THE EQUINE HEAD

The Proceedings of the 2011 Equine Chapter Meeting at the ACVSc Science Week

30 June-2 July 2011

Gold Coast International Hotel Gold Coast, Queensland, Australia

Proceedings Editor – John Chopin

2

SPONSORS

3

4

PRESENTERS:

RADIOLOGY

Belinda Hopper graduated from Murdoch University commenced a Residency in Diagnostic

Imaging at Murdoch University and was awarded her Fellowship of the Australian College of

Veterinary Scientists in 2004. A longstanding member of staff in the Imaging section of

Murdoch University Veterinary Hospital, Belinda provided imaging services for the hospital and

teaching for undergraduate veterinary students.

Karon Hoffmann is a Veterinary Sonologist with both a Masters Degree and PhD in

Veterinary Diagnostic Ultrasound and has extensive experience in both equine and small animal

and exotic sonology. Dr Hoffmann has over 30 publications in the veterinary literature and runs

a number of ultrasound workshops for veterinary practitioners each year.

Jane Day graduated from the University of Queensland in 1994. After graduation Jane worked

in small animal private practice Australia and UK. She completed a Masters in Veterinary

Studies from Murdoch University in 2003 and was awarded Membership in the Australian

College of Veterinary Scientists in Radiology also in 2003. Following her interest area, Jane

began teaching radiology and ultrasound at Queensland University in 2005, and currently

teaches Veterinary Diagnostic Imaging at James Cook University. She is working towards

completing her specialist training in the field, and has recently returned from several months

training in the United States.

Samantha Franklin recently joined the teaching and research team at School of Animal &

Veterinary Sciences, Roseworthy Campus. Dr Franklin qualified from the University of Bristol in

1995. After four years in practice, she returned to Bristol to complete a PhD in upper airway

disorders of the horse using the dynamic endoscope and also ran the equine sports medicine

referral centre at the University of Bristol. Dr Franklin will be lecturing in physiology, and

conducting research into airway problems, heart problems, and other performance problems in

horses.

Mika Frances graduated from Murdoch University in 1999 and has extensive experience as a

general practitioner in Australia, where she worked in Adelaide and Perth, and in the UK. Mika

has a long-standing passion for veterinary imaging and has completed a number of distance

education programs in radiology and ultrasound. Mika sat examinations to become a Member

of the Australian College of Veterinary Scientists in Radiology in 2009 and in 2010 started a

Radiology Residency at the Veterinary Imaging Centre. Mika will undergo 3 years of on-the-job

training in the specialty at the VIC, and will spend time in the Europe and the USA as part of her

training. Mika is a keen cyclist.

5

Charles Ley is a Diplomate of the European College of Veterinary Diagnostic Imaging and

works at the Diagnostic Imaging Unit at the Swedish University of Agricultural Sciences,

Uppsala. Charles is also completing a PhD in diagnostic imaging.

DENTISTRY

Ian Dacre graduated from Massey University Veterinary School in 1991. He spent 5 years in

mixed practice before working for 5 years in animal welfare (predominantly equine) in

Morocco. There he developed an interest in equine dentistry, and so commenced and

completed his PhD in equine dentistry under Prof Padraic (Paddy) Dixon at Edinburgh. He then

returned to NZ to work with MAF (animal welfare) and was senior lecturer at Massey (equine

medicine) 2005-2007. Ian completed the MACVSc in Equine Dentistry in 2007, and was the first

to be awarded this new certificate. He passed the ICEVO diplomate exam in Canada in 2010.

Teerapol Chinkangsadarn (known as Tum to his Australian friends) is a veterinary graduate

from Thailand. Most of his work involves equine dentistry and he is a full time lecturer in the

Equine Department at the Veterinary Faculty of Mahanakorn University of Technology,

Bangkok. Tum was the first veterinarian from Thailand to develop a special interest in equine

dentistry, and attended a workshop in Australia in 2009. Currently, he is researching

periodontal disease in horses as part of a PhD under Assoc Prof Gary Wilson at the University of

Qld.

Rachel Garraway graduated from the University of Qld with a Bachelor of Dental Science

(Honours) in 1992. She then worked in private practice in Toowoomba before returning to the

University of Qld to undertake her specialty training in Periodontics. She was awarded the

Australian Periodontology Research Foundation prize for her publication on Periodontal

Regeneration. She has spent time lecturing and demonstrating in Periodontics at the University

of Qld Dental School.

Liz Thompson runs a mobile equine veterinary practice with a particular interest in equine

dentistry in New Zealand, as well as practicing dentistry and postural rehabilitation on a referral

basis throughout New Zealand. She graduated from the University of California at Davis School

of Veterinary Medicine in 1988 and entered equine practice in California. Following time

training in Pennsylvania in acupuncture and chiropractic, she moved to New Zealand, where

she performed the equine work for four practices for Te Awamutu Animal Health Centre (now

Vet Ent). In 2003 she began her study of equine dentistry with Gary Wilson and Oliver Liyou

and in 2004 completed the Sydney Postgrad Foundation’s course in Equine Dentistry. She

regularly attends overseas dental conferences and workshops and has written numerous

6

articles for Vetscript (NZ) as well as horse magazines and newspapers. For her three part dental

series in Vetscript magazine she received the Jonathan Hope award for the Best Practitioner

Publication of 2010. In 2007, she achieved her MACVSc in Equine Dentistry. She is committed

to improving dental health in horses and has served as a teaching assistant in several dentistry

courses in Australia, New Zealand and in the USA and serves on the NZEVA Executive on the

Dental Subcommittee. She regularly speaks at conferences in New Zealand. Her next goal is that

of becoming a Diplomate of the International College of Equine Veterinary Odontologists.

Shannon Lee is an equine dental veterinarian, running Advanced Equine Dentistry (Victoria’s

only equine veterinary practice dedicated solely to equine dentistry). He has interests in all

aspects of equine dentistry and gained Membership in Equine Dentistry with the Australian

College Dental Chapter in 2010. Shannon is passionate about teaching the art and science of

equine dentistry to other veterinarians and veterinary students.

Since starting Equine Veterinary and Dental Services in 2002, Oliver Liyou has co-ordinated

over 30 short course workshops in equine dentistry - with over 300 vets attending. He has

authored or co-authored several papers and lectured on Equine Dentistry at AVA, AEVA and

Aust College Science Week Functions. EVDS performs approx 1600 dentals per year and has

used equine dentistry to select for good clients who are serious about caring for their horses’

welfare in a proactive manner.

Gary Wilson graduated BVSc from the University of Queensland in 1977. In 1994 he was

awarded MACVSc by examination in veterinary dentistry and completed his MVSc by thesis

titled “Atlas of the radiographic closure of the apices of the teeth of the dog” in 1998. He has

been in full-time veterinary dental referral practice since 1994 and was awarded the 2004

College Prize by the Australian College of Veterinary Scientists, the Meritorious Service Award

from the Australian Veterinary Association in 2000 and the Equine Veterinarians Australia Peter

Irwin Literary Award in 2006. Gary passed the inaugural examinations to become a Diplomate

of the International College of Equine Veterinary Odontologists.

OPHTHALMOLOGY

Simon Hurn graduated from University of Queensland in 1998. In 2002, Simon achieved

Membership of the Australian College of Veterinary Scientists by examination in Small Animal

Surgery. Simon graduated with a Masters of Veterinary Studies from the University of

Melbourne in 2003. Simon started a residency program in Veterinary Ophthalmology in 2002

and achieved Fellowship of the Australian College of Veterinary Scientists by examination in

2006. Simon is a Partner in All Animal Eye Services, in Mount Waverley Victoria.

7

Andrew Turner graduated from the University of Melbourne in 1973. In 1988 Andrew

became a member of the Australian College of Veterinary Scientists by examination in Equine

Surgery. In 1994 Andrew commenced a residency program in Veterinary Ophthalmology with

Dr Rowan Blogg, the founder of Veterinary Ophthalmology in Australia. In 1997, Andrew

became a Fellow of the Australian College of Veterinary Scientists by examination in Veterinary

Ophthalmology. Andrew is a partner in All Animal Eye Services - a clinic dedicated solely to

Veterinary Ophthalmology.

Kelly Caruso is a recent arrival on Australian shores, having moved here from Washington DC,

USA in August of 2010. Kelly has a wealth of veterinary experience in fields other than

veterinary ophthalmology. Kelly received a BSc and then her Doctor of Veterinary Medicine

from the University of Pennsylvania, in 1997. Subsequently Kelly completed internships in

equine medicine and surgery, small animal medicine and surgery, emergency medicine and

critical care and ophthalmology. Kelly was then trained in veterinary ophthalmology essentially

by Dr Seth Koch, but was exposed throughout her training to some of the most highly regarded

veterinary ophthalmologists in the USA. Kelly has published in journals such as JAVMA amongst

others. Kelly currently works in Sydney at the Small Animal Specialist Hospital. She now

understands the various nuances of scrum penalties in rugby union and feels that this means

she is now Australian.

Anu O’Reilly graduated from Murdoch University in 1994. In 1998, Anu undertook an

Internship in Small Animal Medicine and Surgery at the University of Melbourne Veterinary

Clinic and Hospital. During this Internship she completed a Masters of Veterinary Studies. In

2000, Anu achieved Membership of the Australian College of Veterinary Scientists in Small

Animal Medicine. During her residency program in Veterinary Ophthalmology Anu completed a

Certificate in Veterinary Ophthalmology with the Royal College of Veterinary Scientists and then

achieved her Fellowship of the Australian College of Veterinary Scientists in 2003. Anu is a

registered Veterinary Specialist in the discipline of Ophthalmology, currently working with

Animal Eye Care in Malvern East, Victoria.

Harriet Davidson is a Diplomate of the American College of Veterinary Ophthalmology. A

Michigan native, Dr. Davidson has recently returned from Kansas where she had been professor

of ophthalmology at Kansas State University. She and her husband and family make their home

in West Michigan where their household consists of multiple horses, dogs, and cats. She feels

committed to making a difference with each animal she treats.

JD (Dick) Wright graduated from The University of Sydney, School of Veterinary Science, in

1973. He is a Member (Equine Surgery) and a Fellow (Equine Medicine) of the Australian

College of Veterinary Scientists. In 1990, he was awarded Master of Veterinary Clinical Studies

8

by The University of Sydney for investigations titled: Radiological Studies of the Equine Tarsus.

He is currently Lecturer in Veterinary Anatomy and PhD scholar at The University of

Queensland, School of Veterinary Science; his doctoral research investigates the role of

intercellular communication in horse tendons.

SURGERY

Robin Bell obtained his veterinary degree at Sydney University and an internship at the

UVTHC. He completed his residency training and Masters at Massey University in New Zealand,

and after working in referral practice in the UK he was responsible for running the Equine

Lameness and Imaging service at the University of California Davis. He is a European specialist

in Equine Surgery with a particular interest in equine lameness and advanced imaging, in

particular high performance equine athletes and the use of CT and MR.

Samantha Franklin recently joined the teaching and research team at School of Animal &

Veterinary Sciences, Roseworthy Campus. Dr Franklin qualified from the University of Bristol in

1995. After four years in practice, she returned to Bristol to complete a PhD in upper airway

disorders of the horse using the dynamic endoscope and also ran the equine sports medicine

referral centre at the University of Bristol. Dr Franklin will be lecturing in physiology, and

conducting research into airway problems, heart problems, and other performance problems in

horses.

Safia Barakzai graduated from Bristol in 1998 and spent two years working in mixed practice

before working as a locum equine radiographer at Liverpool. From 2000 to 2003, she was the

Horserace Betting Levy Board senior clinical training scholar in equine surgery at Edinburgh,

where she is now a senior lecturer. She is a diplomate of the European College of Veterinary

Surgeons and an RCVS registered specialist in equine surgery.

NEUROLOGY

Joe Mayhew is a New Zealand graduate who has worked in many universities in North

America, latterly in Florida then at the Animal Health Trust in Newmarket and The Royal (Dick)

School of Veterinary Studies, University of Edinburgh. He is now Head of Massey Equine and

Professor of Equine Studies at the Institute of Veterinary, Animal and Biomedical Sciences,

Massey University.

9

Jonathan Hirst coordinates pharmacology teaching at the University of Newcastle and is a

Senior Scientist at the Mothers and Babies Research Centre, at the Hunter Medical Research

Institute. His research interests are in the role neurosteroids have in pregnancy and in the

control of fetal CNS activity. The objectives of his current work are to develop neurosteroid

based therapies for reducing brain injury in neonates following compromised pregnancies and

preterm birth.

Jane Axon is a registered specialist in Equine Medicine and has numerous publications in

peer-reviewed journals, conference proceedings and veterinary textbooks. She is a well

renowned local and international speaker on foal medicine and intensive care. Jane’s interests

are in neonates, ultrasonography, equine emergency and critical care and teaching. She is

actively involved in the Australian College of Veterinary Scientists and Equine Veterinarians

Australia, and she regularly mentors interns and fellowship candidates.

BEHAVIOUR

Amanda Warren-Smith has extensive experience working with horses from all disciplines.

Her specific interest areas include applied animal behaviour and animal welfare. Her experience

as a coach and as an equitation scientist has led to numerous requests to speak nationally and

internationally. Having completed a PhD that focused on training horses, her knowledge of

applying learning theory to the training of horses is world-class. Amanda has conducted

numerous studies which have been published in the peer-reviewed literature and have been

widely cited. Amanda has also written and edited several book chapters and is frequently asked

to review manuscripts for international journals. Amanda is currently involved in research

projects including objective measures of performance and improving training of domesticated

horses.

Lesley Hawson originally studied psychology and physiology before embarking on a career in

industrial relations and human resource management for ten years. She then undertook a

Veterinary Science degree at University of Sydney. She went on to practice in both small

animals and horses while completing the graduate diploma of Animal Chiropractic at RMIT. In

2009, she started a full time PhD candidature under the supervision of Prof Paul McGreevy and

Dr. Andrew McLean. The project is “The science of horse training: implications for rider safety

and rider welfare.” This exciting project is looking at the communications processes between

horse and rider within the context of applied learning theory.

10

2011 Equine Chapter Program

Thursday 30 June

Combined Session between Equine and Radiology Chapters

9.00 Practical Radiography of the Equine Head Belinda Hopper

9.30 Advanced Imaging of the Equine Head Karon Hoffman

10.00 MORNING TEA

10.30 Ultrasound Examination of the Orbit Jane Day

10.50 Ultrasound examination of the Equine larynx Sam Franklin

11.10 Digital Radiography Mika Frances

11.50 Standing MRI for the distal limb Charles Ley

12.10 MRI of the distal tarsal osteoarthritis Charles Ley

12.30 LUNCH

Combined Session between Equine and Dentistry Chapters

1.30 Imaging techniques for diagnosing dental disease Ian Dacre

2.00 Overview and current state of knowledge of periodontal disease in the horse

Teerapol Chinkangsadarn

2.20 Current evidence of link between periodontal disease and infertility in humans

Rachel Garraway & Liz Thompson

3.00 AFTERNOON TEA

3.30 Equine Odontoclastic Tooth Resorption and Hypercementosis

Shannon Lee

3.50 Canine extractions in the standing equine patient Shannon Lee

4.10 Prevalence and risks of causing Pulp Exposures in horses in Australia

Oliver Liyou

11

4.40 Root canal therapy in horses Gary Wilson

Friday 1 July 2011

Combined Session between Equine and Ophthalmology Chapters

8.30 Nerve blocks around the eye and placement of palpebral lavage tubes

Simon Hurn

8.50 Equine neonatal ophthalmology Andrew Turner

9.10 Ocular manifestations of systemic disease Kelly Caruso

9.30 Medical management of bacterial and fungal keratitis

Anu O’Reilly

10.00 MORNING TEA

10.30 Surgical management of bacterial and fungal keratitis

Andrew Turner

10.50 Ophthalmic findings in Thoroughbred horses in Australia

Simon Hurn

11.10 Diagnosis and management of equine recurrent uveitis

Andrew Turner

11.30 Use of nonsteroidal anti-inflammatory agents, corticosteroids and gastrointestinal

protectants in horses Dick Wright

12.10 Equine eyes – stories of mischief (eyelid and corneal problems)

Harriet Davidson

12.30 LUNCH

Equine Chapter

1.30 Standing surgery of the horse’s head Robin Bell

12

1.50 Neuromuscular physiology of the upper airways; mechanisms of obstructions

Sam Franklin

2.30 Complications associated with laryngoplasty, including results of their study

Safia Barakzai

3.00 AFTERNOON TEA

3.30 Laser surgery of the equine upper respiratory tract Safia Barakzai

4.10 Dynamic assessment of the equine upper respiratory tract

Sam Franklin

Saturday 2 July

Equine Chapter

8.30 What I look for on a neurological examination Joe Mayhew

8.50 Ryegrass Staggers Joe Mayhew

9.10 Stringhalt Joe Mayhew

9.30 Vertebral canal measurements in CVM Joe Mayhew

10.00 MORNING TEA

10.30 Seizures, Syncope, Sleep attacks Joe Mayhew

10.50 Neonatal hyponatraemic seizures Jane Axon

11.10 Neurosteroids: key regulators and protectors in the foetal brain

Jon Hirst

12.10 Horner’s Syndrome verses Facial Paresis Joe Mayhew

12.30 LUNCH

Combined Session between Equine and Animal Welfare Chapters

1.30 Overview of how horses learn Amanda Warren-Smith

1.45 Welfare implications Lesley Hawson

13

1.55 Interpretation of horse’s responses Amanda Warren-Smith

2.10 Bridle’s nosebands, halter types Amanda Warren-Smith

2.20 Rein tension with accelerometry Amanda Warren-Smith

2.30 Laterality Lesley Hawson/Amanda Warren-Smith

2.40 Elvis Lesley Hawson

3.00 AFTERNOON TEA

3.30 Rider laterality, handedness, saddle fit and applied learning theory

Lesley Hawson

3.40 Positive and negative reinforcement Amanda Warren-Smith

3.50 Timing of reinforcement when leading Amanda Warren-Smith

4.10 The future Lesley Hawson & Amanda Warren-Smith

14

CONTENTS

Sponsors 2 Presenter Biographies 4 Equine Chapter Program 10 Contents 14 PRACTICAL RADIOGRAPHY OF THE EQUINE HEAD

Belinda Hopper 17 ADVANCED IMAGING OF THE EQUINE HEAD

K.L.Hoffmann 22 EQUINE EYE ULTRASOUND

Jane Day 23 LARYNGEAL ULTRASOUND

Samantha Franklin 28 DIGITAL RADIOGRAPHY WITH AN EQUINE FOCUS

Mika Frances 32 STANDING MRI FOR THE DISTAL LIMB

Charles Ley 40 MRI OF DISTAL TARSAL JOINT OSTEOARTHRITIS

Charles Ley 44 IMAGING TECHNIQUES FOR DIAGNOSING EQUINE DENTAL DISEASE

Ian Dacre 48 OVERVIEW AND CURRENT STAGE OF KNOWLEDGE OF PERIODONTAL DISEASE IN HORSE

Teerapol Chinkangsadarn 51 PERIODONTAL DISEASE AND ADVERSE PREGNANCY OUTCOMES

Rachel Garraway 53 EQUINE ODONTOCLASTIC TOOTH RESORPTION AND HYPERCEMENTOSIS

S Lee 55 STANDING CANINE EXTRACTION IN THE EQUINE PATIENT

S Lee 56 PREVALENCE AND RISKS OF CAUSING PULP EXPOSURES IN HORSES IN AUSTRALIA.

Oliver Liyou 57 ENDODONTICS IN THE HORSE

Gary Wilson 59 NERVE BLOCKS

Simon Hurn 67 EQUINE NEONATAL OPHTHALMOLOGY

Andrew Turner 69 OCULAR MANIFESTATIONS OF SYSTEMIC DISEASE IN HORSES.

Kelly Caruso 73 MEDICAL MANAGEMENT OF EQUINE BACTERIAL AND FUNGAL KERATITIS

Anu O’Reilly 74 SURGICAL MANAGEMENT OF EQUINE BACTERIAL AND FUNGAL KERATITIS

Andrew Turner 76

15

OPHTHALMIC EXAMINATION FINDINGS OF THOROUGHBRED RACEHORSES IN AUSTRALIA Simon Hurn and Andrew Turner 78

DIAGNOSIS AND MANAGEMENT OF EQUINE RECURRENT UVEITIS Andrew Turner 84

NSAIDS, CORTICOSTEROIDS & GASTRIC PROTECTANTS IN THE HORSE Dick Wright 87 EQUINE EYES OR STORIES OF MISCHIEF (EYELID AND CORNEAL PROBLEMS)

Harriet Davidson 97 STANDING SURGERY OF THE HORSE’S HEAD

Robin JW Bell 98 NEUROMUSCULAR PHYSIOLOGY OF THE UPPER AIRWAYS: MECHANISMS OF OBSTRUCTIONS

Samantha Franklin 99 COMPLICATIONS ASSOCIATED WITH LARYNGOPLASTY

Safia Barakzai 106 LASER SURGERY OF THE UPPER RESPIRATORY TRACT

Safia Barakzai 110 DYNAMIC ASSESSMENT OF THE EQUINE UPPER RESPIRATORY TRACT

Samantha Franklin 113 WHAT I REALLY LOOK FOR ON A NEUROLOGIC EXAMINATION

Joe Mayhew 119 A CLINICAL STUDY OF INDUCED PERENNIAL RYEGRASS [LOLITREM-B] INTOXICATION

Joe Mayhew & Laura Johnstone 128 STRINGHALT AND OTHER PELVIC LIMB MOVEMENT DISORDERS

Joe Mayhew 130 VERTEBRAL CANAL MEASUREMENTS IN ADULT HORSES PRESENTING AS WOBBLERS

Joe Mayhew 137 SEIZURES, SYNCOPE AND SLEEP ATTACKS

Joe Mayhew 145 HYPONATRAEMIC SEIZURES IN FOALS

JE Axon, JB Carrick, CM Russell, NM Collins 150 NEUROSTEROID: KEY REGULATORS AND PROTECTORS OF THE FETAL BRAIN

Jonathan J. Hirst, Meredith A. Kelleher, David W. Walker, Hannah K. Palliser 152

HORNER’S SYNDROME VERSES FACIAL PARESIS Joe Mayhew 154

OVERVIEW OF HOW HORSES LEARN Amanda Warren-Smith 160

WELFARE (AND SAFETY) IMPLICATIONS FOR APPLYING LEARNING THEORY IN HORSE TRAINING Lesley Hawson 162

INTERPRETATION OF HORSE'S RESPONSES Amanda Warren-Smith 164

BRIDLES, NOSEBANDS AND HALTERS Amanda Warren-Smith 168

16

REIN TENSION WITH ACCELEROMETRY – OBJECTIVELY MEASURING HORSE PERFORMANCE Warren-Smith AK, Bronicki BB, Evans D, Curtis R, Marsh D 171

LATERALITY IN HORSES Amanda Warren-Smith 172

RIDER ASYMMETRY AND HANDEDNESS Lesley Hawson 175

POSITIVE AND NEGATIVE REINFORCEMENT Amanda Warren-Smith, McGreevy PD 178

TIMING OF REINFORCEMENT Amanda Warren-Smith, McLean AN, Nicol HI, McGreevy PD 179

17

PRACTICAL RADIOGRAPHY OF THE EQUINE HEAD

(Base of skull structures)

Dr Belinda Hopper BSc, BVMS, MVS, FACVSc Veterinary Imaging Centre, 305 Selby St, Osborne Park, WA 6017

INTRODUCTION The equine head is a complicated structure and obtaining (and interpreting) radiographs of it can be a very daunting task. These days, help with radiographic interpretation is never far away, but without good images neither you nor any radiologist in the world will be able to make a credible diagnosis. A good radiographic study is invaluable for the diagnosis and management of so many conditions of the head. Dental and sinus radiography will be covered in other sessions this week so in this presentation I will discuss the radiography of the base of skull structures. APPROACH TO IMAGING THE EQUINE SKULL: 1. First formulate your differential diagnosis list 2. Select your radiographic projections based on your differentials (see below) 3. Assemble your equipment

a. Portable machines perfectly adequate b. No grids, Fast or Medium speed screens (or digital) c. Cassette holders - essential d. Ancillary equipment - rope halter, markers, occy straps, chin rest, gag for dental radiographs e. Radiation protection - gowns and gloves essential, thyroid protectors advisable f. Good sedation

4. Obtain your radiographs 5. Make time for considered interpretation – these are complicated images – or refer for a specialist opinion. A BASIC RADIOGRAPHIC STUDY NB/ D: Dorsal, V: Ventral, R: Rostral, L: Lateral, Cd: Caudal, O: Oblique Paranasal sinuses Lateral and DV Left and Right D15oL-VLO and D45oL-VLO (maxillary obliques – ALWAYS radiograph the other side for comparison) Base of skull/pharynx Lateral (and DV for skull, not for pharynx) Left and Right Cd60oL-RLO (30o or “just off” lateral obliques) Temporomandibular joints Lateral and DV Left and Right Cd60oL-RLO (30o or “just off” lateral obliques)

18

Left and Right caudodorsal to rostroventral obliques (Cd75oL70oD-RLV) OR Left and Right rostroventral to caudodorsal obliques (R45oV30oL-CdDL) In skull radiography, never underestimate the value of a lesion oriented oblique! SOME TIPS FOR ACHIEVING GOOD POSITIONING: Skull radiography often requires beam angulation in two planes and repeated projections on opposite sides of the patient. For this reason, maintaining a static head position (with dental chin rest, stool, up-turned buckets, 44 gallon drum etc…) is extremely helpful. Lateral – base of skull Centre on vertical ramus of mandible Maintain slight extension of head and neck

Figure 1. Positioning for the lateral projection using occy straps NB/ Cassette position in this photograph is for radiographs of the paranasal sinuses. It would need to be more caudally placed for base of skull.

