

MICHAEL WEISHAUPT

Department of Veterinary SurgeryUniversity of [email protected]

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AUTHOR INDEX

ANDERSON, B.H. et al., 33; 45; 51

AUER, J.A. see WEISHAUPT, M.A.

et al.

BARAKZAI, S.Z. and DIXON,

P.M., 71

BINNS, M. and SWINBURNE, J., 89

DERKSEN, F.J., 77; 79

DIXON, P.M., 26; 35; 63 and see

BARAKZAI, S.Z. and DIXON,

P.M.; McGORUM, B. and DIXON,

P.M.

DIXON, P.M. and PRATSCHKE,

K.M., 16

DUCHARME, N., 21; 68; 90

ELLIS, D.R. et al., 39

EMBERTSON, R.M., 42

FULTON, I., 60

FÜRST, A. see WEISHAUPT,

M.A. et al.

GOULDEN, B.E. see

ANDERSON, B.H. et al.

GREET, T.R.C., 59 and see

ELLIS, D.R. et al.

HAHN, C., 3; 9

KANNEGIETER, N.J. see

ANDERSON, B.H. et al.

LANE, J.G., 24; 31; 47; 49; 83

and see ELLIS, D.R. et al.

MAYHEW, I.G., 5; 12

McGORUM, B. and DIXON, P.M., 55

PARENTE, E.J., 66

PRATSCHKE, K.M. see DIXON,

P.M. and PRATSCHKE, K.M.

SWINBURNE, J. see BINNS, M.

and SWINBURNE, J.

VOGT, R. see WEISHAUPT, M.A.

et al.

WEISHAUPT, M.A. et al., 81

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