19

Dorsoventral Beam should be perpendicular to the horizontal plane (which is the plane through the facial crests). Using elasticated (occy) straps to hold the cassette flat against the mandibles is very helpful as it eliminates cassette/object movement and facilitates good positioning. Even small errors of beam angle or cassette position can render the DV uninterpretable.

Figure 2. Positioning for a DV projection using occy straps NB/ Cassette position in this photograph is for radiographs of the paranasal sinuses. It would need to be more caudally placed for base of skull. Lateral oblique (30o off lateral, Cd60oL-RLO) The aim of this projection is to separate structures superimposed on the lateral (such as the stylohyoid bones, TMJs). The more caudally projected structure is usually the one easiest to interpret. Angling the beam from caudal to rostral optimises the TMJ and stylohyoid closest to the cassette. Obliques of the TMJs (caudodorsal to rostroventral and rostroventral to caudodorsal obliques) These are roughly the same projection, but made in reverse. The caudodorsal to rostroventral oblique involves positioning the tube above and behind the horse’s poll on the unaffected side with the cassette held vertically against the affected side. The beam is angled from 15o behind lateral and down 70o from horizontal and centred at the base of the ear on the affected side. The rostroventral to caudodorsal oblique is roughly made in reverse. The horse is positioned with its chin supported so that the mandible is horizontal. The tube is positioned low down in front of the horse on the affected side and the cassette is held nearly horizontally above the poll (tilted slightly so that it is higher at the front, lower at the back). The beam is angled up 45o from horizontal and 30o off rostral (60o off lateral).

20

Both of these projections are not usually necessary as they give roughly the same information - which one you choose will probably be dictated by your equipment. The high tube position of the caudodorsal to rostroventral projection really requires a gantry-mounted tube. Cassette positioning is easier (flat against the side of the face) but the image is a little more distorted than in the second projection. The rostroventral to caudodorsal projection would be easier to achieve if you only have a portable machine. You will need a good cassette holder and a strong arm to hold the cassette still. For a full description of these projections see: NEIL B. TOWNSEND, JOHANNA C. COTTON, SAFIA Z. BARAKZAI “A Tangential Radiographic Projection for Investigation of the Equine Temporomandibular Joint” Vet Surg. 2009 Jul;38(5):601-6 ALESSIA J. EBLING, ALEXIA L. MCKNIGHT, GABRIELA SEILER, PATRICK R. KIRCHER “A Complementary Radiographic Projection of the Equine Temporomandibular Joint” Veterinary Radiology & Ultrasound, Vol. 50, No. 4, 2009, pp 385–391 LABELLING OBLIQUES It is absolutely essential that you adequately label your oblique projections so that laterality can be established. You don’t want to flap the wrong sinus! Most projections can be obtained two ways (by reversing the cassette position and beam angle) but this means that the cassette is not always placed on the affected side. Hence labeling the side closest to the cassette is not always going to be correct. Regardless of the radiographic technique (ie which side is closest to plate) the labels should always indicate the anatomical side optimally displayed on the image. Ideally obliques should have a L and R marker so that you know it is an intentional oblique (not just a dodgy lateral), but one accurately placed marker is adequate. Always place the L or R marker on the cassette so that it is adjacent to the corresponding side of the image. (For example, place the marker dorsal to the head for the obliques of the paranasal sinuses as the side being imaged will be projected dorsally in the image). Below is an example of two correctly labeled oblique radiographs. Both are of the right paranasal sinuses but the one on the left is made with the cassette against the right side of the face and the one on the right is made with the cassette on the left side of the face. It is not possible to differentiate the two from the image. Note how the R marker is placed dorsally, adjacent to the right paranasal sinuses. The L marker is ventral, indicating the left side is being projected ventrally.

21

Figure 3: Right Cd60oL- Left RL oblique (lateral oblique) of the left base of skull structures The L marker is at the caudal edge of the cassette to indicate the left structures are projected caudally Special thanks go to Dr Cristy Secombe, MUVH Equine Hospital for her help with preparation of this presentation, and to Dr Mika Frances and Dr Nola Lester of the Veterinary Imaging Centre.

22

ADVANCED IMAGING OF THE EQUINE HEAD

Dr K.L.Hoffmann BVSc MVSc PhD Dip Vet Clin Stud University Veterinary Teaching Hospital, Faculty of Veterinary Science, The University of Sydney NSW 2006 , Australia Telephone: +61 2 9351 3437 FAX: +61 2 0351 4261

ADVANCED DIAGNOSTIC IMAGING OF THE EQUINE HEAD K Hoffmann* and M Spriet � * Diagnostic Imaging , B10, University of Sydney, Camperdown 2006 � Diagnostic Imaging, University of California , Davis

Due to the complexity and superimposition of the anatomical structures of the equine head, there has been a recent surge in interest in the application of the more advanced diagnostic imaging modalities to this region. The advantages of the available techniques include the cross-sectional imaging capabilities of CT and MRI , the superior soft tissue contrast of MR and to a lesser extent CT and the high sensitivity for bone remodeling when using CT or Scintigraphy. This presentation will include case examples seen on recent visits to both the University of California , Davis and the University of Melbourne, Werribee.

23

EQUINE EYE ULTRASOUND

Jane Day BVSc MVS MACVSc (Radiology) Radiology Resident, Melbourne University Veterinary Hospital, 250 Princes Highway Werribee 3030, Victoria

Technical aspects of ocular ultrasound are described below, followed by a list of useful references1-6. The Science Week presentation will also include some recent cases seen at Melbourne University. Indications7-10

1. All or part of the eye cannot be seen with ophthalmoscopic examination eg swelling of the third eyelid or eyelid; opacity in the cornea, aqueous, lens, or vitreous 2. To confirm ophthalmoscopic examination findings 3. Exophthalmos or change in size of the globe 4. Retrobulbar disease 5. Ocular trauma

Specific conditions that benefit from ultrasonography include corneal masses, corneal oedema or infiltrates, anterior uveitis, cataracts, assessment for retinal detachment and posterior uveitis before cataract removal, foreign body detection, globe integrity assessment, lens luxation, lenticonus, vitreal opacities, choroiditis, retinal detachment, retrobulbar and periorbital masses9,11. Anatomy

http://www.equineeyevet.com/images/ocular_anatomy_9eg7.gif

24

The structures able to be seen on ultrasound include the eyelid, cornea, anterior chamber, ciliary body, iris, corpora nigra, lens, vitreous, and posterior eye (the retina, choroid and sclera cannot be differentiated in the normal eye). The posterior chamber is not large enough to be seen. The normal retrobulbar space can be imaged via the globe, or from the supraorbital fossa and is comprised mostly of fat. Within this are the optic nerve, several extraocular muscles, and the bony orbit, all of which may be imaged with ultrasound. Normal eye measurements are12:

Anterior to posterior diameter = 39.4 +/- 2.3mm Anterior chamber depth = 4.22 +/- 1.29mm Vitreous depth = 17.37 +/- 1.98mm Lens thickness = 11.93 +/- 1.10mm

Technique – Sedation and nerve blocks Sedation is recommended for most, if not all, horses for this procedure. In addition an auriculopalpebral nerve block is performed on most horses to provide motor blockade to the upper lid to prevent excessive blinking. Using a 1 inch, 25 gauge needle, approximately 1 - 2ml of local anaesthetic (eg lignocaine (without adrenaline) or mepivicaine) is injected around the nerve where it can be palpated crossing the zygomatic arch13. The onset of action is within 5 minutes and a successful block is indicated by inability (or reduced ability) to blink, mild ptosis of the upper lid, and mild eversion of the lower lid. The block will last up to 90 minutes (lignocaine) and up to 120 minutes (mepivicaine). A supraorbital nerve block may be performed

25

if desensitisation of the middle two thirds of the upper eyelid is required. Topical anaesthesia is necessary for transcorneal examination (eg Opthaine – proparacaine hydrochloride). *If nerve blocks have been used, it is important to instill an ocular lubricant in the eye when the ultrasound examination is finished and after the ultrasound gel has been flushed out of the eye. Technique – Transpalpebral vs Transcorneal; Supraorbital The globe and retrobulbar area may be examined either through the eyelid (transpalpebral) or directly on the cornea (transcorneal). Ultrasound via the supraorbital fossa is an additional window for examination of the retrobulbar area only.

1. Transpalpebral – This approach is better tolerated by the horse. The image quality is reportedly inferior to the transcorneal approach but is similar in our experience. It is best not to clip the hair or apply alcohol to the upper eyelid to avoid contamination of the eye. Instead the hair is wet with a water soaked swab and ultrasound gel is applied. Ideally, sterile ultrasound gel should be used, particularly if the transcorneal approach is used, but nonsterile ultrasound gel has been used without problems10. It is important to flush any ultrasound gel from the eye with saline when the examination is finished11. The eyelid can act as a standoff pad to see the cornea, although a standoff pad on the transducer provides better evaluation of the cornea. It is not necessary for any other ocular structures. Excess pressure and dripping of gel into the eye will cause the horse to blink excessively (unless an auriculopalpebral block has been performed).

2. Transcorneal – This approach may give better images with fewer artifacts. It is not as well tolerated by the horse. A standoff pad is needed if the cornea is to be imaged, otherwise all other structures can be seen without one. Topical anaesthesia (eg Alcaine - proxymetacaine hydrochloride) can be applied with a 1m syringe and is necessary for transcorneal examination. Multiple applications are needed and it is recommended to wait for 10 minutes before scanning. It is important to flush any ultrasound gel out of the eye when the examination is finished (see the comments above).

3. Supraorbital technique – This is used for further assessment of the retrobulbar region via the supraorbital fossa. Because of the shape of the fossa a small convex transducer is needed to get good contact with the skin. The hair needs to be clipped.

Technique - Equipment A high frequency (greater than 8MHz) linear transducer is best for examination of the eye. Lower frequencies (5 – 8MHz) are necessary for the retrobulbar area as 6-10cm depth is required. However any transducer available to the equine practitioner, such as those used for tendon and rectal examinations, may be used to produce an image. Some abdomen transducers may be used depending on the size of the footprint. Technique - Scanning The ultrasound anatomy of the eye and scanning technique are not difficult, so ultrasound examination as part of an ocular examination should be considered by every equine

26

practitioner with any kind of ultrasound machine. Use only light pressure on the eye as excess pressure encourages blinking (if an auriculopalpebral nerve block has not been performed). Ultrasound examination of the eye should be performed with great care or avoided if corneal rupture is a concern. Both eyes should be examined so that measurements can be compared to a ‘normal’ eye, and so that subclinical problems may be diagnosed in the ‘normal’ eye. The eye should be examined in 2 planes – parallel to the palpebral fissure, and perpendicular to it. The transducer should be fanned from one side to the other to completely examine the globe and retrobulbar areas. It is best to examine the globe and retrobulbar areas separately as different machine settings are used. Set the gain (the overall gain and the TGC) to provide the best image, but temporarily increase it while looking at anechoic structures (the anterior chamber, lens and vitreous), to make sure subtle echoes are not missed. Set the depth so that the structure of interest is filling the entire screen. Have the frequency as high as possible while still having enough penetration to see the structure of interest, and lower the frequency as necessary to see deeper structures (eg retrobulbar area). Set the focal zone at the level of interest, as it greatly improves the resolution at that level. The focal zone is very important as the resolution is it provides the Multiple focal zones can be used in ocular imaging. By convention the transducer position marker is placed towards the nose when scanning parallel to the palpebral fissure, and superior (dorsal) when scanning perpendicular to the palpebral fissure. Alternatively, ensure that the aspects are clearly labeled on the images. Acknowledgement: Thank you to Dr Cathy Beck and Dr Kate Savage for their guidance during ocular examinations at Melbourne University. References 1. Bedford P. Auriculo palpebral and palpebral nerve blocks in the horse. In Practice 1987;9:63. 2. Brooks DE, Matthews A. Equine ophthalmologyTeton NewMedia-Verl.; 2002. 3. Miller W. Diagnostic ultrasound in equine ophthalmology 1990. 4. Scotty N, Cutler T, Brooks D, et al. Diagnostic ultrasonography of equine lens and posterior segment abnormalities. Veterinary ophthalmology 2004;7:127-139. 5. Tremaine W. Local analgesic techniques for the equine head. Equine Veterinary Education 2007;19:495-503. 6. Valentini S, Tamburro R, Spadari A, et al. Ultrasonographic Evaluation of Equine Ocular Diseases: A Retrospective Study of 38 Eyes. Journal of Equine Veterinary Science 2010;30:150-154. 7. Whitcomb MB. How to diagnose ocular abnormalities with ultrasound 2002;272-275. 8. Hallowell G, Bowen I. Practical ultrasonography of the equine eye. Equine Veterinary Education 2007;19:600-605. 9. Diaz OS. Ultrasound of the equine eye and adnexa and clinical applications. Clinical Techniques in Equine Practice 2004;3:317-325. 10. Reef VB. Equine diagnostic ultrasound WB Saunders Company.; 1998. 11. Scotty NC. Ocular Ultrasonography in Horses. Clinical Techniques in Equine Practice 2005;4:106-113.

27

12. Rogers M, Cartee RE, Miller W, et al. Evaluation of the extirpated equine eye using B mode ultrasonography. Veterinary Radiology & Ultrasound 1986;27:24-29. 13. Taylor FGR, Hillyer MH. Diagnostic techniques in equine medicine Saunders; 1997.

28

LARYNGEAL ULTRASOUND

Samantha Franklin BVSc PhD MRCVS School of Animal and Veterinary Sciences, University of Adelaide, Roseworthy Campus, SA5371.

Introduction: Ultrasonography of the equine larynx was first described by Chalmers in 2005 (1), with full details of the technique published in 2006 (2). The technique was previously described in other species where it has been used to diagnose laryngeal masses, laryngeal paralysis and for assessment of vocal fold function (3-5). In horses, laryngeal ultrasonography can be readily performed in the standing horse and is a useful addition to the repertoire of diagnostic aids available to examine the upper airways. Laryngeal ultrasound enables detailed visualisation of the cartilages and associated musculature as well as portions of the hyoid apparatus that cannot be seen using endoscopy. It has been used clinically to provide useful information relating to a number of conditions affecting the larynx and surrounding structures. In cases where exercising endoscopy is unavailable it is useful to augment the findings of a resting endoscopic examination. Technique: Laryngeal ultrasonography can be performed readily in the standing horse. Sedation, using xylazine or detomidine, is useful in most cases and allows the horses’ head to be held in an extended position. This is important in order to move the larynx caudally in relation to the mandible and access the acoustic windows. In most cases it is not necessary to clip the hair but simply to saturate the region with 70% isopropyl alcohol or echogenic gel. However, if the coat is thick or coarse clipping will improve image quality. A linear or curvilinear transducer may be used for the examination, with a frequency of 8 -12 MHz. The laryngeal ultrasound technique involves imaging the throat region from a number of acoustic windows on the lateral and ventral aspects of the larynx (2, 6): The lateral aspect of the larynx can be examined on the left and right sides in the dorsal and transverse planes. The arytenoid cartilage, thyroid cartilage, cricoid cartilage, cricoarytenoideus lateralis muscle (CALM) and vocalis muscle can be evaluated in longitudinal and transverse planes from a lateral window. In transverse plane the arytenoid cartilage is trumpet shaped and the CALM & vocalis muscle can be visualized between the thyroid & arytenoids cartilage (figure 1). In some horses it is possible to distinguish the vocalis muscle from the CALM, whilst in others the distinction between the two muscles cannot be defined. In the dorsal plane, it is possible to image the lateral aspect of the cricoarytenoideus dorsalis muscle (CADM).

29

Figure 1: View from the lateral window, in transverse plane. (A = artenoid cartilage, T = thyroid cartilage, CALM = cricoarytenoideus lateralis muscle)

The ventral aspect of the larynx can be examined from a number of windows: rostral, middle and caudal. From the rostro-ventral window it is possible to image the basihyoid and its’ lingual process (figure 2). The position of the thyroid cartilage relative to the basihyoid bone can be established from the mid-ventral window (figure 3) and from the caudo-ventral window (cricothyroid notch) it is possible to view the vocal folds. Clinical applications: Recurrent Laryngeal neuropathy: Ultrasonographic assessment of the CALM has been found to be useful in the assessment of RLN (7, 8). One of the hallmarks of RLN is denervation atrophy. This affects both the laryngeal abductor and adductor muscles. The adductor muscles in fact appear to be affected earlier and more severely than the abductor muscles, even though the clinical appearance is of decreased arytenoid movement associated with loss of abductor muscle function (9). Denervation atrophy results in a hyperechogenic appearance, in comparison with normal muscles, when assessed ultrasonographically (10, 11). This is proposed to occur due to an increase in the amount of connective and adipose tissue within the muscle or changes (10).

30

Chalmers et al. 2006 (7) first demonstrated a link between increased echogenicity of the CALM and abnormal arytenoid movement characteristic of RLN. Subsequently, a study by Garrett et al. in 2011 (8) compared results of resting endoscopy and laryngeal ultrasonography with treadmill endoscopy in 79 horses. They found that laryngeal ultrasonography was extremely accurate in predicting arytenoid dysfunction during exercise, with a sensitivity of 90% and specificity of 98% compared with resting endoscopy (sensitivity = 80%, specificity 81%). Laryngeal ultrasonography is therefore considered to be a useful diagnostic modality for assessment of arytenoid function in horses with equivocal resting findings, especially where exercising endoscopy is unavailable. Dorsal displacement of the soft palate: Chalmers et al., 1999 (12) found differences in the depth of the basihyoid bone between horses with intermittent dorsal displacement of the soft palate (DDSP) & control horses. However, this was only small (< 2mm) and a subsequent report by Garret (6) was unable to reproduce these findings. Furthermore, radiographic findings in horses with persistent DDSP appear to contradict these findings (13). Therefore at this stage it is recommended that decisions relation to diagnosis of DDSP are not based upon ultrasonographic findings. Ultrasonography may however be useful in examining horses following tie-forward surgery and can be used to assess the integrity of the sutures. Arytenoid chondritis: Ultrasonography has been found to be extremely valuable in the assessment of horses with laryngeal chondritis (2, 6). Videoendoscopy of these patients only enables visualisation of the corniculate process. However, laryngeal ultrasonography will enable a more extensive examination of the arytenoid in order to determine the extent of the cartilage involvement. The arytenoid cartilage is best viewed from the lateral window. Some horses may only have evidence of a granuloma or chondroma on the axial surface, which will appear as a focal irregularity of the axial margin. In horses with more extensive involvement, the cartilage will be thickened, with irregular margins. 4th Branchial arch defects (Laryngeal dysplasia): Garrett et al., 2009 (14) reported the use of laryngeal ultrasonography for diagnosis of laryngeal dysplasia in 5 horses and compared the technique to MRI. Features including lack of the cricothyroid articulation, dorsal extension of the thyroid cartilage laminar and absence or hypoplasia of the cricopharyngeus muscle were identified in all cases, using both modalities. Laryngeal & retropharyngeal masses: Ultrasound examination is also likely to be useful for examination of soft tissues associated with or around the larynx including: masses, abscesses, mucocoeles & subepiglottal cysts. Indeed, a recent case report described how laryngeal ultrasonography was paramount in making a diagnosis & facilitating biopsy in a horse with a laryngeal neuroendocrine tumour (15). Summary: Laryngeal ultrasonography is a recent addition to the diagnostic repertoire in the evaluation of the equine upper airways. It has the advantage of being noninvasive and a number of useful clinical applications have been described. Whilst endoscopy remains invaluable for assessment

31

of laryngeal function and examination of the luminal aspect of the airways, ultrasonography allows for a more detailed examination of the cartilages and associated musculature. Laryngeal ultrasonography can also provide additional information relating to laryngeal function in cases where exercising endoscopy is not possible. References: 1) Chalmers, HJ. (2005) Ultrasonography of the equine larynx. Proc 3rd WEAS, Ithaca. 2) Chalmers, H.J., Cheetham, J., Yeager, AE. And Ducharme, NG. (2006) Ultrasonography of the equine larynx. Vet Radiol & Ultrasound. 47 (5): 476-481. 3) Friedman, EM. (1997) Role of ultrasound in the assessment of vocal cord function in infants and children. Ann Otol Rhinol Laryngol. 106: 199-209. 4) Rudorf, H., Brown, P. (1998) Ultrasonography or laryngeal masses in six cats and one dog. Vet Radiol Ultrasound 39: 430-435. 5) Rudorf H, Barr, FJ., Lane, JG. (2001) The role of ultrasound in assessment of laryngeal paralysis in the dog. Vet Radiol Ultrasound 42: 338-343. 6) Garrett, K.S. (2010) How to ultrasound the equine larynx. Proc AAEP 56: 249-256. 7) Chalmers, HJ., Cheetham, J. Mohammd, HO. And Ducharme, NG. (2006) Ultrasonography as an aid in the diagnosis of recurrent laryngeal neuropathy in horses. Proc of the 2006 ACVS Vet Symposium. pp 3-4. 8) Garrett, KS., Woodie, JB and Embertson, RM. (2011) Association of treadmill upper airway endoscopic evaluation with results of ultrasonography and resting upper airway endoscopic evaluation. Equine Vet J. 43 (3): 365-371. 9) Duncan, ID., Amundson, J, Cuddon, PA., Sufit, R., Jackson, KF. And Lindsay WA. (1991) Preferential denervation of the adductor muscles of the equine larynx I: muscle pathology. Equine Vet J. 23: 94-98. 10) Gunreben, G. and Bogdahn, U. (1991) Real-time sonography of acute and chronic muscle denervation. Muscle Nerve 14: 654-664. 11) Walker, FO. (2004) Neuromuscular ultrasound. Neurol Clin 22: 563-590. 12) Chalmers, H.J., Yeager, AE and Ducharme, NG. (2009) Ultrasonographic assessment of laryngohyoid position as a predictor of dorsal displacement of the soft palate in horses. Vet Radiol Ultrasound. 50 (1): 91-96. 13) Ortved KF., Cheetham, J., Mitchell, LM. And Ducharme, NG. (2010) Successful treatment of persistent dorsal displacement of the soft palate and evaluation of laryngohyoid position in 15 racehorses. Equine Vet J. 42 (1): 3-9. 14) Garrett, KS. Woodie, JB., Embertson, RM. And Pease, AP. (2009) Diagnosis of laryngeal dysplasia in five horses using magnetic resonance imaging and ultrasonography. Equine Vet J. 41 (8): 766-771. 15) Koenig, J., Silviera, H., Chalmers, H., Buenviaje, G. and Lille, BN. (2011) Laryngeal neuroendocrine tumour in a horse. Equine Vet Educ. (Early view, published online 25 May 2011).

32

DIGITAL RADIOGRAPHY WITH AN EQUINE FOCUS

Dr Mika Frances BSc BVMS MACVSc (Radiology) Veterinary Imaging Centre, 305 Selby St, Osborne Park, WA 6017

Overview

· Methods of digital image capture · Image processing and artifacts

o How to take images of good quality repeatably · Image format, storage and transfer · Advantages and disadvantages of digital imaging · Choosing a digital imaging system

Digital radiography has two basic forms

1 : CR = Computed Radiography 2: DDR = Direct Digital Radiography, sometimes called just DR Film Screen Radiography = FSR

· Methods of digital image formation and capture o Both systems use same x-ray generator / x-ray tube as FSR ie the exposure is produced using the same machine. o Systems may be fixed (stand alone) or mobile

CR

· Photosensitive image plate which replaces the film and intensifying screen used in FSR · The imaging plate is housed in a cassette for physical protection · The cassette is used in the same way the FSR cassette is used ie can be inserted into floating table under bucky, cassette holders etc. · The plate is exposed and captures a latent image · In the processor the image plate is read by a laser.

The cassette may be inserted directly into the processor where it is opened by the machine, which removes the image plate for reading. OR The image plate may need to be manually removed from the cassette by you and inserted into the processor, then replaced in the cassette after reading.

This process may result in damage to the plate and therefore cost of replacement · This process takes ~25-180 seconds. The plate is erased in the processor allowing the cassette to be re-used.

DDR

· The imaging plate is exposed and captures the image · The plate is read directly and converted into a digital image · Faster than CR · Two types of detectors

33

Flat panel Direct and indirect In product information sometimes only the compound in the detection system is listed, this can be a clue as to what type of detector it is Direct – commonly = cesium iodide Indirect – commonly = amorphous selenium / amorphous silicon

Charged couple Optic minification → exposed CCD chip →electrical charge → digital signal Due to the optical minification requirements the x-ray beam must always be at right angles to the plate, therefore these detectors are not suitable for equine use as small abnormalities of incident angle may result in a non-diagnostic radiograph.

CCD detectors also reduce the detection efficiency thus reducing radiation dose efficiency. Cheaper than flat-panel detectors

Image processing and quality

· Digital image captured and processed o Image detection – finds collimated borders

May result in artifact o Re-sizing o Contrast and brightness enhancement o Perceived spatial enhancement

· Post processing o Annotation o Image inversion/flip o Window and levelling o Edge enhancement

Exposure Index

Exposure Index = measure of the amount of exposure received by the image receptor Dependent on mAs Detector area irradiated Beam attenuation The EI is an indicator of whether noise levels are acceptable, an indicator of image quality.

FSR – image quality obvious as direct reflection of blackness of film. Post processing of DR, however, may make assessment of quality/appropriateness of initial exposure more difficult. Also developed for technologists to assess initial images prior to assessment by radiologist, this may have been done at a viewing station of poorer quality than where final interpretation was made. Bear this in mind if viewing images in field on small mobile devices.

34

Image noise Image noise = Grainy image

Reduced noise, better image quality, better contrast resolution Derived from a graph of all the pixel intensities created by the exposure and adjusted for body region. Although always calculated from exposure, different equipment manufacturers calculate the ranges differently using different definitions, ranges and units. Eg Fuji = “S” number, Kodak CR uses “EI”, AGFA uses “LgM”, Philips uses “EI” / “S”, Canon DR uses “REX”, Siemens uses “EXI” etc

These values are not directly comparable between one system and another Post processing

LUT = look up table = non-linear function applied to image which alters brightness of pixels relative to one another to alter the appearance.

Increase/decrease overall contrast for an anatomic region Can be used to compensate for large density differences in different anatomic areas These mathematical functions are also responsible for the interactive windowing and levelling we use

Spatial enhancement – post processing eg makes edges sharper, smoothing filters can be applied

Again, different equipment manufacturers use different LUT’s and spatial enhancement methods therefore images will have different appearance TRY system before you buy

Artifacts – pre-exposure

Storage scatter – due to background radiation Expose/clear plates each morning

Cracks – more common in periphery, due to damage to the plate in CR reading Partial erasure – image remains due to faulty white light in processor Phantom image – if there is a long delay between exposures the previous image may reappear Memory – after exposure there is a brief delay required for the photodiodes and photoconductors to return to their ground state. If expose again – get either a negative or positive summation of the previous image.

Ensure functional electrical conduction and grounding, a brief delay may be necessary

Dead Pixels – fault of manufacture or damage over time This may be compensated for by processing to a degree, the computer will extrapolate from neighbouring images however will eventually need to replace detector

35

Artifacts - exposure Upside down cassette – lead backing will partially attenuate image Backscatter – degrades image, reduced by lead backing on cassette, attenuates scatter Grid cutoff – as with film Double exposure – unlike film, with CR a double exposure may produce a uniform image of reasonable contrast (overexposed with film) therefore may be more difficult to detect initially. With DR, interruptions to power supply or data transfer may result in double exposure. Quantum mottle (noise)

Increase mAs Note edge enhancement techniques increase delineation of object borders but also increase quantum mottle.

Saturation – DR and CR have a wider dynamic range than FSR. The lower end of the dynamic range is limited by noise, the upper end by saturation. Pixels that are saturated appear completely black and are unable to be windowed/levelled to their original intensity. Paradoxic overexposure – when functioning in the system’s dynamic range, more exposure results in a blacker image, however with DR systems, further increasing the exposure in some cases results in a lighter image. Unknown cause.

Higher kVp and lower mAs may correct this Planking – DR detectors occur in arrays, at higher exposures these arrays may be visible as separate sections. Radiofrequency interference – Large amounts of RF interference, proximity to a source, breaks in RF shielding may lead to repetitive linear streaks of lighter and darker shades of white and grey. This artifact may be intermittent making it difficult to detect Artifacts – post – processing and reading artifacts Light leak – into CR cassette – takes longer for artifact to occur than with FSR, however looks similar Fading – if not processed immediately, a faded, grainy image of reduced quality will result. Dirty light guide on internal laser – results in a white line/dotted line across the image Skipped scan-lines – caused by physical jarring during processing, this may result in a missing line of image, and a “stepped” appearance to the adjacent image. Moire – no of lines read per unit distance = sampling frequency (differs for different systems) – if this corresponds to a regularly repeated attenuator (eg grid) → Moire.

Use a mobile bucky for best results Workstation artifacts

Faulty transfer – need stable connection Border detection – if automatic, border may be applied to the wrong part eg to area of high attenuation (such as spine) rather than actual border. This may result in omission of part of image. More likely in above scenario or if imaging plate rotated relative to incident x-rays.

Can remove border detection and re-process the image.

36

Diagnostic specifier – picking wrong ROI →wrong histogram used for image processing May correct after processing by selecting correct algorithm.

Clipping – when image/file is compressed for transfer may remove useful information Density threshold – eg when implants used, histogram/look up table used may widen the grey scale resulting in biologic tissues appearing dark and with reduced contrast. Uberschwinger – a result of edge enhancement techniques in region of metallic implants. To edge-enhance, a narrow, black line is inserted adjacent areas of high attenuation, may be added to area adjacent to implants, can appear similar to bone lysis.

Image formats

DICOM = digital imaging and communications in medicine Image plus header

Differs from other data formats in that is contains patient information as well as information about how the image was made within the file, can’t be separated from the image. All types of radiology equipment will use DICOM Necessary for legal identification of digital images

JPEG = joint photographic expert group

Commonly used format for digital cameras Storage and transmission, compresses image therefore tradeoff between file size and image quality Works best for photos Not used for quantitative studies due to effects of compression Usually achieves 10:1 compression with little perceivable loss of quality

TIF = tagged image format (or TIFF tagged image file format)

Originally created in an attempt to get desktop scanner vendors to use same image format Flexible and adaptable, allows storage of images in a wide range of resolutions colours and grayscales Uses lossless compression system Supported by many systems, commonly used format for scanned images such as photos

Image compression

· 2 view study = 16 MB approx, slow transmission time, limited storage space. · Forms of compression

o Reversible (lossless) and irreversible (lossy) compression · Compression ratio initial file size: compressed file size · Lossless limited to 5:1 ratio · Lossy up to 100:1

37

· 10:1 to 20:1 no reduction in image quality however as an exact compression ratio can’t be given there will be variation between individual images

Standard JPEG inadequate for teleradiology, OK for clients. JPEG 2000 – excellent quality at high compression ratios JPEG LS standard form of lossless compression

Image storage

Laptop at acquisition. Commonly store ~3000 images. PACS = picture archival and communications system

Stores multiple modalities Server capable of organizing and distributing Archival system – key to choosing PACS

Short and long term access Off site disaster recovery Economic balance depending on how much on-site/off-site storage Remote access – if regularly email images eg for teleradiology Can import DICOM images directly into PACS for records and viewing

Monitors Viewing environment important, consider light, viewing conditions Monitors –

Best are medical grade black and white LCD $$$ High quality LCD monitors are available with resolution of 2-5 MP, contrast ratio 1000:1, luminescence of 350-1000 cd/m2 (higher the better)

Weblink: http://www.animalinsides.com/learn/digital-imaging/131-veterinary-monitorselection.html Resolution – affects what happens to the image when zoomed. If you open an image with a large matrix on a 2MP display it will appear large. When you then zoom in , the computer makes assumptions about the relative blackness of individual pixels compared to the neighbour and then reduces size of image. The original data is then lost so future zooming/manipulation will only be proportional to the new image. “DOWN PROCESSING”. Luminescence = brightness. Increased luminescence can improve diagnostic usefulness of a lower resolution monitor. Contrast ratio 100:1 means the black is 100 times darker than the white. Consumer grade monitors generally 250:1-350:1, medical grade 1000:1. This improves the number of gray scales displayed. A large contrast ratio is necessary to display all the shades of grey in the dark end of the scale. Colour monitors have a decreased contrast ratio compared to grey scale as use three colours to display black/white. Commercial colour monitors typically

38

Advantages/Disadvantages of CR/DR Advantages of digital detectors

PACs Higher patient throughput Increased dose efficiency Greater dynamic range with possible reduction of x-ray exposure

CR Cassette based and can be integrated into regular systems Mobile Can replace a single faulty or damaged plate

DR Rapid image acquisition and processing time Dose reduction

Disadvantages of digital systems

· may over process images, potential for causing artifacts · Dosage creep – due to ability to correct for overexposure by windowing and levelling it is possible that a higher exposure than is required may be used eg when turn patient 90 degrees and don’t change exposure. · Spatial resolution not as good as film screen, however this is outweighed by multiple other benefits

Choosing your system

Who are my patients ? Equine only Mixed Small animals?

What type of practice ? Mobile Fixed facility

DR versus CR ? DR = Faster, more $ to purchase

Volume of cases a key factor CR = Cheaper and cassette based, can be incorporated into existing FSR cassette-based systems

Issues to consider Image quality – minor differences in spatial resolution (CR resolves up to 10lp/mm, DR resolves ~3-5 lp/mm).

Insert reference comparing CR/DR image quality Film/processing costs versus rate of plate (DR) or cassette (CR) replacement

DR cable can be a significant hazard around horses and has implications for radiation safety

39

If damaged, individual CR cassettes are cheaper to replace than DR plate CARE with CR systems that require you to manually remove the imaging plate – a cause of artifacts and easily damaged. For a DR system – check range of sizes of detector panels, also check weight (commonly ~3kg) and ease of manipulation to ensure adequate radiation safety (cassette holders etc).

Choosing your system

How are images viewed? Pressure to make a diagnosis in the field with poor quality viewing equipment - care

Viewing equipment must be of sufficient quality to allow adequate assessment of image quality prior to leaving property

What PACs is appropriate for all elements of my practice? Other modalities within the practice may be able to use this eg ultrasound, nuclear medicine Capacity Disaster recovery/back up

How are images stored? DICOM JPEG Other

How easily are images downloaded, transferred and accessed? To consult rooms To email To a remote server To practice management software

Cornerstone, others Via wireless connection Choosing your system

What level of support can I expect? Technical support from staff with veterinary experience

Parts Labour Phone support

Pre-purchase trial

40

STANDING MRI FOR THE DISTAL LIMB

Charles Ley, BVSc, MACVSc (Radiology), MVetMed (Diagnostic Imaging), Dipl. ECVDI Department of Clinical Sciences, Section for Diagnostic Imaging, Swedish University of Agricultural Sciences, Uppsala, Sweden.

Magnetic Resonance Imaging (MRI) is now established as an important diagnostic method for equine distal limb lameness. When cases are selected appropriately, the technique allows accurate diagnosis of soft tissue and bone abnormalities that cause lameness, so that treatments can be specific for the problem/s detected. Currently the most common MRI system used for examining the limbs of horses is the Hallmarq 0.27T standing equine scanner with over 20 000 horses now scanned with the system, and 47 sites located around the world. Several other MRI systems are used for horses, these are both low (approximately 0.3T) and high Tesla (1.5-3T), and these systems require the horse to be under general anaesthesia for the scan. It is also possible to use the Hallmarq scanner for anaesthetised horses. All systems have advantages and disadvantages. High Tesla systems have the potential for higher resolution images with larger fields of view, but these systems are more expensive to run and only specialised non-magnetic equipment can be used in the MRI room. Low Tesla systems are cheaper to run and often routine monitoring and anaesthetic equipment can be used in the room. For the standing MRI examination horses are sedated (usually a combination of an alpha2-adrenergic agonist and an opioid) with regular ‘top up’ doses or infusions. Average examination times vary between about 30-60 minutes but can be up to 2 hours, and each sequence usually takes between 2-6 minutes. Currently, most examinations using the standing MRI system are of the hoof but it is possible to examine most legs to the level of the carpus/tarsus. The further proximally you examine the more motion will become a problem, and anaesthesia can be considered in these cases. There is currently a lot of interest in scanning the fetlock region (particularly in Thoroughbred horses) and the proximal metacarpal/metatarsal regions. The Image An MRI image is an image representation of the behaviour of the protons in the body in response to strong magnetic fields and pulses of radiofrequency. Most of the protons in animals are in the form of hydrogen atoms in water molecules. There are fast spin echo sequences and gradient echo sequences. Gradient echo sequences generally have the shortest acquisition time, and the T2 weighted fast spin echo sequences have the longest acquisition time. Fast spin echo sequences available on the Hallmarq system include T1W SE, T2W FSE, PD and STIR. Gradient echo sequences available on the Hallmarq system include T1W 3D, T2*W 3D, T1W GRE and T2*W GRE. During an MRI examination images are made in several different planes. This is done since anatomical structures and abnormalities of these structures are most clearly seen when the plane is perpendicular to the structure of interest. The basic planes are sagittal, transverse, and dorsal/frontal.

41

The maximum field of view for the Hallmarq system is about 15 cm, but image quality is poor in peripheral 2-3 cm of the image. To examine regions proximal or distal to the field of view the magnet must be mechanically lifted/lowered and this usually requires repositioning of the horse. Thus, localisation of the lameness to a 10-12cm diameter region is ideal. Common image artefacts that need to be recognised and understood in the MRI images include; motion, partial volume averaging, susceptibility, magic angle and fat/water cancellation artefacts. Essential pre-MRI information For a horse to have an MRI examination there must be a clear and convincing reason and the possibility of a potential benefit. Horses must have a complete lameness examination and it should be possible to localise the lameness to a region that is ideally less than 15cm in diameter. Causes of lameness that can be detected using radiology and/or ultrasound should be excluded. It is important that the veterinarian doing the MRI receives a request with a brief, relevant and accurate history that clearly states the requested region of examination, plus any radiographs of/ultrasound reports from the region of interest. There should not be metal implants in the region of examination. Image interpretation MRI images give information about the size, shape, number, relationship and position of anatomical structures, and the signal intensity and signal homogeneity from these structures and any lesions detected. Some sequences give mainly anatomical/spatial information (e.g. proton density), others give mainly intensity information (e.g. STIR) and many give a combination of both. MRI gives the most signal from fluid containing tissues and soft tissues, and thus these tissues give the most information in an MRI image. The MRI anatomy of the distal limb is well described in the literature with several excellent textbooks and articles (Denoix et al. 1993; Martinelli et al. 1997; Denoix 2000, Dyson et al. 2003, Busoni et al. 2004; Murray et al. 2007; Smith et al. 2010; Murray 2011). In a routine clinical MRI images objects as small as 1-2mm can usually be defined in images that do not have significant artefacts. Normal variations/incidental findings Several normal anatomical and intensity variations are commonly seen. There can be mild size variation between individuals in the medial and lateral collateral ligaments of the distal interphalangeal joint and the collateral (proximal) ligaments of the navicular bone, and the assessment of whether or not this is normal is usually made by comparing the right and left legs, and the presence/absence of intensity and other changes. Heterogeneous hyper intensity can be seen normally in the short, cruciate, oblique, and straight sesamoidean ligaments, and the insertions of the suspensory ligament branches (Dyson and Murray 2007). The magic angle artefact is a relatively common in the collateral ligaments of the distal interphalangeal joint, the deep digital flexor tendon, and the oblique sesamoidean ligaments. When hyper intensity is seen in a normal sized ligament the magic angle artifact should always be considered (Spriet et al. 2007; Smith et al. 2007; Spriet and McKnight 2009; Spriet and Zwingenberger 2009). The

42

amount of filling of the distal interphalangeal joint is variable in standing horses; once again, comparison of right and left legs can be useful. MRI has been shown to be accurate for the detection of osteophytes on joint margins (Olive et al. 2010) but care must be taken not to over interpret normal peak shaped joint margins as osteophytes, particularly in T2*W images. Changes suspected to be unrelated to the current lameness of the horse (for example in the non-lame leg) are also detected occasionally. Such changes include regions of bone formation, mild tendon or ligament lesions, and small mild regions of STIR hyper intensity. Hypoechoic tracts from old now healed penetrating injuries in the heel region of the hoof can be seen, and it is of course very important in these cases to carefully evaluate adjacent structures for lesions. The conclusion about the future clinical significance of such changes is usually impossible or extremely uncertain. Lesions Injuries in soft tissues and bone often result in increased signal intensity in T2W and STIR images, and this is often called edema like signal/change. When such injuries are examined with histology the microscopic abnormalities detected include; edema, necrosis, hemorrhage, fibrosis, congestion, perivascular mononuclear cellular infiltration (Schramme et al. 2005, Blunden et al. 2006, Murray et al. 2006a). Edema like signal is detected quite often in asymptomatic human athletes (Kornaat et al. 2008) and has been detected in horses that are not lame (Murray et al. 2006b, Dyson and Murray 2007b). A recent publication (Holowinski et al. 2010) found that resolution of edema like signal in follow up examinations of tendon and ligament lesions was associated with clinical improvement, although this association was not found with bone marrow lesions. It is suspected in most cases that acute/active lesions are usually hyper intense in T2W images (including STIR) and hypo intense in T1W images, and the inactive/old lesions can be hyper intense in T1W images but not usually hyper intense in T2W images. There are certainly exceptions to this pattern and until more is known about the spectrum of possible MRI appearances for specific and combinations of histological changes, then caution is recommended in interpreting lesions as acute/active verses inactive/old. Contrast techniques are being evaluated in an effort to accurately classify lesions as acute/active lesions verses old/inactive lesions, and help monitor response to treatment (Judy 2011). A decrease in intensity in all sequences in a bone is caused by sclerosis/increased bone density. This change can be exercise induced, but if there is evidence of lameness originating from the region and evidence of STIR hyper intensity close to the decreased signal region then a bone injury is usually suspected. When abnormalities are detected in the hoof and fetlock regions it is more common to detect multiple lesions rather than single lesions (Murray et al. 2006b, Gonzalez et al. 2010). This suggests that injuries are occurring concurrently in several structures in a region, or that an injury in one structure increases the risk of injuries occurring in surrounding structures. This is

43

also supported recent findings that abnormalities in the distal portion of the navicular bone are significantly correlated histological abnormalities in the impar ligament (Dyson et al. 2010). The Future Further improvements in MRI hardware and software, and our expanding knowledge regarding image interpretation and its application will make MRI even more valuable in the future. There is now a good knowledge base regarding the image appearance of the distal limb and the common lesions. A major challenge that remains is to learn more about the clinical significance of specific imaging patterns in specific locations (Holowinski et al. 2010). A developing focus in equine MRI research is investigation of long-term outcomes of treatments that target specific lesions (Gutierrez-Nibeyro et al. 2010). This will hopefully result in development of new or modified effective site specific lesion therapies, and improve the certainly of prognosis predictions. References Blunden, A., et al. Equine Vet J (2006), 38, p23. Busoni, V., et al. Vet Radiol Ultrasound (2004), 45, p198. Denoix, J.-M., et al. Vet Radiol Ultrasound (1993) 34, p405. Denoix, J.-M., The Equine Distal Limb (2000) Manson Publishing/The Veterinary Press. Dyson, S. and Murray, R. Clin Tech Eq Prac (2007a) 6, p62. Dyson, S. and Murray, R. Equine Vet J (2007b) 39, p340. Dyson, S., et al. Equine Vet J (2003) 35, p18. Dyson, S., et al. Equine Vet J (2010) 42, p332. Gonzalez, L.M, et al. Vet Radiol Ultrasound (2010), 51, p 404. Gutierrez-Nibeyro, S.D, et al. Equine Vet J (2010) 42, p680. Holowinski, M.,et al. Vet Radiol Ultrasound (2010), 51, p 479. Judy, C. In Equine MRI Ed Murray, R. (2011) Wiley, p63. Kornaat, P.R, Radiology (2008), 67, p49. Martinelli, M.J., et al. Vet Radiol Ultrasound (1997), 38, p193. Murray, R. C., Equine MRI (2011), Wiley. Murray, R., et al. Vet Radiol Ultrasound (2006a), 47, p17. Murray, R., et al. Vet Radiol Ultrasound (2006b), 47, p1. Murray, R., et al. Clin Tech Eq Prac (2007), 6, p26. Olive, J., et al. Vet Radiol Ultrasound (2010) 51, p267. Schramme, M.C., et al. Ann Con Am Ass Eq Prac (2005) 51, p348. Smith, M.A., et al. Vet Radiol Ultrasound (2008), 49, p509. Smith, M.A., et al. Vet Radiol Ultrasound (2011), 52, p61. Spiret, M., et al. Vet Radiol Ultrasound (2007), 48, p95. Spriet, M. and McKnight A., Vet Radiol Ultrasound (2009) 50, p32. Spriet, M. And Zwingenberger A., Equine Vet J (2009), 41, p498. Werpy, N.M., et al Vet Radiol Ultrasound (2010) 51, p2.

44

MRI OF DISTAL TARSAL JOINT OSTEOARTHRITIS

Charles Ley, BVSc, MACVSc (Radiology), MVetMed (Diagnostic Imaging), Dipl. ECVDI Department of Clinical Sciences, Section for Diagnostic Imaging, Swedish University of Agricultural Sciences, Uppsala, Sweden.

Distal tarsal joint osteoarthritis (dTOA), also called bone spavin, is osteoarthritis (OA) of the centrodistal tarsal joint, the tarsometatarsal joint and occasionally the talocentroquartal joint in horses. In Sweden, a recent study found that joint problems are the most common cause of death or euthanasia in horses and dTOA is one of the leading causes of these joint problems (Egenvall et al. 2006). This correlates well with another study done in Sweden between 1973 and 1981 where dTOA accounted for approximately 9% of all cases of equine lameness that resulted in loss of use (Bergsten 1983). There is a high rate of incidence of dTOA in Icelandic horses living in Iceland (30.3%) and Sweden (23%) (Axelsson et al. 1998, Björnsdottir et al. 2000a) and is the most common cause of culling due to disease in 7-17 year old Icelandic horses used for riding in Iceland (Björnsdottir et al. 2003). The cause and aetiology of equine dTOA is not fully understood, and it is uncertain whether dTOA develops differently in different horse breeds. The heritability of dTOA for Icelandic horses is estimated to be medium to high (Björnsdottir et al. 2000b), age and tarsal angle are risk factors in Icelandic horses, but work load and type of training are not (Axelsson et al. 2001). A recent study of a small group of Thoroughbred and Warmblood horses found a higher incidence of osteochondral lesions in ridden horses compared to pasture exercise horses suggesting a link between exercise type and dTOA (Tranquille et al. 2011). Distal TOA changes have been detected with histology and high detail radiology in young Icelandic horses (Björnsdottir et al. 2004), and weanling Thoroughbreds (Laverty et al. 1991), suggesting an early onset and slow progression of the disease. For many years there has been debate in the medical and veterinary literature regarding the development of osteoarthritis and the location of the earliest changes (Burstein and Hunter 2009; Heinegård and Saxne 2011, Thambyah and Broom 2009). Where does the disease begin and what are the pathogenic pathways? Traditionally osteoarthritis was considered to be characterised by articular cartilage degeneration and reactive changes in the joint margin and joint capsule (Pool and Meagher 1990). Recently, there has been more emphasis on the concept that osteoarthritis is a disease of the entire synovial joint organ, and that injury to one component of the joint leads to damage of other joint components (Peterfy et al. 2004; Burstein and Hunter 2009; Heinegård and Saxne 2011). This concept does not limit the disease to the cartilage and joint margins. The location of the highest frequency of dTOA radiographic changes has been investigated. Verschooten and Schramme (1994) consider the dorsolateralplantaromedial oblique projection as the most informative for dTOA, implying that more changes are present on the dorsomedial joint aspect. A study of Icelandic horses shows that the highest relative frequency of radiological changes is on the dorsolateral aspect of the distal tarsal joints (Eksell et al.

45

1999). Histological examination from standard sites has been used to examine young Icelandic horses and there was no significant difference between the incidence of the changes being located in the lateral compared to the medial region of the centrodistal joint (Björnsdottir 2004). The normal magnetic resonance imaging (MRI) anatomy of the equine tarsal joint is described (Blaik et al. 2000; Latorre et al. 2006; Branch et al. 2007a). MRI abnormalities of the tarsal joints are seen in clinically normal and lame horses (Branch et al. 2004; Branch et al. 2007b). Using MRI a normal pattern of subchondral bone thickness has been described and high intensity exercise is associated with greater subchondral bone thickness (Branch et al. 2004, Branch et al. 2005, Branch et al. 2007a; Branch et al. 2007b, Murray et al. 2007, Tranquille et al. 2009). Care must be taken when using MRI to assess subchondral bone thickness since chemical shift artefacts can result in over and under estimation of compact bone thickness (Dimock and Spriet 2010). To allow the development of methods to prevent or treat equine OA an understanding of the pathogenesis of the first stages of the disease is required. Since it is possible that these early changes could develop in specific and focal regions/structures in the joint, a technique is required that allows evaluation of the entire joint organ. High resolution and three-dimensional (3D) cross sectional diagnostic imaging techniques, such as (MRI) and computed tomography (CT) allow reconstructions to be made in unlimited planes so that all areas of a joint can be examined from multiple angles and thus evaluation of the entire joint organ is possible. High resolution 3D MRI cartilage specific sequences are very useful for detecting the early changes of OA in the articular cartilage (Batiste et al. 2004; Calvo et al. 2004), and using several techniques of image acquisition provides information about the different specific tissue types and structures in the joint. It is also possible to use image registration so that several different imaging modalities can be used together to investigate OA (Batiste et al. 2004). Studies that link diagnostic imaging abnormalities with the microscopic appearance of the lesion are also extremely valuable in understanding the relevance of lesions and the development of disease (Murray et al. 2006). The accuracy of MRI correctly detecting low-grade changes of osteoarthritis, especially articular cartilage defects, is currently a very active area of research in both human and veterinary medicine. Several human studies performed in the 1990s concluded that MRI is highly sensitive for detecting focal cartilage defects and thinning (Kawahara et al. 1998; Bredella et al. 1999), but more recent human studies have questioned the accuracy of MRI for detecting lowgrade cartilage abnormalities (Bittersohl et al. 2009; Hofmann et al. 2010). The predictive value of MRI using current clinical sequences at 1.5T for detecting low-grade cartilage lesions in human stifle OA was recently considered to be limited and the inter-observer variance high (Hofmann et al. 2010). The capability of FLASH and DESS sequences in diagnosing early cartilage lesions in human stifle OA with high accuracy could not be proven (Bittersohl et al. 2009). Studies of equine articular cartilage have shown that there is good to moderate correlation between measurements of cartilage thickness with highfield MRI compared to histology

46

(Murray et al. 2005; Olive et al. 2010). MRI has moderate sensitivity and high specificity for detecting full thickness cartilage erosions but the size of cartilage defects are often under estimated (Olive et al. 2010; Werpy et al. 2010). Using a low-field MRI system with clinical sequences, 5mm diameter experimentally created full thickness cartilage defects could not be detected and several false positive lesions were detected (Werpy et al. 2010). Partial volume averaging artefacts and low contrast in the articular cartilage are reasons for the poor detection rate of cartilage lesions in low-field MRI. We are using high resolution 3D MRI and CT, combined with microscopy to investigate the early changes of dTOA a group of young Icelandic horses. The parents of the study horses were selected so that approximately half of the study group have parents with radiological changes of dTOA, and the other half have parents with no radiological changes of dTOA. The study horses lived together since birth, and so were exposed to the same environmental factors. The horses lived in a large ‘natural’ paddock and did not receive any training. Horses were slaughtered at 2.5 years of age and their tarsal joints were removed for MRI and CT examinations. The microscopy techniques we are using include histology, confocal scanning light microscopy (CSLM) and back-scattered electron scanning electron microscopy (BSE SEM), and samples are taken using diagnostic image guidance. Boyde et al. (2005) developed a technique combining CSLM and BSE SEM that results in extremely high resolution images of bone and cartilage. This technique has been used to investigate changes in subchondral bone density of the equine third metacarpal bone (Boyde and Firth 2005) and a modification of this technique has been used to investigate the third metacarpal articular calcified cartilage and subchondral bone of 2-year-old thoroughbred horses (Boyde and Firth 2008). Using this technique it was possible to detect several previously undescribed changes and possible to see in unparalleled detail some of the commonly detected ‘early OA’ changes. The characteristics and locations of these changes provide information that can help to explain the sequences of events and pathogenesis of equine OA. BSE SEM and CSLM give the opportunity to study the earliest changes of OA in the tarsal joints of Icelandic horses and the possibility of combining this technique with high resolution 3D diagnostic imaging make it possible to examine specific regions of interest which could otherwise be overlooked using standard sampling techniques. References Axelsson, M., et al. Acta Vet Scand (1998), 39, p349. Axelsson, M., et al. Equine Vet J (2001), 33, p84. Batiste, D.L., et al Osteoarthritis Cartilage (2004), 12, p614. Bergsten, G., Svensk Veterinärtidning (1983), 35 (S3), p14. Bittersohl, B., et al Eur J Rad (2009), 70, p561. Björnsdottir, S., et al. Equine Vet J (2000a), 32, p268. Björnsdottir, S., et al. Liv Proc Sc (2000b), 63, p77. Björnsdottir, S., et al. Acta Vet Scand (2003), 44, p161. Björnsdottir, S., et al. Equine Vet J (2004), 36, p5. Blaik, M.A., et al. Vet Radiol Ultrasound (2000), 41 p131.

47

Boyde, A., et al. Eur Cell Mater (2005), 9, p33. Boyde, A. and Firth, E.C. N Z Vet J (2005), 53, p123. Boyde, A. and Firth, E.C. Micros Res Tech (2008), 71, p477. Branch, M., et al. Am Ass Eq Prac, Focus on Joints (2004), p28. Branch, M., et al. Equine Vet J (2005), 37, p450. Branch, M., et al. Clin Tech Eq Prac (2007a), 6, p96. Branch, M., et al. Equine Vet J (2007b), 39, p101. Brendella, M., et al. Am J Roentgenol (1999), 172, p1073. Burstein, D., and Hunter, D.J, Osteoarthritis Cartilage (2009), 17, p571. Calvo, E.I., et al. Osteoarthritis Cartilage (2004), 12, p878. Dimock, A.N, and Spriet, M. Vet Radiol Ultrasound (2010), 51, p 415. Egenvall, A., et al. Vet Rec (2006), 158, p397. Eksell, P., et al. Vet Radiol Ultrasound (1999), 40, p228. Heinegård, D. and Saxne, T. Nat. Rev. Rheumatol. (2011) 7, p50. Hofmann, G.O., et al. Pathophysiology (2010), 17, p1. Kawahara, Y., et al. Acta Radiol (1998), 38, p120. Kawcak, C.E., et al. Osteoarthritis Cartilage (2008), 16, p1519. Latorre, R., et al. Am J Vet Res (2006), 67, p756. Murray, R.C., et al. Am J Vet Res (2005), 66, p1999. Murray, R.C., et al. Vet Radiol Ultrasound (2006), 47, p17. Murray, R.C., et al. J Applied Physiol (2007), 102, p2194. Olive, J., et al. Vet Radiol Ultrasound (2010), 51, p107. Peterfy, C.G., Osteoarthritis Cartilage (2004), 12, p177. Pool, R.R., and Meagher, D.M., Vet Clin N Am, Eq Prac (1990), 6, p1. Schramme, M. et al. Vet Radiol Ultrasound (2009), 50, p 606. Thambyah, A. and Broom, N. Osteoarthritis Cartilage (2009), 17, p456. Tranquille, C. A., et al. Am J Vet Res (2009), 70, p1477. Tranquille, C. A., et al. Am J Vet Res (2011), 72, p33. Verschooten, F. And Schramme, M., Eq Vet Ed (1994), 6 p323. Werpy, N.M, et al. Vet Radiolo Ultrasound (2011), 52, p154.

48

IMAGING TECHNIQUES FOR DIAGNOSING EQUINE DENTAL DISEASE

Ian Dacre

Introduction

In the thesis entitled ‘A Pathological, Histological and Ultrastructural Study of Diseased Equine

Cheek Teeth’ (Dacre, 2004) the author describes several revised and new techniques for the

examination of extracted equine cheek teeth for the determination of pathological conditions

present. Many previously undescribed conditions of equine dentition were identified as a result

of this work. This presentation aims to show how these techniques may be used to give

researchers further tools in the advancement of the understanding of equine dental pathology.

As an example the technique used to produce undecalcified equine dental sections has been

described below in the hope that researchers in this field may become aware of such

techniques.

Teeth Sectioning Twelve control CT were sectioned in a rostro-caudal plane, and 88 control CT in a transverse

plane using a water-cooled Logitech CS10 saw with diamond blade. Thirty-six apically infected

CT were also transversely sectioned using the above diamond saw. A further 14 apically

infected CT were latterly transversely sectioned at Easter Bush Veterinary Centre using a 99-

TS230M tile-saw with an 8” Thin CR diamond blade. This saw was also used for sectioning 20 CT

with idiopathic fractures and latterly CT examined with unknown dental histories.

As CT curve in three dimensions (x, y and z axes), sectioning them in a longitudinal direction

with a rigid blade does not allow the anatomical features of interest (e.g. infundibula or

endodontic pulp chambers) to be followed for their full course. Consequently all quantitative

measurements recorded from pathological specimens were taken from transverse sections and

only qualitative assessments were made of longitudinal sections.

In an initial pilot study of 16 maxillary-infected CT the CT were transversely sectioned at 3mm

intervals (with 1.0mm being lost with each saw cut), from the occlusal surface to the apical

region. This produced up to 23 sections per tooth. Sections from each tooth were randomly

assigned for light microscopy following decalcification, undecalcified light microscopy, scanning

electron microscopy or transmission electron microscopy.

All sections were placed in individual histokinette chambers before being returned to the

formalin solution. In some cases, transverse sections of (the larger) maxillary CT were divided

into rostral and caudal halves, in order to allow their placement in individual histokinette

chambers.

49

Undecalcified Thin Sections

Eighty-eight control CT transverse sections, 50 diseased CT transverse sections and 21 sections

from fractured teeth in various orientations, were dehydrated through a series of graded

ethanol on a semi-automatic histokinette. Following removal from ethanol, they were air dried

at room temperature for 24 hours. The samples were then placed into a foil mould and cast

into blocks using Buehler Epo-Thin resin - with 2% petropoxy blue dye added to help identify

any remaining covering resin during the hand-grinding phase - and samples were left to set at

room temperature for 24 hours.

Once set, samples were removed from the mould and excess resin was trimmed away using a

diamond saw. The desired face of the sample was then hand ground, using a series of

incrementally finer silicon carbide grit papers (240, 400, 800, 1200, 2500, and 4000 grit) to

obtain a flat surface. Castrol Ilocut 430 was used as non-water based lubricant for this and all

further processing requiring cutting or grinding. Samples were then rinsed clean with Analar

acetone.

The hand-ground surface was then bonded to a glass slide using Buehler Epo-Thin resin and left

in a spring-loaded jig for 24 hours. The samples were then removed from the jig and using a

Buehler Petrothin cut-off saw with a diamond blade and vacuum mount, the mounted tissue

blocks were cut to a thickness of 500µm. At this stage the calcified tissues were already

translucent to transmitted light and were checked for potential processing faults. In some cases

it was necessary to re-mount the section, if bonding to the slide was thought inadequate to

hold it through the remaining processing.

The 500µm thick sections were then placed onto a Logitec LP30 rotary lapping machine for 20

minutes with ethanediol as an initial lubricant, and 600 grit silicon carbide powder with

ethylene glycol constantly being drip-fed onto the contact surfaces. Following this, the sections

were hand-lapped on a glass plate using 800 grit silicon carbide paper to give a fine finish and a

final thickness of 60-70µm. The exposed surface was gently cleaned with acetone before being

covered with a glass cover-slip using Eukitt adhesive.

Dentinal measurements were made of 26 undecalcified control CT slides and the results

compared to the adjacent control decalcified transverse sections from the same CT.

This data was correlated to the respective CAT scan image data when available. Control

undecalcified slides were qualitatively assessed for artefact and any anatomical irregularities

recorded.

Undecalcified slides of apically infected CT and those with idiopathic dental fractures were

examined under dissecting and light microscopy for any evidence of dental caries. The

50

undecalcified slides from CT with idiopathic fractures had their fracture planes categorised, and

any other pathological features recorded whilst being viewed under dissecting and light

microscopy.

Reference List

Culling,C.F.A. (1974) Handbook of Histopathological and Histochemical Techniques. 3rd 66-

Butterworth & Co. Ltd.

Dacre, I.T. (2004) Thesis: A Pathological, Histological and Ultrastructural Study of Diseased

Equine Cheek Teeth. University of Edinburgh

Dixon,P.M. & Copeland, A. N. (1993) The radiological appearance of mandibular cheek teeth in

ponies of different ages. Equine Vet Edu. 5 (6) 317-323

Getty,R. (1975) Sisson and Grossman's The anatomy of domestic animals. W.B.Saunders Co.

Kilic,S. (1995) A light and electron microscopic study of calcified dental tissues in normal horses.

1-193 University of Edinburgh

Kirkland,K.D. et al. (1996) Effects of aging on the endodontic system, reserve crown, and roots

of equine mandibular cheek teeth. Am.J.Vet.Res. 57 (1) 31-38

Richardson,J.D. et al. (1995) An evaluation of the accuracy of ageing horses by their dentition:

changes of dental morphology with age. Vet.Rec. 137 (5) 117-121

Acknowledgements Professor Padraic Dixon; Dr Sue Kempson; Mr Mike Hall

The Home of Rest for Horses

51

OVERVIEW AND CURRENT STAGE OF KNOWLEDGE OF PERIODONTAL DISEASE IN HORSE

Teerapol Chinkangsadarn D.V.M.* *Faculty of Veterinary Medicine, Mahanakorn University of Technology, 140 Nong-Jok Bangkok, THAILAND 10530

Periodontal disease can be found clinically significant in mature horses, with an incidence of

60% in horses over 15 year of age.1 Moreover, it also has been documented in the veterinary

literature for many years and continues to be a main cause of dental pathology.5

The periodontium includes gingiva, periodontal ligament, cementum, and alveolar bone.

Whereas, the general term of the altered state of the periodontium is called Periodontal

Disease which can be categorized into 2 stages, the Periodontitis and the Gingivitis that affect

the periodontium and the gingival, respectively.2 The periodontal ligament is consisting of

collagen bundles called Sharpey’s Fibers that attach the tooth cementum to alveolar bone.

More study under electron microscope found the presence of blood vessels and nerves above

the clinical crown, which can be concluded that the cementum above the gingival margin is

living tissue for at least a short distance.4

The pathophysiology of the periodontium starting from the shift in population of bacteria then

leads to gingivitis and periodontitis.3 The increase in the number of Gram-negative aerobes,

anaerobes and spirochetes results in the loss of deep tissue attachment of periodontal

ligament. The basic host defense mechanism of horses starting from the release of gingival

crevicular fluid (GCF)6 which contain leukocytes, antibodies, enzymes and electrolytes in order

to flush the gingival sulcus. In combination with releasing of saliva which not only form a barrier

known as the salivary pellicle that protects against minor trauma and prevents adherence of

bacteria to the tooth surface, but also maintain specific oral cavity’s pH level to prevent

pathologic bacteria to be able to flourish.2 The further process of the response is to isolate the

infection to local tissue and prevent spread of the disease to the rest of the body. This may

result in rejection of the infected tooth. The periodontal disease can be easily detected by oral

examination with dental mirror and periodontal probe to measure the depth of pocket and

gingival sulcus. It is important that the veterinary examiner should be able to determine the

degree of advancement of the disease in order to formulate a prognosis and plan for the

treatment. The staging of periodontal diseases can be categorized into 5 stages (0-4) by

following parameters, the characteristic of gingival, the depth of gingival sulcus, the present of

feed debris packed in a pocket and the radiographic change of supporting structures. Where

“stage 0” means normal periodontium and “stage 4” is severely periodontal disease just before

the end stage of periodontal disease or exfoliation.

52

The treatment strategies of periodontal disease can be performed in the stages 0 to 3 include:

occlusal equilibration, pocket debridement and perioceutic therapy. Since equine teeth

undergo an elongated eruption time, the success of the treatment can be achieved with a

reduction in pocket size and re-establishment of gingival attachment. However, the true

character of the adherent tissue is unknown.

References

1 Baker GJ (1991) Diseases of the teeth Colahan PT, ed. Equine Medicine and Surgery, American

Veterinary Publications 550-570

2 David O.Klugh (2005) Equine Periodontal Disease Clin TechEquine Pract 4:135-147

3 Haake SK, Newman MG, Nisengaard RJ, et al (2002) Periodontal microbiology Carranza’s

Clinical Periodontology (ed4) Saunders 96-112

4 Kempson S. (2003) Equine Cementum: the Cinderella tissue Proceedings of the 17th Annual

Veterinary Dental Forum 206-210

5 Scott KG, Tony PB (2002) Recognition and Treatment of Equine Periodontal Disease AAEP

Proceedings Vol.48 Page 463-466

6 Weinstein E, Mandel ID, Salkinf A, et al (1967) Studies of gingival fluid Periodontics 5:161-166

53

PERIODONTAL DISEASE AND ADVERSE PREGNANCY OUTCOMES

Rachel Garraway Periocare, 800 Gympie Rd, Chermside 4032

rg@periocare.com.au

Periodontal disease is a complex, multifactorial disease. It is the result of the host response to

pathogenic oral bacteria. Research has traditionally focused on the bacterial aetiology and

more recently, risk factors associated with periodontal disease. The impact of periodontal

disease on overall health has been the focus of much research over the last couple of decades,

with epidemiological evidence linking periodontal disease to cardiovascular disease, adverse

pregnancy outcomes and respiratory infections (Genco and Williams 2010)

Since the first publication that linked periodontal disease with pregnancy complications in 1996,

there have been numerous studies exploring the association (Offenbacher et al 1996). The

obvious medical and financial implications of an association are enormous but do we have the

evidence to support this association? Many studies have shown an association between

periodontal disease and pregnancy complications, however others have demonstrated no

association (Bobetsis et al 2006, Xiong et al 2006). These differences in findings could be related

to the presence and management of aetiologic and risk factors, and the difficulties in defining

periodontal disease. Different population groups may also contribute the variation in results. A

significant association between periodontal disease and adverse pregnancy outcomes has

consistently been found in populations with a high incidence of preterm deliveries, including

African-American women and those from economically disadvantaged families (Offenbacher et

al 1996).

Hypothetical models of the association between maternal periodontal inflammation and foetal

development have been proposed. Inflammatory cytokines and acute phase reactants such as

C-reactive protein are produced as a result of periodontal disease activity and such mediators

could trigger a series of events, culminating in preterm delivery.

Despite the evidence supporting an association and the biological data suggesting causality, the

evidence relating the ability of maternal periodontal treatment to reduce the risk of pregnancy

complications is still limited. Although some studies have shown beneficial effects of

periodontal treatment, a recent meta-analysis has shown that periodontal treatment during

pregnancy is unlikely to reduce the risk of preterm birth or low birthweight infants (Polyzos et al

2010).

54

Perhaps the relationship is not a cause and effect relationship but an association due to an

underlying inflammatory phenotype? More studies with better methodological quality are

needed to confirm that periodontitis in pregnant women is an independent risk factor for

adverse pregnancy outcomes.

Bibliography

Bobetsis v, Barros S, Offenbacher S. Exploring the relationship between periodontal disease and

pregnancy complications. JADA 2006;137(10) 7s-13s.

Genco R and Williams R (2010). Periodontal Disease and Overall Health: A Clinician’s Guide.

Pennsylvania USA. Professional Audience Communications, Inc.

Offenbacher S, Katz V, Fertik G, Collins J, Boyd D, Maynor G, McKaig R, Beck J. Periodontal

infection as a possible risk factor for preterm low birth weight. J Periodontol 1996;67(10

Suppl):110-1113.

Polyzos N, Polyzos I, Zavos A, Valachis A, Mauri D, Papanikolaou E, Tzioras S, Wever D, Messinis

I. Obstetric outcomes after treatment of periodontal disease during pregnancy: a systematic

review and meta-analysis. BMJ 2010;341:7017-7030

Xiong X, Beukens P, Fraser W, Beck J, Offenbacher S. Periodontal disease and adverse

pregnancy outcomes: a systematic review. BJOG 2006;113:135-143.

55

EQUINE ODONTOCLASTIC TOOTH RESORPTION AND HYPERCEMENTOSIS

S Lee Advanced Equine Dentistry 394 Tylden Rd Woodend Victoria 3442

info@advancedequinedentistry.com.au

This paper details the identification of equine odontoclastic tooth resorption and

hypercementosis (EOTRH) in Australia. The five cases described below occurred in Victoria,

however discussions with interstate equine dental veterinarians suggest the disease has been

identified in South Australia, New South Wales, Queensland and The Northern Territory. The

disease involves the progressive destruction of alveolar structures, increasing tooth mobility,

resorption of dental material and production of excess cementum (hypercementosis). Reported

to primarily affect older horses from their late teens onwards, development of EOTRH has been

linked to incisor length,1 however as incisor length also tends to be a function of horse age it is

the authors opinion that this is an over simplification. Symptoms associated with EOTRH include

tooth mobility, gingival recession, discharging sinuses associated with tooth roots and gingival

inflammation and radiographic evidence of areas of lysis and hypercementosis. Diagnosis is

made on the basis of clinical signs, patient history and radiographic evidence.

EOTRH has been previously described in North America and Europe1, this paper describes the

first discussed cases of EOTRH in Australia. All five horses were seen in Victoria, Australia and

involved the incisor teeth of horses aged between 17–23 years-old.

References

Bienert A, Kreutzer R, Simhofer H, Staszyk C, Wohlsien P (2008) Equine odontoclastic tooth

resorption and hypercementosis The Veterinary Journal 178 :372

56

STANDING CANINE EXTRACTION IN THE EQUINE PATIENT

S Lee Advanced Equine Dentistry 394 Tylden Rd Woodend VIC 3442 Australia

info@advancedequinedentistry.com.au

Equine canine teeth are large brachydont teeth, found predominantly in males. Due to injury,

periodontal or endodontic considerations, extraction may be required. This paper describes a

surgical technique for removal in the standing equine patient. Indications, equipment,

techniques, outcomes and potential complications are discussed.

57

PREVALENCE AND RISKS OF CAUSING PULP EXPOSURES IN HORSES IN AUSTRALIA.

Dr Oliver Liyou BVSc (Hons) MACVSc (Eq Dent) Equine Veterinary and Dental Services, PO Box 95, South Grafton, NSW, 2460.

Abstract

REASONS FOR PAPER

Pulp exposure in horses is a relatively common occurrence, and frequently referred to by

persons practicing equine dentistry at whatever level they operate. However, a thorough

appreciation of its relevance, prevalence and risk factors is not as well understood by many of

these practitioners. This paper aims to define and discuss some of these topics.

BACKGROUND

Any of the 4 types of equine teeth (incisors, canines, premolars and molars) can be subjected to

the effects of a pulp exposure. The definition of a pulp exposure, along with the relevance to

both the long and short term effects on the health of the tooth and horse need to be

appreciated. The causes of the pulp exposures are many, but iatrogenic causes are the ones of

special significance to equine dental practitioners, as highlighted by Bettiol and Dixon, EVJ Mar

2011. The other important factors to consider are the limitations to accurately diagnosing a

pulp exposure, and subsequently investigating and managing them appropriately.

Horses, having hypsodont teeth containing highly active odontoblasts laying down secondary

and tertiary dentine, may be able to deal with acute pulp exposure better than humans, dogs

and cats with brachydont teeth. However studies to prove or disprove this theory are difficult

to set up with the strict animal ethics requirements for studies on live animals in Australia.

METHODS

A survey of 3000 dental charts from 2 equine dental veterinarians who both routinely use the

examination aids of:

a) Sedation and dental halter,

b) Mouth thoroughly rinsed out with hose spray,

c) Thorough inspection of occlusal surfaces of incisors,

d) Thorough examination of canines following scaling of calculus,

58

e) Full mouth speculum, bright light, mirror and probe for examination of cheek teeth

(premolars and molars).

RESULTS and CONCLUSION

The results of this survey showed the prevalence of pulp exposures is highest in incisor teeth

when compared to premolars, molars and canines. However, due to the increased difficulties of

thoroughly examining the occlusal surfaces of cheek teeth, the incidence of pulp exposures in

cheek teeth could be higher than this survey indicates, given that rigid endoscopy and

individual probing of the occlusal surfaces of ALL pulp horns in every cheek tooth were not

routinely performed, due largely to economic and subsequent time constraints of these

practitioners and their clients.

59

ENDODONTICS IN THE HORSE

Assoc Prof Gary Wilson Advanced Animal Dentistry Pty Ltd, PO Box 2095, Wellington Point, Qld 4160

Endodontics is the branch of dentistry dealing with diseases of the dental pulp.

The majority of veterinarians in practice have no desire to perform endodontic treatments.

However these treatments are available and can offer a viable alternative to extraction for

endodontically affected teeth.

In the horse, most endodontics will be performed on the canine, incisor and lower cheek teeth.

Endodontic anatomy

Endodontic anatomy is the anatomy of the pulp, the root canals and pulp chambers and the

dentine of the tooth i.e. the anatomy of the pulp cavity structures and its contents.

The dental pulp of equine teeth has not been studied in detail but is assumed to be similar to

that of brachydont teeth such as dogs. It is composed of connective tissue, fibroblasts, collagen

fibres, blood vessels, lymphatics and nerves. The periphery of the dental pulp (adjacent to the

dentin) is a layer of cells called odontoblasts.

The dentine of the tooth is a solid structure that contains large numbers of microscopic tubules

running approximately perpendicular to the long axis of the tooth. These tubules are filled with

fluid and contain processes from the odontoblasts (odontoblastic processes) which are sensory.

The odontoblasts are responsible for producing dentine and do so more rapidly when

stimulated.

A thin layer of predentine is found between the odontoblasts and the dentine.

In the young horse the pulp chambers are large and the dentine of the wall is thin. Dentine is

laid down rapidly initially then slows down but continues throughout life. With occlusal wear,

stimulation of the odontoblasts (which appear to be more reactive than in brachydont teeth)

causes production of dentine as the pulp retreats away from the attrition. This prevents pulp

exposure and subsequent abscessation.

The cheek teeth of the horse contain at least 5 pulp horns independent of the number of roots

present. The 06s and 11s usually have 6 pulp horns.

Root canal therapy (pulpectomy)

60

The basic indication for root canal therapy is a tooth with non-vital (i.e. not living) pulp. A

common cause of this is tooth fracture with pulp exposure leading to pulp infection. 100% of

teeth with pulp exposure will eventually become abscessed and should always be treated by

root canal therapy or extraction.

The aim of the treatment is to prepare the canal by filing (with K-files or Hedstrom files) until

clean dentinal shavings are found on the files, sterilizing the canal and obturation (filling of the

canal). In other words, all of the organic material is removed and replaced by an inorganic

material that won’t support bacterial growth. This is difficult, if not impossible, in equine cheek

teeth.

Root canal therapy of equine incisors is similar to that in the brachydonts. A crown down

technique is usually performed. The canal is shaped and cleaned with Hedstrom files and

obturated with zinc oxide/eugenol and gutta percha. Access is restored with a composite

restoration. It is important that the canal is sealed effectively at the apex (root end). In the

equine it must be remembered that the restoration will be lost and bacteria can gain access to

the obturated canal. Hence an effective apically seal is imperative to long-term success.

Pulp stones and calcifications are relatively common findings with the equine incisor and may

necessitate performance of an apicoectomy to complete the root canal.

Root canals in the cheek teeth are very technically difficult and can only be performed by

apicoectomy. Access to the root apices is difficult especially in the maxillary cheek teeth. The

success of the process is reasonable in mandibular teeth but poor in the maxilla. It is

impossible to completely clean the canals of premolar and molar teeth due to the complexity of

the pulp horns. Long-term studies of the effectiveness of root canal treatments have not been

done in the horse.

The affected tooth should be able to function normally after root canal therapy.

Pulp capping

This procedure can be done by most veterinarians in practice with a little training and the

purchase of a minimal amount of equipment. The technique is used for recent fractures where

the pulp is still vital or where accidental pulp exposure has occurred with crown reductions.

The procedure allows the tooth to stay alive and mature normally. A complete pulp capping

would also include a final composite restoration where possible.

61

Requirements

Drill

Sterile round bur

Small dental spoon curette

Paper points

Calcium hydroxide (in the form of powder or paste)

Hard setting calcium hydroxide cement

Small mixing spatula

Technique

The tooth is taken out of occlusion as well as the opposing tooth. This will help prevent loss of

the cement material whilst healing occurs.

The exposed (and bleeding) pulp is amputated to approximately 10mm using a round bur. It is

essential to cut the pulp cleanly or bleeding will be difficult to control.

62

The blunt end of a paper point is inserted to apply pressure to the bleeding pulp and left for

several minutes. The paper point is removed and, if bleeding is still evident, replaced. Dry

paper points may remove the clot when they are removed (if this occurs, moisten with saline).

63

Ready for pulp capping

Once bleeding has stopped, a layer of calcium hydroxide (Calcipulp) is placed using a paper

point to pack it. The walls of the cavity are cleaned using the spoon curette.

64

Layer of CaOH in place

A layer of hard setting calcium hydroxide cement (mixed and applied as per manufacturers’

directions) follows this.

Once dried, the surface of the tooth is scraped clean with the spatula. The calcium hydroxide

cement layer is then “dished out” with the spatula to ensure that it is slightly below the occlusal

surface of the tooth.

65

CaOH cement finished

appearance

The reason calcium hydroxide is used is that it is bacteriostatic and will also irritate the

odontoblasts. These will then produce a layer of reparative dentine under the restoration in

the form of a "dentinal bridge" which further protects the pulp from exposure should the filling

be lost.

A radiograph is taken in approximately 3 months to assess the formation or otherwise of the

dentinal bridge. If the bridge has not formed, the tooth has most likely died and a root canal

procedure or extraction is required.

66

Layer of sterile necrosis

Dentinal bridge

67

NERVE BLOCKS

Dr. Simon Hurn All Animal Eye Services, 5 Andrew Street, Mt. Waverley, Victoria, 3149

Phone: (03) 9808 2822 Fax: (03) 9808 2844

clinic@allanimaleyes.com

a. Supraorbital block

The supraorbital (frontal) block is performed by first locating the supraorbital foramen above

the eye in the supraorbital process of the frontal bone where it widens

Once the foramen is located, clip a small area with a pair of blunt curved scissors. This serves as a marker

Surgically prep the area

Using a 13mm 25G needle, inject 2-3 ml of local anaesthetic (prilocaine or lignocaine) subcutaneously over the foramen

Using a 25mm 22G needle inserted deep into the canal, I then inject 2 ml of local anaesthetic and inject a further 2 ml as I withdraw the needle.

This should block motor (palpebral branches) and sensory nerves to the upper eyelid making examination much easier in the painful eye.

b. Auriculopalpebral block

The auriculopalpebral block is performed by first locating the caudal border of the ramus of the mandible and the zygomatic arch.

A depression in the zygomatic bone is palpated just caudal. The nerve cannot be palpated at this point

Using a 13mm 25G needle inject a 2ml bleb of local anaesthetic subcutaneously followed by 5-6 ml of local anaesthetic into the depression just caudal to the highest point of the zygomatic arch using a 25mm 22G needle. This technique may not block all sensory nerves to the upper eyelid.

Placement of Subpalpebral Lavage Tubes

With frequent treatment of painful equine eyes, a SPL allows for safe, convenient and frequent

eye treatment. Traditionally SPL systems were placed in the upper lateral eyelid or nasolacrimal

duct (for retrograde instillation of medications). More recently a SPL system has been designed

for placement in the medial lower eyelid (Mila Eye Lavage kits, Mila International Inc. Medical

68

Instruments for Animals, via Vetquip in Sydney) 1. In my experience, medial placement of SPL

systems helps prevents migration of tubing and subsequent corneal ulceration.

Sedation is essential before commencing. A line block is then placed in the medial lower eyelid.

Topical anaesthesia is then placed in the lower conjunctival fornix – 1 drop or 0.1mls every 30

seconds for 2-3 minutes. The trocar with the tubing attached is used to penetrate the medial

lower eyelid from the conjunctival surface– be careful not to damage the lower eyelid punctum.

It is then threaded through the lower eyelid until the footplate is sitting flat and secure in the

conjunctival fornix. The trocar is removed and an injection port is fixed at the distal end. Tubing

can then be sutured into place on the face after tape is fixed along its length. The distant length

of tubing can be platted into the mane and drugs administered safely from the shoulder.

Ointments and viscous suspensions cannot be administered through the tubing.

References:

1. Giuliano et al. Inferomedial placement of a single entry subpalpebral lavage tube for the

treatment of equine eye disease. Veterinary Ophthalmology 2000;3:153-156

69

EEQQUUIINNEE NNEEOONNAATTAALL OOPPHHTTHHAALLMMOOLLOOGGYY

Andrew Turner All Animal Eye Services, 5 Andrew Street, Mt. Waverley 3149

NNEEOONNAATTAALL PPEERRIIOODD

Humans - first 4 weeks Foals - longer as often not presented or recognized early in life Often noted at yearling inspection

EEXXAAMMIINNAATTIIOONN OOFF TTHHEE FFOOAALL’’SS EEYYEE

Pupil not normal shape for some days PLR - not brisk especially if foal is excited Menace response - absent until 4th to 8th day and very poor up to 2 weeks of age Reduced corneal sensitivity especially if sick/dehydrated Dark stable or black curtain material essential Sedation (Xylazine 0.5 – 1.0 mg/kg IV) Local nerve blocks may be necessary if eye is very painful – supraorbital and auriculopalpebral

EESSSSEENNTTIIAALL EEQQUUIIPPMMEENNTT NNEECCEESSSSAARRYY FFOORR AA TTHHOORROOUUGGHH EEXXAAMMIINNAATTIIOONN OOFF TTHHEE CCOORRNNEEAA

Finoff transilluminator Magnification – binocular loupe, Voroscope, Optivisor, Welch Allyn head set, Slit lamp biomicroscope Ophthalmoscope - direct, Panoptic Topical anaesthetic (Alcaine) Microscope slides Sterile spatula - bottom end of a scalpel blade Cytology stains – Diff-Quick, Gram, Methylene Blue Stain – fluorescein Saline for flushing

CCOORRNNEEAA

Corneal sensitivity is significantly less in sick foals Foals have significantly lower tear production than adults High incidence of corneal ulceration in sick foals

OOCCUULLAARR AABBNNOORRMMAALLIITTIIEESS IINN FFOOAALLSS

Congenital Inherited Acquired

70

CCOONNGGEENNIITTAALL AABBNNOORRMMAALLIITTIIEESS

Dermoid Rocky Mountain Horse Disease Microphthalmia Anterior uveal dysgenesis Cataract

DDEERRMMOOIIDD

Usually temporal conjunctiva, occasionally involves cornea and eyelids

RROOCCKKYY MMOOUUNNTTAAIINN HHOORRSSEE DDIISSEEAASSEE

Multiple Ocular Anomalies Megalocornea Iris hypoplasia Cataract Lens luxation

EENNTTRROOPPIIOONN

Primary - inherited Secondary - seen in foals born to poorly doing mare or foal not doing well - scouring, dehydrated, enophthalmic Lower eyelid rolled in, epiphora, corneal ulceration, spasm of orbicularis oculi muscle Treatment - digital trauma to lids or tacking sutures, occasionally Hotz-Celsus procedure

AATTRREESSIIAA OOFF TTHHEE NNAASSOOLLAACCRRIIMMAALL PPUUNNCCTTUUMM

Distal punctum Unilateral or bilateral Epiphora, mucopurulent discharge Not always obvious in newborn

CONJUNCTIVA

Conjunctival haemorrhages common Dorsally and dorsonasally Blunt trauma or thoracic compression Usually resolved by 10 days of age

MMIICCRROOPPHHTTHHAALLMMIIAA

Differentiate from phthisis bulbi secondary to uveitis Small, usually blind eye, microcornea Small palpebral fissure, prominent third eyelid

71

Often corneal ulceration secondary to entropion May need to correct entropion or enucleate

DDEEFFEECCTTSS OOFF TTHHEE AANNTTEERRIIOORR UUVVEEAA

Absence of iris (aniridia) rare Iridal hypoplasia presenting with undeveloped iris bud, limbal dermoids and cataract Persistent pupillary membranes - remnants of foetal blood supply to the lens. Strands across pupil from iris collarette to iris collarette Heterochromia iridis - variation in normal dark brown iris colour. Common in Appaloosa, palamino, paint, grey, chestnut, spotted and white horses.

CCAATTAARRAACCTT

Common in foals Inherited, post-inflammatory, toxic, traumatic, and possibly nutritional 33-35% of congenital ocular defects Causes include heritable, post-inflammatory, toxic, traumatic and nutritional May be present with other anomalies including aniridia, and persistent pupillary membranes Surgery possible but beware if uveitis present

RREETTIINNAA AANNDD OOPPTTIICC NNEERRVVEE

Variations in appearance in normal retina - depending on age and colour Retinal haemorrhages - 16% of normal foals examined within 96 hrs of birth. Possibly birth trauma especially if prolonged stage 2 of parturition Coloboma – optic nerve or retina Retinal detachment

NNEEOONNAATTAALL GGLLAAUUCCOOMMAA

In adults, usually secondary to uveitis Reported in foals - Haab’s stria, buphthalmos, corneal oedema Haab’s stria - break in Descemet’s membrane Severe corneal oedema

AACCQQUUIIRREEDD

Corneal ulceration Corneal laceration Corneal stromal abscess Traumatic retinal detachment Uveitis secondary to neonatal septicaemia

UUVVEEIITTIISS

Usually associated with neonatal septicaemia

72

History of colostrum deficiency Full blood examination

RREEFFEERREENNCCEESS

Turner AG. Ocular conditions of neonatal foals. Vet Clin North Am: Equine Pract 20:429-440, 2004 Gilger BC. Equine Ophthalmology. 2nd edition. Maryland Heights: Elsevier Saunders; 2011

73

OCULAR MANIFESTATIONS OF SYSTEMIC DISEASE IN HORSES

Dr Kelly Caruso It has been said that the eye is the window to the soul. As veterinary ophthalmologists we believe never a truer word has been said. The eye has a tremendous blood supply, courtesy of the uveal tract, and per gram of tissue has 2-3 times the blood flow of the kidneys. This means that many systemic diseases have a propensity to manifest with ocular abnormalities. The eye also gives the only visible access to a cranial nerve. In light of these facts, it makes sense to include a thorough ocular examination as part of a workup for any systemic disease. In this lecture Kelly will discuss some of the ocular manifestations of systemic disease equine practitioners may face in clinical practice. Some of the diseases discussed may be rare in Australia, but with the increase in international horse transportation from outside of Australia, it would be prudent to briefly cover some of these exotic diseases. The recent outbreak of Equine Influenza is a case in point. In this lecture Kelly will cover viral diseases such as equine viral arteritis, equine infectious anaemia, equine herpes virus and West Nile Virus. Bacterial diseases such as strangles, brucellosis, leptospirosis and systemic fungal diseases such as Aspergillosis will be covered as well. Finally a number of neurologic conditions, such as tetanus, botulism and Horner's syndrome amongst others will be covered. Participants are sure to learn an awful lot from Kelly in this informative lecture, and come away with a new respect for the value of an ophthalmologic examination.

74

MEDICAL MANAGEMENT OF EQUINE BACTERIAL AND FUNGAL KERATITIS

Dr Anu O’Reilly BVSc; MVS; MACVSc (Small Animal Medicine); FACVSc (Veterinary Ophthalmology) Registered Veterinary Specialist, Animal Eye Care 181 Darling Rd, Malvern East, Victoria, 3145 Phone: (03) 9563 6488

The purpose of this presentation is to discuss the medical treatment options for bacterial and

fungal keratitis.

Ulcerative keratitis is a common complaint in equine ophthalmology. The horse’s prominent

cornea lends itself to traumatic injuries and bacterial or fungal infections can quickly follow.

Early diagnosis and appropriate treatment are vital to secure a successful outcome.1

The clinical symptoms of bacterial keratitis can include blepharospasm, photophobia, epiphora,

ocular discharge corneal oedema, vascularization, keratomalacia and anterior uveitis.1 Fungal

infections can have a more varied appearance. There are five typical patterns recognized.2

Bacterial like ulcers, superficial fungal ulcers, keratomycosis with surrounding furrows,

keratomycosis with cake-frosting and keratomycosis stromal absess.2

The clinical approach for the majority of corneal ulcers should be systematic.2 Ideally samples

for culture and sensitivity are collected first followed by corneal scrapings for cytology. It is

important to scarp with careful vigor to get diagnostics samples. In some cases repeat

scrapings are required. Mixed infections are not uncommon and some fungal organisms have a

predilection for the deeper corneal layers.4 Deep fungal infections often require a biopsy in

order to make a diagnosis. After the diagnostic tests are completed fluorescein dye can then be

applied to determine the depth of the lesion.

Medical therapy is aimed at destroying the infectious agent, controlling the proteolytic activity

in the tear film and controlling the secondary uveitis.

Bacterial keratitis

The choice of antibiotics is based upon the results of the culture and sensitivity. Pending these

results a broad spectrum bactericidal agent with adequate corneal penetration should be

selected.5 Where Pseudomonas is suspected gentamicin, tobramycin and amikacin are good

choices and for -haemolytic Streptococcus cephazolin and fusidic acid are appropriate.5

Clinicians should be made aware of the increasing problem of resistance of pathogens to

fluoroquinolone antibiotics. These antibiotics should NOT be used for minor infections or for

routine prophylaxis.5

75

Mycotic keratitis

Mycotic keratitis is a serious disease that is challenging to diagnose and treat. Early aggressive

intervention with systemic and or topical medications is required.1 The choice of anti-mycotic

agent can be influenced by geographical location, tissue penetration, cost and mode of drug

delivery. Voriconazole is the author’s current preference for a topical anti-fungal agent and

fluconazole is the preferred choice of treatment for the oral anti-fungal.

Antiprotease therapy

Stopping the inflammatory cascade that follows ulcerative disease is vital for successful

treatment. Destructive mediators like MMP-2, MMP-9 and serine proteinases can cause more

damage to the cornea than the pathogen itself.3 Autologous serum, N-acetylcysteine, disodium

EDTA, tetracycline are some anti-proteolytic drugs.

Pain relief

Controlling the secondary uveitis and managing patient pain is accomplished by using a topical

cycloplegic eg. atropine and a systemic non-steroidal anti-inflammatory drug.1 Failure to

control the secondary uveitis may result in iris adhesion to the lens or cornea, cataract,

glaucoma and phthsis bulbi.1

In summary ulcerative keratitis in the horse is a diagnostic and therapeutic challenge. A

systematic and thorough approach is necessary to yield a positive outcome.

References

1. Andrew S.E. and Willis A.M: Diseases of the cornea and sclera. In Gilger BC: Equine Ophthalmology, Philadelphia, 2005, Elsevier Saunders, pp173-182

2. Gaarder JE, Rebhun WC, et al: Clinical appearances, healing patterns, risk factors, and outcomes of horses with fungal keratitis: 53 cases (1978-1996) Journal of American Veterinary Medical Association: 1998: 213:1:105-112

3. Brooks DE. Inflammatory stromal keratopathies: medical management of stromal keratomalacia, stromal abscess, eosinophilic keratitis, and band keratopathy in the horse. Veterinary Clinics Equine 2004:20:345-360

4. Grahn B, Wolfer J, Keller C, Wilcock B: Equine Keratomycosis: Clinical and Laboratory findings in 23 cases. Progress in Veterinary and Comparative Ophthalmology Vol 3:No1 pp 3-7

5. Matthews AG. Tutorial Article: Equine Veterinary Education: 2009:21:5 271-280

76

SSUURRGGIICCAALL MMAANNAAGGEEMMEENNTT OOFF EEQQUUIINNEE BBAACCTTEERRIIAALL AANNDD FFUUNNGGAALL KKEERRAATTIITTIISS

Andrew Turner All Animal Eye Services, 5 Andrew Street, Mt. Waverley 3149

SSuurrggiiccaall iinnssttrruummeennttss

Need some form of magnification - essential Fine instruments for gentle control of fragile ocular tissues Usually expensive, so look after them – use appropriate tray Dramatically improve surgical outcome Reduce anaesthesia time

OOpphhtthhaallmmiicc SSuuttuurree MMaatteerriiaall

3/0-4/0 monofilament absorbable or non-absorbable with CUTTING needle for skin & eyelids 4/0-6/0 multifilament absorbable with TAPER POINT needle for conjunctiva 7/0-8/0 multifilament absorbable with SPATULA needle for cornea

PPaattiieenntt PPrreeppaarraattiioonn

Minimal clipping Avoid trauma Lubricate cornea 1:50 Iovone in saline Ophthalmic drapes Can make your own drape – use sterile latex glove

CCoolllleecctt ccoorrnneeaall ssaammpplleess –– ccyyttoollooggyy vveerryy iimmppoorrttaanntt

Fungal isolates from Equine keratitis At least 40 different fungal isolates in normal eyes Most common pathogen is Aspergillus We have also cultured Pseudoallescheria, Cladosporium, Scedosporium, Fusarium

BBaacctteerriiaall iissoollaatteess ffrroomm eeqquuiinnee uullcceerraattiivvee kkeerraattiittiiss

Pseudomonas aeruginosa Streptococci equi subspecies zooepidemicus Staphylococcus aureus

77

SSttrroommaall aabbsscceessss

Off-white stromal opacity Often very painful Zone of opacity around abscess (white cells)

SSuurrggeerryy

Keratectomy Conjunctival flap/graft Deep lamellar keratoplasty

CCoonnjjuunnccttiivvaall GGrraaffttss//FFllaappss

Used to increase mechanical/vascular support of cornea, prevent infection and promote rapid healing Necessary if corneal defect greater than 1/4-1/3 of cornea depth (some exceptions)

Hood, pedicle, island, “360” Flaps must be thin and contain little Tenon’s capsule

78

79

80

81

82

83

84

DDIIAAGGNNOOSSIISS AANNDD MMAANNAAGGEEMMEENNTT OOFF EEQQUUIINNEE RREECCUURRRREENNTT UUVVEEIITTIISS

Andrew Turner All Animal Eye Services, 5 Andrew Street, Mt. Waverley 3149 WHAT IS THE UVEA? Iris Ciliary body Choroid

UUVVEEIITTIISS

Breakdown of the blood-eye barrier followed by a series of immune-mediated events

IINNIITTIIAATTOORRSS OOFF UUVVEEIITTIISS

Mechanical Chemical Viral Parasitic Bacterial Idiopathic

MMEEDDIIAATTOORRSS OOFF UUVVEEIITTIISS

Neuropeptides Lipid and arachidonic acid metabolites Cytokines including interleukins and interferon Oxygen metabolites Free radicals Others including nitric oxide

EEQQUUIINNEE UUVVEEIITTIISS

Primary - equine recurrent uveitis (ERU) Secondary - to other ocular disease

UUVVEEIITTIISS -- AACCUUTTEE SSIIGGNNSS

Blepharospasm Corneal vascularisation Photophobia Miosis Aqueous flare and/or hypopyon

85

UUVVEEIITTIISS -- CCHHRROONNIICC SSIIGGNNSS

Phthisis bulbi Subtle perilimbal corneal vascularisation Cataract formation Posterior synechia Retinal detachment Hyperpigmented iris Vitreous opacity Lens luxation Glaucoma

EEQQUUIINNEE RREECCUURRRREENNTT UUVVEEIITTIISS

Approximately 15% of horses affected Episodic intraocular inflammation Tends to increase in severity Often leads to blindness Breed predilection Appaloosa - 8 x greater than all other breeds combined Appaloosa ERU - possibly a distinct entity Related to equine MHC, autoaggressive T cell reaction against retinal proteins

EEQQUUIINNEE RREECCUURRRREENNTT UUVVEEIITTIISS iinn tthhee AAPPPPAALLOOOOSSAA

Often insidious onset and course with NO obvious signs 80% bilateral Secondary complications common

EERRUU iinn tthhee AAPPPPAALLOOOOSSAA

SSEECCOONNDDAARRYY CCOOMMPPLLIICCAATTIIOONNSS

Corneal ulcers - 40% Glaucoma - 20% Iris atrophy - greater than 50% Posterior synechia - 50% Cataract - 75% Lens luxation - about 30% Posterior segment changes - vitritis, chorioretinitis and retinal detachment Phthisis bulbi - 25%

86

EEQQUUIINNEE RREECCUURRRREENNTT UUVVEEIITTIISS

CCAAUUSSEESS

Immune-mediated Leptospira interrogans

EEQQUUIINNEE RREECCUURRRREENNTT UUVVEEIITTIISS

Retinal autoantigens (S-antigen and interphotoreceptor retinal binding protein) - molecular mimicry Bystander activation Epitope spreading Autoaggressive T cell reaction against retinal proteins Leads to subsequent destruction of intraocular structures Uncovers other epitopes (part of antigen recognized by immune system)

TTRREEAATTMMEENNTT

Timely anti-inflammatory therapy Inadequate treatment leads to loss of vision Anti-inflammatory therapy Mydriatics - atropine to effect

AANNTTII--IINNFFLLAAMMMMAATTOORRYY aanndd IIMMMMUUNNOOSSUUPPPPRREESSSSIIVVEE TTRREEAATTMMEENNTT

Topical - corticosteroids, NSAIDs Oral - corticosteroids, phenylbutazone Local - intravitreal depot corticosteroids, cyclosporine implants

SSUURRGGIICCAALL TTRREEAATTMMEENNTT

Pars plana vitrectomy Intrascleral/suprachoroidal cyclosporin implant

87

NSAIDS, CORTICOSTEROIDS & GASTRIC PROTECTANTS IN THE HORSE

Dick Wright FACVSc (Equine Medicine) PAIN •Physiological parameters (heart rate) used alone DO NOT adequately detect and quantify pain •Multifactorial pain behaviour rating scales used in conjunction with physiological parameters are best •Primary inflammatory pain arising from peripheral tissues can be amplified by central secondary hyperalgesia and by neuropathic pain PAIN MANAGEMENT •Select drugs that better control the type of pain elicited by the insult –DON’T JUST REACH FOR THE BUTE! •Select techniques of analgesic drug administration that act on pathways or anatomical locations where the nociceptive information is being processed or from site of origin •Combine analgesic drugs that act on different pathways –MULTIMODAL ANALGESIA •Provide best possible comfort for the horse HOMEOSTATIC RESPONSE TO PAIN •Horses are characterised by their instinctive flight response to stressful situations –PRE-EMPTIVE ANALGESIA may dramatically improve outcomes •Pre-emptive analgesia invariably requires lower dose and more profound positive response ANALGESIA •Combination of drugs may give best outcome: enhancing analgesia and minimising side-effects •NSAID + opioid + a-2agonist + regional anaesthesia •Continuous peripheral neural blockade for acute distal limb lameness –placed between suspensory ligament and accessory ligament of the DDFT; 10 ml of 0.5% bupivacaine over 3 days via battery-powered pump (or manual bolus 0.85 ml TID) [Watts et al (2011) JAVMA 238(8)1032-39] CHRONIC PAIN •ANALGESIA is not sufficient by itself –is necessary to provide analgesia but also need to address the pathophysiological events that have resulted in neuropathic pain (central sensitisation secondary to nociception) •Persistence of central involvement means pain control is difficult, often incomplete, requiring higher and repetitive doses of analgesics CENTRAL SECONDARY HYPERALGESIA AND NEUROPATHIC PAIN •Both characterised by increased pre-and post-synaptic neuronal sensitivity and activity at the level of the spinal cord •BUTORPHANOL and other opioids (morphine; methadone) provide central analgesia by inhibiting nociceptive transmission

88

•KETAMINE at a low dose IM (0.5 mg/kg QID) is an NMDA receptor antagonist and reduces nociceptive amplification and hypersensitivity at the spinal level •Pentoxifylline (8.8 mg/kg PO TID) •Gabapentin (2.0 mg/kg PO BID) •Aspirin (4 mg/kg PO SID) •Omega-3 fatty acids (30 ml PO SID) •Dutton et al (2009) Equine Vet Educ21, 37-43 •Jones et al (2007) Pain 132, 321-331 (Mayhew) OF INTEREST •No current evidence that intra-articular local anaesthetics (bupivacaine) damage cartilage •Inflammation up-regulates joint opioid receptors (morphine 0.1 mg/kg diluted in saline at 1 ml/10 kg –6 h analgesia) •Transdermal analgesia -FENTANYL patches: 2 x 10 mg; shaved antebrachium; bandaged; rapid absorption < 1 h; 96% bioavailability; continuous administration 8-9 days with patch replacement 48-72 h COMPLICATIONS OF SYSTEMIC CORTICOSTEROID ADMINISTRATION •Transient neutrophilia and lymphopaenia •Muscle wastage •Adrenocortical suppression and dysfunction •Hepatopathy (hyper-adrenocorticoidism): 412 mg IM over 4 weeks •Laminitis •Altered bone metabolism •Increased susceptibility to infection •Decreased response to vaccination INTRA-ARTICULAR (IA) CORTICOSTEROIDS •POSITIVE EFFECTS: •Reduce capillary dilation, margination, migration and accumulation of inflammatory cells •Inhibit interleukin-1 and TNFa •Inhibit prostaglandin release (pain relief) •Inhibit phospholipaseA2 and COX-2 expression •Betamethasone esters •Methylprednisolone acetate (MPA) •Triamcinalone acetonide (TA) •Repetitive administration of IA MPA alters mechanical integrity of articular cartilage •Greater efficacy if combined with hyaluronate (HA) + post-injection rest •No definitive evidence linking IA CS administration with catastrophic injury (no harmful effect on subchondral bone) •Considerable variability in published pharmokinetic data •PHARMOKINETICS = pharmacological presence •PHARMOCODYNAMICS = clinical effectiveness

89

•Chen et al(1992): TA; 6 mg; rapid absorption from joint with peak serum levels within 4 h; undetectable in joint fluid by Day 15 and in serum by 48 h •200 mg IA MPA caused plasma cortisol suppression for 240 h post-injection McIlWRAITH (2010) and IA CORTICOSTEROIDS •9 issues: 1 Potent anti-inflammatory agents -product variability –benefits v deleterious effects (DE): betamethasone esters (BE) have no DE; TA is chondroprotective; MPA has DE 2 Generalisation about harmful effects inappropriate 3 Prolonged clinical effectiveness: 50-70 days 4 Up-regulation at the cellular level responsible for prolonged effect 5 Period of rest post-injection facilitates improved absorption and efficacy but exercise does not promote negative effects (except for MPA) 6 No evidence that IA CS cause catastrophic fractures or harm subchondral bone 7 Good evidence linking laminitis to CS injection is lacking and generalisation of risk is inappropriate 8 Required minimal dose is well-defined for TA and BE and MPA should not be used 9 HA has chondroprotective effects and is beneficial when used with TA and betamethasone esters but will not ameliorate DE of MPA AEROSOLISED CORTICOSTEROIDS •Commonly used for treatment of COPD and other inflammatory airway diseases •Maximise treatment and minimise adverse effects? •High doses of beclomethasone impaired ACTH-stimulated cortisol release (returned to normal 2-4 days after cessation of treatment) •Long-term fluticasone treatment did not alter HPA axis or immune function TOPICAL CORTICOSTEROIDS •50 g dexamethasone-containing ointment applied twice daily to 30 x 50 cm area of skin for 10 days •Significant suppression of resting plasma cortisol levels (>75-98%) within 2 days and continued decrease until Day 10 •Markedly reduced rise in plasma *cortisol+ in response to ACTH stimulation test •Decreased plasma ACTH levels •Increase in neutrophils, decrease in lymphocytes and eosinophils •SIGNIFICANT SUPPRESSION OF HYPOTHALAMUS-PITUITARY-ADRENAL AXIS •Hydrocortisone –also penetrates skin CORTICOSTEROIDS and BONE •Glucocorticoids (GC) commonest cause of drug-induced osteoporosis in people •Prolonged exposure required (>3 months) •Inhibit bone remodelling •Increase fracture risk

90

•Lepageet al (1993): single dose of triamcinolone acetonide at 0.09 mg/kg IM significantly reduced serum osteocalcinin horses (return to pretreatment levels 28-150 days) •Osteocalcinis produced by osteoblasts •2 main effects: 1. Stimulate osteoclast-mediated bone resorption 2. Reduce osteoblast-mediated bone formation GS induce apoptosis in osteoblasts and osteoclasts thereby decreasing bone formation 4. Prolong lifespan of osteoclasts thereby increasing bone resorption ANAPHYLACTIC SHOCK, ALLERGIES, etc •COCHRANE CENTRAL REGISTER OF CONTROLLED TRIALS: no evidence from high-quality studies for the use of steroids in the emergency management of anaphylaxis (neither refute nor support) •ALLERGIES: 1. Is the horse suitable candidate –no laminitis or infection 2. Beware of obese ponies 3. Long term maintenance therapy –alternate-day therapy only when clinical signs eliminated: reduce dose by 20% every 2 weeks to minimal effective alternate-day dosage 4. Side-effects: polyuria/polydypsia SUITABILITY OF CORTICOSTEROIDS FOR LONG-TERM USE

DRUG Equivalent anti-

inflammatory

potency

Duration of action

(hours)

Suitable for long

term alternate day

therapy

Hydrocortisone 1 8-12 No

Prednisolone 4 24-36 Yes

Methylprednisolone 5 24-36 Yes

Triamcinolone 5 36-48 No

Betamethasone 30 36-54 No

Dexamethasone 30 36-54 No

Taken from Paterson (2003) In Practice, 25 (2), 86-91

91

CORTICOSTEROID DOSES FOR ANTI-INFLAMMATORY AND IMMUNOSUPPRESSIVE THERAPY

Dosage Prednisolone Dexamethasone

Induction* Maintenance# Induction* Maintenance#

Anti-inflammatory 0.5-1.5 mg/kg 0.2-0.5 mg/kg 0.02-0.1 mg/kg 0.01-0.02 mg/kg

Immunosuppression 1.5-2.5 mg/kg 0.5-1.0 mg/kg 0.1-0.2 mg/kg 0.01-0.02 mg/kg

*Daily #Maintenance Taken from Paterson (2003) In Practice, 25 (2), 86-91 LAMINITIS and CORTICOSTEROIDS •No definitive evidence linking CS administration to laminitis •Letter in Vet Record -Eustace and Redden (1990) •Dutton (2007) –2 x 80 mg IA and 20 mg IM •Bailey and Elliott (2007) –review of the literature •Bathe (2007) –retrospective study of clinical cases [3/2000 cases; TA; majority 20-45 mg] •McCluskey and Kavenagh (2004) –up to 80 mg TA as a single dose •Keep total dose of TA to < 18 mg? (Genovese 1983) •Corticosteroid-potentiated vascular responses of the equine digit: a possible pharmacologic basis for laminitis (Eyre et al1979) •Ryu et al (2004) –Glucocorticoid-induced laminitis with hepatopathy in a Thoroughbred filly: 10 x 20 mg/day TA CORTICOSTEROIDS •PREDNISONE is rapidly absorbed and metabolised to the active drug PREDNISOLONE in people but this does NOT happen in horses NSAID COX-1 INHIBITION •Gastrointestinal ulceration •Nephrotoxicity COX-2 INHIBITION •Reduction of inflammation and pain FENAMIC ACID DERIVATIVES (FENAMATES) •Mefenamic acid •Meclofenamic acid •Flufenamic acid •Tolfenamic acid SELECTIVE COX-2 INHIBITORS (COXIBS) •Firocoxib (Equiox) •Robenacoxib •Specific COX-2 inhibitors •Chewable tablets (dogs) ACETIC ACID DERIVATIVES •Indomethacin

92

•Diclofenac–interestingly, may have anti-leukotriene activity (5-lipoxygenase inhibition) [VOLTAREN]; high concentration in synovial fluid •Eltenac–used in horses (TELZENAC injectable solution); Australian registration in 2000 ENOLIC ACID (OXICAM) DERIVATIVES •Piroxicam •Meloxicam (METACAM) •Relatively specific COX-2 inhibitors •Long half-live in dogs but shorter in horses •Foals 0.6mg/kg bodyweight (1mL suspension/20kg) or as directed by the consulting veterinarian. Draw an accurate volume of suspension from the tube using the syringe supplied. To administer, place the syringe nozzle into the side of the mouth and deposit the suspension as far back over the tongue as possible PROPRIONIC ACID DERIVATIVES •Ibuprofen •Naproxen •Ketoprofen •Vedaprofen •COX-1 and -2 INHIBITORS •Ketoprofen patches VARIOUS •Flunixin meglumine–highly substituted derivative of nicotinic acid •SALICYLATES –aspirin •SULPHONALIDES -hepatotoxic •Licofelone–5-LOX/COX inhibitor COX-1 versus COX-2 INHIBITORS •Inflammation is a major component of injury and pain •NSAIDS –inhibitory actions on cyclo-oxygenase enzymes (COXs) necessary for prostaglandin production (pro-inflammatory) •COX-1: important in homeostasis (gastric mucosa; renal perfusion; platelet function) •COX-2: important in inflammation BUT also has role in homeostasis (kidney perfusion; gastrointestinal healing) •Based on in vitro studies NSAIDS should be more specific for COX-2 BUT in vivo both can cause adverse side-effects •Plasma concentrations don’t always correlate with analgesic effects •Consider as adequate for mild-moderate pain particularly when used in combination with other analgesic drugs NSAID •PBZ, FLUNIXIN, KETOPROFEN •All COX-1 inhibitors •PBZ is the most toxic •Toxicity –inappetance, depression, colic, gastrointestinal ulceration, weight loss •PBZ –single dose may cause toxicity

93

•8.8 mg/kg, PO, q24 h, 21 days –hypoalbuminaemia, neutropaenia, increased RDC blood flow, changes in VFA production •4.4 mg/kg (2 mg/kg q12 h) versus 8.8 mg/kg (4 mg/kg q 12 h) –PO, 4 days, chronic forelimb lameness: no difference in lameness scores •FLUNIXIN MEGLUMINE •Commonly used for abdominal pain •Foals < 24 h: pharmacokinetic data suggest need to increase dose by 1.5 to achieve comparable adult therapeutic dose rates BUT longer dose intervals are necessary to avoid toxicity •PBZ and flunixin available in oral and IV •Eyes; endotoxaemia •KETOPROFEN •Injectable formulation only •2.2 mg/kg IV SID •Foals < 24 h: longer elimination half-life but volume of distribution larger (higher doses but less frequent) •Good synovial concentrations with IV injection lasting up to 4 h CARPROFEN •0.7 mg/kg IV •Longer elimination half-life and clearance than ketoprofen and vedaprofen •Very good penetration into synovial fluid (peaks at 12 h in normal joints; still detectable at 48h) MELOXICAM •0.6 mg/kg IV •Short half-life and large clearance therefore probably should be dosed more than once daily (horse versus dog) COXIBS 1 •Firocoxib (Equiox) at 0.05 mg/kg daily (SID) did not reduce lameness score more than control group (box rest for 7 days) [both groups improved] BUT 0.1 mg/kg improved lameness compared to controls (0.25 mg/kg was no better than 0.1 mg/kg) •Oral paste •Back et al (2009) Equine Vet J 21(1), 309-312 COXIBS 2 •0.1 mg/kg firocoxib PO SID was compared with 1.0 mg/kg vedaprofen paste PO BID for 14 days •83% horses showed clinical improvement with firocoxib; 65% with vedaprofen •No changes in haematology or biochemistry with any group •1 horse (2%) and 4 horses (8%) respectively showed adverse effects (mucous membrane oedema; hypersalivation; decreased appetite; lip erosion) •Prospective, randomised, controlled, double-blinded, multicentre trial –Koene et al (2010) J Equine Vet Sci30(5), 237-243 COXIBS 3 •Cook et al(2009) Am J Vet Res 70(8), 992-1000 •Compared firocoxib with flunixin meglumine on recovery of ischemic-injured equine jejunum •Both effective for visceral analgesia

94

•Flunixin retarded mucosal recovery NSAID CLEARANCE TIMES •PBZ + flunixin: donkeys >horses •Fast clearance requires more frequent administration •BUT •Carprofen: donkeys<horses DOSES OF NSAIDS IN THE HORSE

Dose (mg/kg)

Route Frequency Notes Reference

Phenylbutazone 2-4 PO, IV q 12 h Reduce to 2 mg/kg Day 2

MacCallister Raekallio et al

Flunixin 1 PO,IV, IM

q 12 or 24 h

Crisman et al

Ketoprofen 2-3 IV q 24 h Coakley et al

Carprofen 0.7 IV q 24 h Armstrong et al

Eltenac 0.5 IV q 24 h Goodrich et al

Vedaprofen 1 IV q 24 h Lees et al

Meloxicam 0.6 IV q 12 h Sinclair et al

PROSTAGLANDINS (PGs) •Anti-secretory and mucosal protective effects •Phospholipids metabolise into PGs and leukotrienes by the COX and lipoxygenase enzymatic pathways •COX-1 is the house-keeping enzyme in gastric mucosa •COX-2 is induced by inflammation •NSAIDs reduce PG production by inhibiting expression of COX-1 and COX-2 in gastric mucosa BUT also increase leukotriene levels (relatively) •H2-antagonists and PPIs increase mucosal levels of PGs (PGE2) but only PPI have any effect on leukotriene (LTB4) levels GASTRIC ULCERATION •Not only secondary to reduced PROSTAGLANDIN secretion (COX-1 and COX-2 inhibition) BUT also influenced by upregulation of leukotrienes such as 5-lipoxygenase (5-LOX) GASTRIC PROTECTANTS •ANTACIDS •SUCRALFATE •H2 RECEPTOR ANTAGONISTS •PROTON PUMP INHIBITORS •MISOPROSTOL –synthetic PG

95

ANTACIDS •Neutralise acid within stomach •Mixture of aluminium hydroxide and magnesium hydroxide •Short-lived effect on equine stomach pH (250 ml raises gastric pH to 4 for 2 hours) •May be useful to alleviate ACUTE clinical signs •TOO MUCH, TOO OFTEN SUCRALFATE •Hydroxyl aluminium salt of sucrose octasulphate •pH <4: sticky viscous gel, 6 hours •Adheres to epithelial cells and base of ulcer craters (affinity for ulcers > epithelium) •Inhibits pepsin secretion •Inhibits bile absorption •Inhibits absorption of fluroquinolones and H2-RECEPTOR ANTAGONISTS (10%) •Thickens mucosal layer •Reduces degradation of mucus •Foals experimentally intoxicated with PBZ still developed ulcers despite 4 g sulcralfate but ulcers scores were less than CONTROLS •22 mg/kg QID –7 month-old foals with sub-clinical ulcers did no better than foals given CORN OIL* only •Horses in active training on sulcralfate less likely to have moderate-severe ulcers than those on H2-receptor antagonists BUT not significant when compared to NO TREATMENT (duration and dose not given?) H2-RECEPTOR ANTAGONISTS •Decrease basal acid (HCl) secretion by blocking interaction of histamine with H2receptors on gastric parietal cell •No toxicity noted in horses (unlike humans) •Poor oral availability •Significant inter-horse variation in response at lower doses (use at higher end of dose range) •DO NOT USE concurrently with NSAID or corticosteroids and expect ULCER PREVENTION •Cimetidine<ranitidine and nizatidine(4x)<famotidine(2-3x) •Ranitidine 6.6 mg/kg PO TID –healed ulcers in adult horses and prevented ulcers forming in a feed-deprived horse model •Cimetidine PROBABLY doesn’t work in horses (oral availability 14%; half-life 1-2.2 h); 20 mg/kg PO TID did not improve ulcer score after 30 days of treatment •Famotidine–half-life 2 h •13% bioavailability after oral administration •0.3 mg/kg IV BID or 2.8 mg/kg PO BID •Mild colic in one horse when given at three times recommended dose IV PROTON PUMP INHIBITORS (PPIs) •Substituted benzimidazoles •Rapidly move from blood to acid secretory canaliculi of parietal cells

96

•Block acid secretion •Irreversible inhibition of hydrogen-potassium adenosine triphosphate •Anti-secretory effects are prolonged (once daily dosing) •Omeprazole, lansoprazole •Metabolised in liver, excreted in urine and bile •Parenteral IV versus oral paste (enteric versus non-enteric-coated) •Safe in all age-groups •Gastric pH did not rise after single oral dose but 5 doses reduced gastric acid secretion by 70% (@ 1.4 mg/kg/day) •Single dose of omeprazole @ 0.5 mg/kg IV significantly increased gastric pH within 2 hours in adult horses (basal levels @ 8 hours) •After 5 daily 0.5 mg/kg IV doses, basal levels depressed for at least 27 hours (another study 5 days PO @ 1.5 mg/kg/day –basal levels returned after 19 days) •BID no better than SID •Response to oral dosing slower (maximum response 3-5 days) than with IV (hours) •FOALS: •Higher bioavailability cf adults •Has been administered safely @ 4 mg/kg orally •Efficiency varies between products: commercial paste versus compounded formulations (pH?) •SUSPENSIONS LESS or NOT EFFECTIVE (related to concentration, degree of protection from gastric acid, ease of absorption?) •Has been used safely @ 5 mg/kg/day in adults •Multi-centre study; adults •Omeprazole @ 4 mg/kg/day orally •28 days: complete healing 77%; improved ulcer scores 92% •90% (18/20) of horses’ taken-off drug at 28 days re-developed ulcers by Day 58 •Maintenance omeprazole @ 2 or 4 mg/kg/day –only 16% re-developed ulcers •LOWER DOSE preventative effect after initial high treatment dose? •SOME HORSES WILL NOT HEAL, SMALLER NUMBER MAY NOT SHOW IMPROVED SCORES

97

EQUINE EYES OR STORIES OF MISCHIEF (EYELID AND CORNEAL PROBLEMS)

Harriet Davidson MS, DVM, DACVO

GD Veterinary Ophthalmology

Acute eyelid problems

Acute lesions are most often secondary to trauma. Traumatic eyelid lesions may be a result of

external injury or internal lesions rupturing outwards. Common rule outs for externally induced

damage include lacerations, puncture wounds, or foreign objects lodged within the eyelid.

Internal lesions include extension of neoplasia from an orbital mass or metastatic lesion.

Abscess from previous trauma or neoplasia.

Achieving a diagnosis may be combined with treatment in order to maximize the efficiency of

animal handling. Cleaning the wound, sample collection for culture, cytology and/or

histopathology may need to be combined with surgery. Treatment must include complete

removal of all abnormal tissue. Planning for surgical intervention can be extensive if the

primary lesion is large enough to require secondary wound closure. Eyelid margin alignment is

necessary for corneal health. Subsequent follow-up treatment can add additional

complications depending on the cause of the initial lid abnormality. Therapy may need to

include long term antibiotics or chemotherapy.

Acute corneal problems

Initial rule outs for corneal problems include foreign body, lacerations/punctures, ulceration

both infected and non-infected, non-ulcerated keratitis, dermoid and neoplasia with squamous

cell carcinoma being the primary form. Diagnosis prior to surgery is helpful to determine if

additional treatment will be necessary. However, in some cases surgical biopsy may be

necessary to achieve a diagnosis as well as a cure. Histopathology of removed tissue should

always be encouraged. Mass resection for biopsy in a standing horse is possible; however,

complete surgical resection is safer with the horse under general anesthesia. Initial therapy

following keratectomy should include ophthalmic antibiotics to prevent bacterial infection and

systemic anti-inflammatory medication for secondary uveitis. Post-operative examination is

necessary to confirm resolution of the problem.

98

STANDING SURGERY OF THE HORSE’S HEAD

Dr Robin JW Bell BVSc MVSc MACVSc DipVetClinStud DipECVS Equine Performance and Imaging Centre, University Veterinary Teaching Hospital Camden

Numerous surgical procedures can safely be performed standing under sedation in horses.

These range from laceration repair, mass removal and enucleation to surgery of the paranasal

sinuses. In particular surgery of the paranasal sinus lends itself to being performed standing and

can involve either trephination of the maxillary and/or the frontal sinuses, or an osteoplastic

frontonasal or maxillary bone flap. Indications for performing standing sinus surgery are

decreased risks associated with general anaesthesia, decreased cost and superior visualisation

at surgery due to a decrease in the amount of haemorrhage. Lesions that can be treated via

standing sinus surgery include removal of a mass, cyst or ethmoid haematoma, biopsy of

abnormal tissue, removal of inspissated material from the ventral conchal sinus and evaluation

of the maxillary cheek teeth. Sedation for the procedure is usually achieved with a continuous

rate infusion of detomidine. Local anaesthetic is used to provide analgesia at the incision, and if

a previous trephine hole does not exist, local is also injected into the sinus via a 14 gauge

needle that is hammered through the skin and frontal bone with a mallet, providing analgesia

to the lining of the sinus. Draping may be used, although some horses do not tolerate this. The

flap itself is created with an oscillating saw used at a 45˚ angle, which is then elevated with an

osteotome and fingers, to create a break at its base and reflected axially. Due to the decreased

amount of haemorrhage, packing the sinus is not usually necessary, but this can be

accomplished through the creation of sinonasal opening in either the ventral or dorsal conchal

sinus. The bone flap is replaced and the skin is closed routinely. A foley catheter is placed

through a new or existing trephine hole to facilitate post operative lavage.

99

NEUROMUSCULAR PHYSIOLOGY OF THE UPPER AIRWAYS: MECHANISMS OF OBSTRUCTIONS

SAMANTHA FRANKLIN BVSc PhD MRCVS School of Animal and Veterinary Sciences, University of Adelaide, Roseworthy Campus, SA5371.

Introduction:

Dynamic collapse of the upper respiratory tract (URT) describes the respiratory obstruction

caused by the collapse of one or more soft tissue structures into the airway during exercise.

Certain structures within the airway are at particular risk of collapse. These include parts of the

nasopharynx and larynx, which rely on muscular activity to maintain airway patency. Any

weakness (either pathological or physiological) may result in an inability to resist the increased

negative airway pressures associated with exercise and hence will result in dynamic airway

collapse.

Nasopharyngeal collapse: The nasopharynx is a musculo-membraneous tube leading from the nasal cavity to the larynx. This region has no direct bony or cartilaginous support and is particularly prone to dynamic collapse during exercise. The most common form of nasopharyngeal collapse is due to palatal dysfunction, which includes palatal instability (PI) and dorsal displacement of the soft palate (DDSP). Indeed, a recent study that modelled airflow patterns within the URT confirmed that the ventral aspect of the nasopharynx is subject to the most negative wall pressures & turbulence, perhaps explaining the high prevalence of these conditions (1). Dynamic collapse of the lateral and / or dorsal pharyngeal walls may also occur, although this appears to be less common. Nasopharyngeal patency is achieved through the activation of a combination of the palatal

muscles, the extrinsic tongue muscles, the hyoid muscles and the pharyngeal constrictors.

Activation of these muscles is stimulated during exercise by laryngeal pressure-sensing

mechanoreceptors and chemoreceptors that detect increased levels of carbon dioxide (2,3).

Dilation and stabilisation of the dorsal and lateral walls of the nasopharynx is achieved by

contraction of the stylopharyngeus muscle and the pharyngeal constrictor muscles (4, 5). The

stylopharyngeus muscle is the major dilator of the dorsal nasopharynx. This muscle originates

from the medial surfaces of the distal stylohyoid bone and ramifies in the dorsal wall of the

nasopharynx, passing between the pterygopharyngeus and palatopharyngeus muscles (6).

Motor function is provided by the glossopharyngeal nerve and bilateral blockade of this nerve

has been shown to produce dorsal nasopharyngeal wall collapse in horses (5). The pharyngeal

constrictor muscles include the superior (dorsal) pharyngeal constrictor (composed of the

palatopharyngeus and pterygopharyngeus muscles), the middle pharyngeal constrictor

(hyopharyngeus) and inferior pharyngeal constrictor (thyropharyngeus) (4, 6). These muscles

100

are innervated by branches of the vagus nerve. They have a dual role in deglutition and

respiration. Tonic activity of these muscles during respiration aids dilation of the pharyngeal

walls (4). It is possible that dysfunction of one or more of these muscles may be implicated in

dynamic pharyngeal wall collapse.

The soft palate makes up the ‘floor’ of the nasopharynx and acts to separate the oropharynx and nasopharynx. It plays an important role in both breathing and swallowing. In the horse the soft palate extends from the hard palate (via a broad tendinous aponeurosis) to the larynx where the caudal border lies ventral to the epiglottis, except during deglutition, thereby rendering the horse an obligate nasal breather. The position of the soft palate is determined by the co-ordinated action of the intrinsic muscles, which include: the levator veli palatini, tensor veli palatini, palatinus and palatopharyngeus muscles. The palatinus muscles are two fusiform muscles that lie either side of the midline. They extend

from the caudal aspect of the palatine aponeurosis and terminate near the caudal free margin

of the soft palate. A connective tissue sheath surrounds the palatinus muscles, onto which

other palatal muscles attach (7). It has been suggested that this sheath may also contribute to

the intrinsic support of the dorsal soft palate controlling its stiffness and preventing distortion

(8).

The tensor veli palatini is a flat fusiform muscle that travels along the lateral walls of the

nasopharynx and the lateral lamina of the guttural pouch. Its tendon is reflected around the

hamulus of the pterygoid bone and inserts laterally onto the caudal aspect of the aponeurosis.

The tensor veli palatini shows respiratory related activity (9). The action of this muscle is to

tense the rostral portion of the soft palate in a lateral direction, rather than to depress it

towards the tongue and although electrical stimulation of this muscle has been shown to

reduce collapsibility of the airway, the role of this muscle is probably small (10, 11). It has been

suggested the coordinated activation of the palatopharyngeal muscles is required to maximally

increase upper airway tension and decrease collapsibility (11). In the horse, experimental

transection of the tendons has been shown to induce instability of the rostral portion of the

soft palate in exercising horses although this did not result in DDSP (12).

The palatopharyngeus muscle originates from the palatine aponeurosis lateral to the palatinus

muscle and further fibres attach ventrally along the length of the connective tissue sheath of

the palatinus muscle (7). The palatopharyngeus muscle travels caudally along the lateral wall of

the nasopharynx to the pharyngeal raphe, forming part of the superior constrictor muscle

group. The main role of this muscle relates to pharyngeal airway closure during swallowing.

However, it is also active during respiration (13, 14) and is involved in stiffening of the

pharyngeal walls and dilation of the airways (13). In the horse it is has been suggested that the

combined action of the palatopharyngeus and palatinus is to depresses the soft palate (14, 15).

101

The levator veli palatini muscles arise from the muscular process of the petrous temporal bone and lateral lamina of the auditory tube (7). They insert in the midline, ventral to the palatinus muscle, forming a sling-like structure. Their action is to raise the soft palate during deglutition and vocalisation and to aid oral ventilation in non-obligate nasal breathers (16). Although the pathogenesis of DDSP is not completely understood, there is some evidence that

neuromuscular dysfunction of the palatal musculature (specifically the palatinus and

palatopharyngeus muscles) plays an important role. Temporary blockade of the pharyngeal

branch of the vagus that provides motor supply to these muscles has been shown to result in

persistent DDSP at rest and during exercise (15). However, more recent research suggests that

factors affecting laryngohyoid position may also play a role in the development of DDSP (17,

18).

The tongue is important in the positioning of the hyoid apparatus. There are four extrinsic

muscles of the tongue that attach to the hyoid apparatus: The genioglossus and geniohyoideus

are tongue protruders, and pull the hyoid apparatus rostrally whilst the styloglossus and

hyoglossus are tongue retractors (19). These muscles are all innervated by the hypoglossal

nerve: the medial branch innervates the genioglossus and geniohyoid, and the lateral branch

innervates the styloglossus and hyoglossus. The genioglossus & geniohyoideus have been

shown to have respiratory related activity during exercise (20). Furthermore, bilateral blockade

of the hypoglossal nerve at the level of the ceratohyoid has been shown to result in DDSP

during high-speed exercise (18). In other species also there is evidence that these muscles have

respiratory-related activity and that electrical stimulation of the hypoglossal nerve increases

upper airway dilation.

Other muscles that attach to the hyoid apparatus may also affect the position of the hyoid

apparatus and hence may also play a role in nasopharyngeal stability. These include the “strap”

muscles (sternohyoideus and omohyoideus) and the thyrohyoideus muscles. The strap muscles

act in the opposite direction to the genioglossus and geniohyoid muscles and result in caudal

traction of the hyoid apparatus and larynx. Transection of the sternothyrohyoid muscle has

been shown to impair airflow in horses during exercise (21). In other species, caudal

displacement of the trachea has also been shown to improve pharyngeal stability and this is

further enhanced when in combination with displacement of the tongue (22).

The paired thyrohyoid muscles attach to the caudal border of the thyrohyoid bones and run to

the lateral surface of the ipsilateral thyroid cartilage lamina. These act to move the basihyoid

caudally and the larynx rostrally and dorsally and help to prevent caudal retraction of the larynx

during exercise. Bilateral resection of these muscles resulted in DDSP at slow speed exercise in

7/10 horses and led to the development of the “tie-forward” procedure as a treatment for

DDSP (17).

102

Laryngeal collapse The larynx is suspended by the hyoid apparatus and forms the connection between the pharynx and tracheo-bronchial tree. This is an important structure within the URT because it is a further source of resistance to breathing and a potential site of obstruction to airflow. A number of abnormalities leading to obstruction are now well recognised, including arytenoid cartilage collapse (most commonly as a result of recurrent laryngeal neuropathy) vocal cord collapse, axial deviation of the aryepiglottal folds and, less commonly, collapse of the apex of the corniculate process of the left arytenoid cartilage and epiglottal retroversion. During exercise, laryngeal dilation occurs which reduces resistance and maximises airflow (23). This is achieved by maximal abduction of the arytenoid cartilages through contraction of the intrinsic muscles, specifically the cricoarytenoideus dorsalis (CAD), which is the principal abductor muscle. The remaining intrinsic muscles of the larynx have an adductory role, narrowing the rima glottidis and protecting the lower airway during swallowing. It is well known that recurrent laryngeal neuropathy (RLN) leads to atrophy of the CAD muscle,

ultimately resulting in complete collapse of the left arytenoid cartilage and the associated vocal

fold, both at rest and during exercise. The aetiology of RLN remains unknown; however, recent

evidence has confirmed that it is a bilateral mononeuropathy rather than a polyneuropathy

(24). A number of horses with equivocal or even ‘normal’ laryngeal movements at rest may also

experience dynamic collapse of the left arytenoid cartilage and / or vocal cord (s) during

exercise. Recent studies suggest that this condition may be progressive (25), which might

explain the findings of dynamic collapse during exercise despite normal function during a

resting examination, when airway pressures are much lower.

Bilateral dynamic laryngeal collapse has also been reported in some horses (26, 27). The cause

of this condition remains unclear but differs from RLN because affected horses have normal

laryngeal function when exercised with a free head carriage but develop dynamic laryngeal

collapse when the poll region is flexed.

Another, less common, condition affecting the arytenoid cartilages during exercise is that

associated with collapse of the apex of the corniculate process of the left arytenoid during

exercise (28). Although the cause remains unclear, it has been suggested that the arytenoid

transversus muscle or transverse arytenoid ligament may be implicated. (28,29). Affected

horses are able to maintain abduction of the ventral aspect of the corniculate process.

However, they may exhibit concurrent vocal fold collapse and/ or axial deviation of the

aryepiglottal folds (28).

Axial deviation of the aryepiglottic folds (ADAEF) is now a commonly recognised form of

dynamic collapse and is often, but not invariably, associated with DDSP or other forms of

dynamic airway collapse. The folds are composed of a doubled layer of mucous membrane

103

which is continuous rostrally with the glosso-epiglottal mucosa lying between the base of the

tongue and the ventral aspect of the epiglottis. They have limited muscular attachments and

only a collagenous fibre layer is present to strengthen the dorsal margin of the fold (30). The

cause of this condition is currently not well understood. In humans, the condition has been

associated with redundant aryepiglottic tissue and laryngeal neuromuscular dysfunction (31,

32). Similar factors may be associated with the condition seen in horses. In cases of complex

dynamic collapse is possible that laxity of these folds may arise secondary to the dorsal

‘flattening’ of the epiglottis that is observed before displacement occurs, or secondary to

dynamic collapse of other structures.

Retroversion of the epiglottic cartilage had been described as a rare dynamic obstructive

condition in exercising horses. The normal position of the epiglottis is determined by

contraction of the hyoepiglotticus muscle and epiglottal retroversion has been shown to be

induced experimentally by anaesthesia of the hypoglossal nerves at the level of the guttural

pouch (33), leading to the hypothesis that this impairment of this muscle is implicated in the

clinical condition.

Conclusions:

It is now well recognised that both the intrinsic and extrinsic musculature of the URT plays a key

role in maintaining dilation of the airway. Neuromuscular dysfunction of the supporting

musculature may be responsible for a number of forms of dynamic collapse during exercise.

This occurs due to the inability of the musculature to maintain dilation of the airway in the face

of the high airflows and pressures generated during exercise.

References:

1) Rakesh, V., Ducharme, N.G., Datta, A.K., Cheetham, J. and Pease, A.P. (2008) Development of equine upper airway fluid mechanics model for Thoroughbred horses. Equine Vet J 40 (3): 272-279. 2) Sant'Ambrogio G, Tsubone H, Sant'Ambrogio FB (1995). Sensory information from the upper airway: role in the control of breathing. Resp Physiol 102:1-16.

3) Holcombe SJ, Derksen FJ, Berney C, Becker AC, Horner NT.(2001)Effect of topical anesthesia of the laryngeal mucosa on upper airway mechanics in exercising horses. Am J Vet Res. 62(11):1706-10. 4) Kuna, S.T. and Vanoye, C.R. (1999) Mechanical effects of pharyngeal constrictor activation on pharyngeal airway function. J. Appl. Physiol. 86 (1): 411 – 417. 5)Tessier, C., Holcombe, S.J., Derksen, F.J., Berney, C. and Boruat, D. Effects of styolpharyngeus muscle dysfunction on the nasopharynx in exercising horses. Equine Vet J. 36 (4): 318 – 323. 6) Sisson and Grossman (1975) Anatomy of Domestic Animals. 5th Ed. Philadelphia: WB Saunders Co. 471-475.

104

7) Richardson, L.E., Wakley, G.K. and Franklin, S.H. (2006). A quantitative study of the equine soft palate using histomorphometry. The Vet J. 172: 78-85. 8) Kuehn, D.P., Folkins, J.W., Linville, R.N. (1988) An electromyographic study of the musculus uvulae. Cleft Palate J. 27: 348-355. 9) Van der Touw, T., O'Neill, N., Brancatisano, A., Amis, T., Wheatley, J. and Engel, L. (1994) Respiratory-related activity of soft palate muscles: augmentation by negative upper airway pressure. J. Appl. Physiol. 76, 424-432. 10) Honjo, I., Okazaki, N. and Nozoe, T. (1979) Role of the tensor veli palatini muscle in movement of the soft palate. Acta Otolaryngol 88, 137-141. 11) McWhorter, A.J., Rowley, J.A., Eisele, D.W., Smith, P.L., Schwartz, A.R. (1999) The effect of tensor veli palatine stimulation on upper airway patency. Arch Otolaryngol Head Neck Surg 125: 937-940. 12) Holcombe, S. J., Derksen, F. J., Stick, J. A. and Robinson, N. E. (1997) Effect of bilateral tenectomy of the tensor veli palatini muscle on soft palate function in horse. Am. J. Vet. Res. 58, 317 - 321 13) Kuna, S.K. (2000) Respiratory-related activation and mechanical effects of the pharyngeal constrictor muscles. Resp Physiol 119: 155-161. 14) Holcombe, S.J., Derksen, F.J. and Robinson, N.E. (2007) Electromyographic activity of the palatinus and palatopharyngeus muscles in exercising horses. Equine Vet J 39, 451-455. 15) Holcombe, S. J. Derksen, F. J., Stick, J. A. and Robinson, N. E. (1998) Effect of bilateral blockade of the pharyngeal branch of the vagus nerve on soft palate function in horses. Am. J. Vet. Res. 59, 504 – 508 16) Kuehn, D.P., Folkins, J.W. and Cutting, C.B. (1982). Relationships between muscle activity and velar position. Cleft Palate J. 19: 25 -35. 17) Ducharme, N.G., Hackett, R.P., Woodie, J.B., Dykes, N., Erb, H.N., Mitchell, L.M. and Soderholm, L.V. (2003) Investigations into the role of the thyrohyoid muscles in the pathogenesis of dorsal displacement of the soft palate in horses. Equine Vet J 35 (3): 258 – 263. 18) Cheetham, J., Pigott, J.H., Hermanson, L.C., Soderholm, L.V., Thorson, L.M. and Ducharme, N.G. (2009) Role of the hypoglossal nerve in equine nasopharyngeal stability. J Applied Physiol. 107: 471–477. 19) Sawczuk A, Mosier KM. (2001)Neural control of tongue movement with respect to respiration and swallowing. Crit Rev Oral Biol Med 12: 18–37. 20) Morello, S.L., Ducharme, N.G., Hackett, R.P., Warnick, L.D., Mitchell, L.M. and Soderholm, L.V. (2008) Activity of selected rostral and caudal hyoid muscles in clinically normal horses during strenuous exercise. AJVR 69 (5): 682-689. 21) Holcombe SJ, Beard WL, Hinchcliff KW, Robertson JT.(1994) Effect of sternothyrohyoid myectomy on upper airway mechanics in normal horses. J Appl Physiol. 77(6):2812-6. 22) Rowley J.A. and Badr, M.S. (2004) Breathing during sleep: ventilation and the upper airway. In Clinical Sleep Disorder. Ed R. Carney, R.B. Berry and J.D.Geyer. 65-68. 23) Lafortuna, C.L., Saibene, F., Albertini, M. and Clement, G. (2003) The regulation of respiratory resistance in exercising horses. Eur J Appl Physiol 90: 396 – 404. 24) Hahn, C.N., Matiasek, K., Dixon, P.M., Molony, V., Rodenacker, K. and Mayhew, I.G. (2008) Histological and ultrastructural evidence that recurrent laryngeal neuropathy is a bilateral mononeuropathy limited to recurrent laryngeal nerves. Equine Vet. J. 40 (7): 666-672.

105

25) 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 in 152 cases of equine recurrent laryngeal neuropathy (RLN). Equine Vet. J. 34, 29 – 34. 26) Strand, E., Hanche-Olsen, S., Gronvold, A.M.R. and Mellum, C.N. (2004) Dynamic bilateral arytenoid and vocal fold collapse associated with head flexion in 5 Norwegian Coldblooded Trotter racehorses. Equine Vet Educ. 16 (5): 242-254. 27) Allen, K.J., Terron-Caned0, N., Hillyer, M.H. and Franklin, S.H. (2011) Equitation and exercise factors affecting dynamic upper respiratory tract function: A review illustrated by case reports. Equine Vet educ. 23 (7):361-368. 28) Dart, A.J., Bowling, B.A. and Smith, C.L. (2005) Upper airway dysfunction associated with collapse of the apex of the corniculate process of the left arytenoid cartilage during exercise in 15 horses. Vet Surg. 34: 543-547. 29) Barakzai, S.Z., Milne, E.M. and Dixon, P.M. (2007) Ventroaxial luxation of the apex of the corniculate process of the arytenoid cartilage in resting horses during induced swallowing or nasal occlusion. Vet Surg. 36: 210-213. 30) Reidenbach, M.M. (1998) Aryepiglottic fold: normal topography and clinical implications. Clin Anat. 11 (4): 223 -235. 31) Peron, D.L., Graffino, D.B. and Zenker, D.O. (1988) The redundant aryepiglottic fold: a report of a new cause of stridor. Laryngoscope 98 (6): 659 – 663. 32) Read, C.T. (1995) Redundant aryepiglottic folds may require surgical removal. Chest 108 (1): 296. 33) Holcombe, S. J., Derksen, F. J., Stick, J. A. and Robinson, N. E. (1997) Effects of bilateral hypoglossal and glossopharyngeal nerve blocks on epiglottic and soft palate position in exercising horses. Am. J. Vet. Res. 58, 1022 -1026

106

COMPLICATIONS ASSOCIATED WITH LARYNGOPLASTY

SAFIA BARAKZAI University of Edinburgh, Roslin, Midlothian, Scotland, EH25 9RG, UK

Laryngoplasty has a high complication rate and some complications can be associated with significant patient morbidity. A detailed account of complications and their management has been recently published by Ahern and Parente (2008).

1. Coughing: Coughing both immediately postoperatively and chronically is a common complication of laryngoplasty with the prevalence of acute post-operative coughing being reported as being as high as 43% and that of chronic coughing being 14% (Dixon et al. 2003). Coughing results from aspiration of food material into the trachea due to the newly fixed arytenoid’s inability to adduct and protect the lower airway during swallowing, or perhaps due to surgically-induced changes in pharyngeal function (Greet 1979). True aspiration pneumonia (as opposed to tracheitis) is thankfully relatively rare after laryngoplasty. The degree of arytenoid abduction is thought to be significantly associated with the severity of postoperative coughing and aspiration of food material (Russell & Slone 1994, and Dixon et al. 2003), however wide abduction is certainly not the only factor that causes dysphagia because the complication is occasionally seen in horses with moderate or minimal arytenoid abduction. Aspiration of food and coughing usually reduces over the first 2-3 weeks after surgery – if this does not occur or if the degree of aspiration and/or cough is very severe, the laryngoplasty suture must be removed.

2. Loss of arytenoid abduction: Some loss of abduction is almost inevitable in almost every case to some degree in the long term (Dixon et al. 2003, Barnett et al. unpublished data). Acute loss of abduction in the immediate post-operative period is often due to suture pull-through or avulsion/fracture of cartilage. This type of surgical ‘failure’ necessitates repeat laryngoplasty or arytenoidectomy and has been reported to occur in 2-15% of cases (Marks et al., 1970; Hawkins et al., 1997; Dixon et al., 2003a; Kraus et al., 2003). Methods to prevent construct failure such as the use of cables and washers (Schumacher et al., 2000), various different trochars, needles and suture materials have been suggested by different authors.

The more insidious loss of abduction reported over the weeks to months following surgery that occurs in the majority of cases (Dixon et al. 2003, Barakzai et al. 2009, Davidson et al. 2010) is problematic and difficult to prevent. Proposed causes of this gradual loss of abduction include the suture ‘cutting in’ to cartilage or soft tissues, suture loosening and stretch and are likely associated with long term cyclical loading of the suture-cartilage construct, particularly during swallowing and coughing (Witte et al. 2010). Several methods to reduce this loss of abduction have been proposed, such as promoting ankylosis of the crico-arytenoid joint by using surgical curettage (Parente et

107

al., 2011) or injection of PMMA (Cheetham et al. 2009), however there is currently no long term information regarding the efficacy of these procedures in large numbers of clinical cases.

Several experimental and clinical studies have suggested that a moderately abducted arytenoid that is fixed in position (i.e. no longer becomes adducted during inspiration at exercise) provides a sufficient airway for non-performance horses. Moderate (grade 3) abduction has also been shown to have no significantly adverse effect on racing performance of National Hunt racehorses as compared to horses with good (grades 1 or 2) abduction (Barakzai et al. 2009). A recent cross sectional dynamic endoscopic study of horses post laryngoplasty has reported that the grade of arytenoid abduction is not correlated with arytenoid stability (Barnett et al., 2011). However, in a population of horses that are returned with recurrent symptoms of respiratory noise and/or poor performance, this is not the case, with Davidson et al. (2010) reporting that arytenoid instability was more common in horses with no residual surgical abduction, compared to those with poor to moderate abduction.

3. Wound infection: As with any surgical site with a permanent implant, the prosthesis and the wound can become infected. Currently, the reported incidence of wound infection is between 0.5 and 6% (Hawkins et al., 1997; Strand et al., 2000; Davenport et al., 2001, Kidd & Slone, 2002; Dixon et al., 2003; Kraus et al., 2003). Treatment of wound infection consists of wound lavage and broad-spectrum antibiotics. In the occasional case where the infection is refractive to conservative management, the prosthesis will need to be removed.

4. Continued respiratory noise and/or poor performance: The aetiology of continued noise and poor performance after laryngoplasty is complex. In one study, experimental horses with higher levels of arytenoid abduction were found to have increased levels of noise compared to those with more moderate abduction (Brown et al. 2004). Three recent studies reporting results of exercising endoscopy in horses that have undergone laryngoplasty have all reported that although arytenoid instability does occur in some cases, there is an alarmingly high incidence (48-59%) of dynamic laryngeal or pharyngeal collapse that is not arytenoid cartilage collapse (Davidson et al. 2010, Compostella et al. 2010, Barnett et al. 2011). These include right vocal fold collapse, dorsal displacement of the soft palate, ary-epiglottic fold collapse, collapse of the axial portion of the corniculate cartilage etc. Clearly, more research must be done in this field, but the take home message is that horses presented for investigation of laryngoplasty ‘failure’ should always undergo dynamic endoscopy before laryngoplasty is repeated because instability of the arytenoid cartilage is often not the cause of ongoing clinical signs.

5. Arytenoid chondritis: Arytenoid chondritis has been reported in 1% of horses following laryngoplasty (Dixon et al. 2003), however more recent studies with longer term (months to years) follow up

108

of cases suggest that the prevalence of this serious complication may in fact be higher at 8-9% (Davidson et al. 2010, Barnett et al., 2011). Infection may enter the arytenoid cartilage via the suture placed at the muscular process, or more likely, through the vocal process if the dorsal vocal cordectomy incision damages the cartilage.

Ahern BJ, Parente EJ.(2008) Surgical complications of the equine upper respiratory tract. Vet Clin North Am Equine Pract. 24:465-84

Barakzai S.Z., Boden L.A., Dixon P.M (2009) Post-operative race performance is not correlated

with degree of surgical abduction obtained after laryngoplasty. Veterinary Surgery, 38, 934-40

Barnett T.P., Dixon P.M., Barakzai S.Z. (2011) A prospective study of horses undergoing

videoendoscopic dynamic assessment of the upper airway following laryngoplasty. ECVS Annual

Congress, July 7-9 2011, Ghent, Belgium

Brown JA, Derksen FJ, Stick JA, et al. (2004) Effect of laryngoplasty on respiratory noise

reduction in horses with laryngeal hemiplegia. Equine Vet J. 36: 420-5

Cheetham J, Witte TH, Rawlinson JJ et al: (2008) Intra-articular stabilisation of the equine

cricoarytenoid joint. Equine Vet J 40: 584-8

Compostella,F., Tremaine, W.H., and Franklin, S.H. (2010) Causes of continuing respiratory

noise following prosthetic laryngoplasty. In: BEVA congress proceedings, pp 218

Davenport CL, Tulleners EP, Parente EJ: The effect of recurrent laryngeal neurectomy in

conjunction with laryngoplasty and unilateral ventriculocordectomy in thoroughbred

racehorses. Vet. Surg. 30: 417, 2001

Davidson EJ, Martin BB, Rieger RH, et al. (2010) Exercising videoendoscopic evaluation of 45

horses with respiratory noise and/or poor performance after laryngoplasty. Vet Surg 39: 942-8

Dixon P.M., McGorum B.C., Railton D.I., et al. (2003) Long-term survey of laryngoplasty and

ventriculocordectomy in an older, mixed-breed population of 200 horses. Part 1: Maintenance

of surgical arytenoid abduction and complications of surgery. Equine Vet J 35: 389-396

Greet, T.R.C., Baker, G.J., and Lee, R. (1979) The effect of laryngoplasty on pharyngeal function

in the horse. Equine Vet J. 11: 153-158

Hawkins JF, Tulleners EP, Ross MW et al: (1997) Laryngoplasty with or without ventriculectomy

for treatment of left laryngeal hemiplegia in 230 racehorses. Vet Surg 26: 484-91

Kidd JA, Slone DE (2002) Treatment of laryngeal hemiplegia in horses by prosthetic

laryngoplasty. Ventriculocordectomy and vocal cordectomy. Vet Rec 150: 481-4

Kraus BM, Parente EJ, Tulleners EP (2003) Laryngoplasty with ventriculectomy or

ventriculocordectomy in 104 draft horses (1992-2000). Vet Surg 32:530-538

Marks D, Kay-Smith MP, Cushing LS et al (1970) Use of a prosthetic device for surgical

correction of laryngeal hemiplegia in horses. J. Am. Vet. Med. Assoc. 157:157-163

Parente EJ, Birks EK, Habecker P. (2011) A modified laryngoplasty approach promoting ankylosis of the cricoarytenoid joint. Vet Surg. 40:204-10

109

Russell AP, Slone DE. (1994) Performance analysis after prosthetic laryngoplasty and bilateral

ventriculectomy for laryngeal hemiplegia in horses: 70 cases (1986-1991). J Am Vet Med Assoc.

204:1235-41.

Schumacher J, Wilson AM, Pardoe C et al. (2000) In vitro evaluation of a novel prosthesis for

laryngoplasty of horses with recurrent laryngeal neuropathy. Equine Vet J 32:43-6

Strand E, Martin GS, Haynes PF et al: (2000) Career racing performance in Thoroughbreds

treated with prosthetic laryngoplasty for laryngeal neuropathy: 52 cases (1981-1989) J Am Vet

Med Assoc 217:1689-1695

Witte TH, Cheetham J, Soderholm LV, et. al. (2010) Equine laryngoplasty sutures undergo increased loading during coughing and swallowing. Vet Surg. 39:949-56

110

LASER SURGERY OF THE UPPER RESPIRATORY TRACT

SAFIA BARAKZAI University of Edinburgh, Roslin, Midlothian, Scotland, EH25 9RG, UK

During the last 15 years the use of lasers in equine patients has increased substantially, with the

most common indication for laser surgery being transendoscopic surgery of the upper

respiratory tract (URT). Although there are numerous types of surgical lasers available, only 2

are commonly used for equine URT surgery, the diode and Nd:YAG lasers. These are applied to

the tissue of interest by transmission down a quartz glass fibre passed through the biopsy

channel of an endoscope. The CO2 laser works via transmission down flexible copper tubing and

is currently being modified so that it can be used in a transendoscopic fashion.

Mechanism of Action

The acryonym L.A.S.E.R. stands for ‘Light amplification by stimulated emission of radiation’.

Lasers are intense beams of light which act by destroying the tissue on which the beam is

focused (non-contact mode) or tissue that is in direct contact with the tip of the laser fibre.

Generation of heat by the laser results in a zone of vaporisation, where tissue is heated to

>100oC, resulting in a ‘laser crater’ and a plume of smoke. Surrounding this zone of vaporisation

is a zone of ‘latent thermal necrosis’ where tissue is heated to >60oC, and undergoes necrosis

over subsequent days. Such necrosis may result in significant injury to tissue adjacent to the

surgical incision, and thus any cuts with a laser should be made conservatively to account for

this further ‘dying back’ of tissue.

Health and safety considerations: The laser beam can cause major ocular injuries if viewed

directly, and therefore protective glasses which are specific for the wavelength of laser being

used must be worn by all attending staff. There must be a designated laser area equipped with

appropriate warning signs to prevent entry of unwanted personnel into the treatment area. In

a modern health and safety conscious veterinary practice, the use of a nasally positioned

suction tube and scavenging system to remove the smoke plume of vaporised tissue is

appropriate, but does mean that an extra intra-nasal or intra-pharyngeal tube is required.

Additionally, if the horse is undergoing laser surgery under general anaesthesia, appropriate

precautions must be taken to ensure that the highly flammable mix of oxygen and anaesthetic

gas is not ignited by the laser beam.

Indications for laser surgery of the URT:

Ventriculocordectomy (Hawkins et al. 2001, Ducharme 2002)

Ary-epiglottic fold excision (King et al. 2001)

111

Axial sectioning of epiglottic entrapment (Tulleners 1990)

Soft palate surgery including laser staphylectomy, and laser palatoplasty (Ortved et al. 2010, Alkabes 2010)

Laryngeal granuloma excision (Hay & Tulleners, 1993)

Choanal atresia

Sub-epiglottal and other pharyngeal cyst excision

Guttural pouch tympany (Tate et al. 1995)

Sino-nasal fenestration (Morello and Parente, 2010)

Progressive ethmoidal haematoma (Nd:YAG laser only, Rothaug and Tulleners [1999])

Patient preparation and aftercare:

The majority of surgeons perform laser surgery in the standing sedated patient and in most cases; the surgery can be performed on an out-patient basis. The author routinely pre-medicates laser surgery patients with procaine penicillin, flunixin and tetanus anti-toxin before sedation with romifidine and either morphine or butorphanol.

The area that is undergoing laser treatment should be liberally sprayed with topical lidocaine (applied via a transendoscopic catheter) and topical anaesthesia of the nasal passages also facilitates passage of the broncho-oesophageal forceps and endoscope. Resting the horse’s head on a headstand greatly reduces movement during surgery and also facilitates grasping of more ventrally positioned tissues such as the vocal fold.

Post operatively, the horse is starved for several hours (to allow topical anaesthesia of the pharynx/larynx to completely wear off) or aspiration of food may result. Some authors recommend the use of SID or BID topical ‘throat spray’, usually containing a mixture of glycerine, DMSO and steroids. I do not routinely recommend it as I believe the efficacy of application of such a mixture to the appropriate area without endoscopic guidance is somewhat questionable. Systemic NSAIDs are continued for 5-7 days, and depending on the lesion operated on and any concurrent surgery performed (e.g. tie-back, tie-forward), the horse can continue with walking exercise and return to full work in 3-6 weeks. Use of an ongoing course of antibiotics is usually reserved for lesions where active infection is already present e.g. arytenoid chondritis, or where extensive soft tissue damage has resulted from the laser surgery. Owners should be notified that a nasal discharge may be present for 2-3 days after laser surgery, caused by the ongoing necrosis of tissue in the ‘latent thermal necrosis’ zone.

It is definitely worthwhile to perform a follow-up endoscopic examination prior to the horse re-commencing work to ensure that all sites have healed adequately, that there is minimal post-surgical inflammation and no resultant complications (such as granuloma formation).

112

Alkabes KC, Hawkins JF, Miller MA et al. (2010) Evaluation of the effects of transendoscopic diode laser palatoplasty on clinical, histologic, magnetic resonance imaging, and biomechanical findings in horses. Am J Vet Res 71:575–582 Ducharme NG, Goodrich L, Woodie B (2002) Vocal cordectomy as an aid in the management of horses with laryngeal hemiparesis/hemiplegia. Clinical techniques in equine practice. 1: 17-21 Hawkins JF, Andrews-Jones L (2001) Neodymium: yttrium aluminium garnet laser ventriculocordectomy in standing horses. AJVR 62: 531-537 Hay WP and Tulleners EP (1993) Excitation of intralaryngeal granulation tissue in 25 horses using a neodymium:YAG laser (1986-1991) . Vet Surg. 22: 129-134 Ortved, KF, Cheetham J, Mitchell LM and Ducharme NG. (2010) Successful treatment of persistent dorsal displacement of the soft palate and evaluation of laryngohyoid position in 15 racehorses. Equine Vet J. 42: 23-29 King DS, Tulleners EP, Martin BB et al. (2001) Clinical experiences with axial deviation of the aryepiglottic folds in 52 racehorses. Vet Surg. 30: 151-160 Morello SL, Parente EJ (2010) Laser vaporization of the dorsal turbinate as an alternative method of accessing and evaluating the paranasal sinuses. Vet Surg. 39: 891-899 Rothaug PG, Tulleners EP. (1999) Neodymium:yttrium-aluminum-garnet laser-assisted excision of progressive ethmoid hematomas in horses: 20 cases (1986-1996). J Am Vet Med Assoc. 214:1037-41. Tate LP Jr, Blikslager AT, Little ED. (1995) Transendoscopic laser treatment of guttural pouch tympanites in eight foals. Vet Surg. 24:367-72. Tulleners EP (1990) Transendoscopic contact neodymium: yttrium aluminium garnet laser correction of epiglottic entrapment in standing horses. JAVMA 196: 1971-1980

113

DYNAMIC ASSESSMENT OF THE EQUINE UPPER RESPIRATORY TRACT

Samantha Franklin BVSc PhD MRCVS School of Animal and Veterinary Sciences, University of Adelaide, Roseworthy Campus, SA5371.

Introduction:

Obstructive disorders of the upper respiratory tract (URT) have been recognised as important

causes of poor performance in the equine athlete for many years. Collapse of structures within

the upper airways results in a reduction in the diameter of airway and causes increased

resistance to airflow, an increase in the work of breathing and a reduction in ventilation,

thereby reducing the oxygen supply to the exercising muscles.

It is now acknowledged that resting endoscopic findings alone are not necessarily

representative of the situation occurring during strenuous exercise and the presence of

complex dynamic airway collapse is common. Exercising endoscopy is therefore necessary in

order to make a definitive diagnosis of dynamic URT collapse in many cases (1-4).

This is perhaps not surprising when we consider the changes that occur within the respiratory

system between rest and fast exercise. The breathing frequency increases from 8-12 breaths

per minute at rest to approximately 120 breaths per minute during galloping. Tidal volume also

increases (approximately threefold) resulting in the minute ventilation increasing from 50 l/min

at rest to over 2000 l/min (5). In order to drive ventilation, the pressures within the airway

increase dramatically during exercise (6). Any weakness (either pathological or physiological) of

the upper airway musculature may result in an inability to resist the increased negative airway

pressures associated with exercise and hence will result in dynamic airway collapse.

For over 20 years diagnosis of dynamic URT collapse has been made possible by performing

endoscopy of the upper airways during high-speed treadmill exercise. However, advances in

technology now allow us to perform endoscopy of the upper airways during ridden exercise.

This presentation will describe how exercise endoscopy may be performed in the field and

discuss clinical applications of this technique.

Treadmill endoscopy:

The use of treadmill endoscopy was first described in 1989 (7). Since that time it has enabled

clinicians to visualise the upper airways during strenuous exercise. This has greatly aided our

understanding of the different forms of dynamic collapse affecting the exercising horse and to

date has been considered to be the “gold standard” for diagnosis of dynamic airway collapse.

This technique has the advantage that testing protocols may be standardised and other

measurements may also be made concurrently, such as measurement of airflow and gas

exchange, thereby enabling the degree of obstruction to be quantified. However, there are a

114

number of disadvantages: Treadmill endoscopy requires the horse to be examined at a

specialist facility. The procedure is labour intensive and time consuming and considered by

many to be too expensive. In addition, there are frequently concerns over the potential risk of

injury, although these may not be justified (8). This has meant that historically, relatively few

horses have undergone exercising endoscopy in order to achieve a definitive diagnosis of

dynamic airway collapse and in many cases the decision for surgery has been based on clinical

history and resting endoscopic findings alone.

Overground endoscopy:

During the past few years, advances in technology have enabled the development of portable

endoscopes that may be used during ridden exercise in the field (9-11). The advantages of

overground endoscopy include the ability to exercise the horse in its’ natural environment with

a rider onboard and without the need for referral to a specialist centre. This is less time

consuming and also potentially has the benefit of examining the horse under conditions similar

to those experienced during competition.

A number of systems are now available commercially and this will doubtless have an important impact on the ability to diagnose dynamic airway collapse in the exercising horse. These systems incorporate a CCD video chip into an insertion tube of varying length. Some systems are mounted on the horse’s head, whilst others have a longer tube with the processor, telemetry unit, battery pack and recording equipment mounted either in a saddle pack or backpack worn by the jockey. All systems record the video image onto a recording device in order for download and viewing after the completion of exercise. Some systems also have the option of wireless transmission for real-time viewing by the veterinarian. The transmission distance varies between systems but currently appears to be in the range of 150 to 1000 m. Transmission distance may be affected by the presence of obstacles between the horse and the viewer. Interference may also occur as a result of other electronic equipment or because of reflection of some stray signals off solid surfaces, for example when used in an indoor arena.

Factors to consider when choosing equipment (12):

1) Ease of use & safety - The system should be easy to apply, should stay in place during the examination, and should not provide a safety hazard for horse or rider.

2) Image quality - This is determined by a combination of the CCD camera chip and lighting. Most systems use LED lighting at the endoscope, which enables miniaturisation of the system by negating the need for an external light source. However, the illumination is considerably lower than that of light sources that are used with standard hospital based videoendoscopes. Only one system currently uses a xenon light source.

3) Ability to flush the endoscope during exercise - The majority of horses will have some mucus within the upper airways during exercise. This emanates from the trachea and may be increased in horses with lower airway disease. In many cases, mucus is cleared from the endoscope tip by the passage of air through the nasal passages at high flow rates during expiration. However, where mucus becomes lodged at the tip, this may significantly impair the

115

image. In these instances it may be necessary to flush the endoscope tip with air and/or water. Ideally a system should enable flushing “on demand” by telemetry and care should be taken in interpreting clinical findings that coincide with flushing, such as swallowing or episodes of dorsal displacement of the soft palate that may be induced by the presence of water within the nasopharynx.

4) Ability to view the image in real time - The ability to view the endoscopic image in real time is important for a number of reasons (a) to ensure a diagnostic image is obtained and (b) to identify the timing of events that may occur during the exercise test. In particular, relaxation of the muscles associated with the nasopharynx occurs as the horse slows, and may result in pharyngeal wall collapse and / or palatal instability and displacement of the soft palate at this time, despite functioning normally during strenuous exercise. Also dynamic airway collapse may be induced or exacerbated by other external factors including poll flexion, whether the horse is pulling hard, or has an open mouth (13). It is important to be able to correlate this information to make appropriate judgements regarding treatment.

5) Ability to review the image in slow motion - This is important because dynamic changes occur rapidly during strenuous exercise when the breathing frequency is in the region of 120 breaths per minute. It is therefore possible to miss subtle forms of dynamic collapse unless the recording is viewed in slow motion or on a frame-by-frame basis.

Setting up the equipment and positioning of the endoscope

Application of the equipment is best performed in a quiet environment (e.g., in a stable) rather than in the arena or start of the gallops, where horses are likely to be more excitable. As for resting endoscopy, passage of the endoscope is via the ventral meatus and is usually straightforward in the majority of horses with or without the use of a nose-twitch. The ability to move the endoscope tip is important for accurate positioning. However, in the majority of cases when the position is set, there is little need to alter it during exercise.

Positioning of the tip of the endoscope (whether for treadmill or field-based endoscopy) is critical. If the endoscope is positioned too far rostrally, it may be difficult to observe all of the structures associated with the larynx (e.g., the vocal cords) and beyond (e.g., the crico-tracheal membrane). This is particularly evident if lighting is suboptimal or if there is pharyngeal collapse that obscures the view of the larynx. However, if the endoscope is positioned too close to the larynx, it may not be possible to identify the presence of pharyngeal wall collapse or palatal instability. Ideally, the endoscope should be positioned so that the tip of the epiglottis is clearly visible. However, in some horses it may be necessary to readjust the endoscope and repeat the exercise test to visualise different parts of the upper airway.

Exercise Testing:

Previously it has been suggested that because treadmill exercise does not entirely replicate field exercise conditions, this may lead to some conditions being under-diagnosed. It has therefore been proposed that overground endoscopy should be more accurate (11). It is, however, important to recognise that the type of exercise test performed is crucial in enabling an accurate diagnosis of dynamic airway obstruction to be made. This applies to both treadmill

116

and field exercise tests (14). In cases where horses make obvious respiratory noise during training conditions, a diagnosis should be straightforward. However, for investigation of those cases that make abnormal respiratory noise only during competition or racing it is essential to replicate the conditions encountered during competition. This also applies to those horses that present with poor performance and a history of “stopping” in races that are not reported to make abnormal respiratory noise. If the clinical signs reported during competition are not replicated, false negative findings may occur. Therefore, for investigation of poor performance in racehorses, it is recommended that exercise testing be performed at an appropriate track where the distance and speeds encountered during racing can be replicated. Treadmill exercise testing, where available, also remains a viable alternative since horses can be run to the point of fatigue (15).

In pleasure and sport horses, overground endoscopy has the benefit that horses can be tested with the rider on board, which may markedly influence the upper airway dynamics. In many cases, dynamic airway collapse in these horses is associated with poll flexion (13, 16-18). Changes in poll flexion are easier to recreate during ridden exercise although it is also possible to induce changes in poll flexion during treadmill exercise, through the use of side reins (17, 19, 20). Summary:

Exercise endoscopy is essential for establishing a definitive diagnosis in horses with dynamic airway collapse. It is likely that the technique of overground endoscopy will revolutionise the way in which dynamic airway collapse is diagnosed, thereby enabling a definitive diagnosis to be established in more horses. This technique also has the potential to facilitate further research into the pathogenesis of URT obstructions. Irrespective of the method of performing exercise endoscopy, the application of appropriate exercise testing protocols is essential if an accurate diagnosis is to be made.

References:

1) Kannegieter, N.J. and Dore, M.L. (1995). Endoscopy of the upper respiratory tract during

treadmill exercise: a clinical study of 100 horses. Aus. vet. J. 72: 101–107.

2) Martin B.B., Jr., Reef V.B., Parente E.J. and Sage A.D. (2000) Causes of poor performance of

horses during training, racing, or showing: 348 cases (1992-1996). J. Am. Vet. Med. Assoc. 216,

554-558.

3) Tan, R.H.H., Dowling, B.A. and Dart, A.J. (2005) High-speed treadmill video-endoscopic examination of the upper respiratory tract in the horse: the results of 291 clinical cases. Vet J. 170: 243-248. 4) Lane, J.G., Bladon, B., Little, D.R.M., Naylor, J.R.J. and Franklin, S.H. (2006) Dynamic obstructions of the equine upper respiratory tract. Part 2: a comparison between endoscopic findings at rest and those recorded during high- speed treadmill exercise of 600 Thoroughbred racehorses. Equine vet. J. 38: 401–408.

117

5) Lekeux, P. and Art, T. (1994) The respiratory system: anatomy, physiology and adaptations to

exercise and training. In: The Athletic Horse: Principles and Practice of Equine Sports Medicine.

Eds: D.R. Hodgson and R.J. Rose, W.B. Saunders, Philadelphia. 79-127.

6) Ducharme, N.G., Hackett, R.P., Ainsworth, D.A., Erb, H.N. and Shannon, K.J. (1994)

Repeatability and normal values for measurement of pharyngeal and tracheal pressures in

exercising horses. Am. J. Vet. Res. 55, 369-374.

7) Stick JA, Derksen FJ.(1989) Use of videoendoscopy during exercise for determination of

appropriate surgical treatment of laryngeal hemiplegia in a colt. J Am Vet Med Assoc.

195(5):619-22.

8) Franklin, SH., Barakzai, SZ., Courouce-Malblanc, A.,Dixon, P., Nankervis, K., Perkins, J.D.,

Roberts, CA., VanErck, Westergren, E. and Allen, K.J. (2010) Investigation of the incidence and

type of injuries associated with high-speed treadmill exercise testing. Equine Vet J. 42 (Suppl.

38): 70-75.

9) Franklin, S.H., Burn, J.F., Allen, K.J. (2008) Clinical trials using a telemetric endoscope for use during over-ground exercise: a preliminary study. Equine Vet J. 40(7):712-5. 10) Desmaizieres, L-M, Serraud, N., Plainfosse, B. Michel, A. and Tamzali, Y. (2009) Dynamic respiratory endoscopy without treadmill in 68 performance Standardbred, Thoroughbred and saddle horses under natural training conditions Equine vet. J. 41 (4) 347-352 11) Pollock, P.J. Reardon, R.J.M., Parkin, T.D.H. Johnston, M.S. Tate, J. and Love, S. (2009) Dynamic respiratory endoscopy in 67 Thoroughbred racehorses training under normal ridden exercise conditions Equine vet. J. 41 (4) 354-360. 12) Franklin SH (in Press). Overground Endoscopy. In, Equine Surgery 4th Ed. Eds Auer JA. and Stick. JA. 13) Allen KJ, Terron-Canedo, N., Hillyer, MH and Franklin SH (2011) Equitation and exercise factors affecting dynamic upper respiratory tract function: a review illustrated by case reports. Equine Vet Educ. 23 (7): 361-368. 14) Allen KJ, Franklin SH (2010) Assessment of the exercise tests used during overground endoscopy in UK Thoroughbred racehorses and how these may affect the diagnosis of dynamic upper respiratory tract obstructions. Equine Vet J 42 (Suppl. 38): 587-591. 15) Allen KJ, Franklin SH (2010) Comparisons of overground endoscopy and treadmill endoscopy in UK Thoroughbred racehorses. Equine Vet J 42 (3): 186-191.

16) Davidson EJ, Martin BB, Parente EJ. and Birks, E.K. (2002) Dynamic evaluation of sport horses with poor performance: 80 cases (1992-2000). Proceedings of the 2002 Conference on

Equine Sports Medicine: The Elite Dressage and Three Day Event Horse, Ed: A. Lindner, CESMAS, Jülich. pp 133-136.

17) Franklin SH, Naylor JRJ, Lane JG. (2006) Videoendoscopic evaluation of the upper respiratory tract in 93 sports horses during exercise testing on a high-speed treadmill. Equine Vet J Suppl 36: 540.

18) Van Erck-Westergren, E., Frippiat, T., Dupuis, M-C., Richard, E., Art, T & Desmaizieres, L-M. Upper airway dynamic endoscopy: are track and treadmill observations comparable? Proceedings of the 4th World Equine Airways Symposium. 254-255.

118

19) Petsche VM, Derksen FJ, Berney CE and Robinson, NE (1995) Effect of head position on upper airway function in exercising horses. Equine Vet J Suppl 18:18-22.

20) Strand E, Fjordbakk CT, Holcombe SJ, Risberg, A. and Chalmers, H.J. (2009) Effect of poll flexion and dynamic laryngeal collapse on tracheal pressure in Norwegian Coldblooded Trotter racehorses. Equine Vet J 41:59-64.

119

WHAT I REALLY LOOK FOR ON A NEUROLOGIC EXAMINATION JOE MAYHEW Massey University, Aotearoa i.g.mayhew@massey.ac.nz

To simply describe all the manipulations that can be performed and observations that can be made when undertaking a neurologic examination doesn’t give the sense of efficiency and flow that is necessary to effectively perform such examinations in practice. This presentation aims to assist the practitioner to develop a flow to the equine neurologic examination without detracting from the clinical dictum that “it is easy to look, but harder to see”; one has to know what one is looking for. PROCEDURE FOR THE NEUROLOGIC EXAMINATION The primary aim of a neurologic examination is to confirm whether or not a neurologic abnormality exists. Because omission of parts is the most common mistake made during the neurologic examination, the order in which the examination is performed becomes important. I give here a precise practical format that is logical in sequence, easy to remember with practice, and emphasizes the need for an anatomic diagnosis [Where is the lesion?] to be made before an etiologic diagnosis [What is the cause of the condition?] is made. The rationale for the sequence of this examination is: firstly, it starts at the head and proceeds caudally to the tail; secondly, it is used for patients of all sizes and whether the patient is ambulatory or recumbent; thirdly, it considers the anatomic location of lesions as the examination proceeds. Even if parts of the examination must be omitted because of the nature of the patient, suspicion of fracture, or financial constraints, the sequence ought to be followed through mentally. Frequently, the presence of a neurologic lesion[s] cannot be deduced until the end of a thorough neurologic examination. An outline of the recommended format for neurologic examination of horses is given in Table 1 and an example of a recording form to record the results of the neurologic examination is given in Figure 1. Some comment as to differences important to recall when evaluating neonates also are indicated. I encourage those readers who are not reasonably well practiced in performing neurologic examinations, and in recording the variety of responses obtained with direct observations, reflex testing and response induction in normal patients, to practice on a friendly, neighborhood, mid-sized dog. The approach for such an examination will be used for young foals and miniature horses. Should the practice dog or such patient be small enough, the close aspects of the procedure used are readily performed by sitting with the patient on one’s knees or standing above and behind the patient for restraint and comfort. Below is given an overview of the practicalities of performing an efficient neurologic examination. This is then followed by interpreting the findings to determine the presence, site(s) and extent of any neurologic lesion.

120

1. Head For the routine equine examination, I evaluate what I can from a distance, preferably before the patient is disturbed, for the first observations of behavior, mentation and head, neck, trunk and limbs. Head and neck deviations need to be assessed closely by straightening the neck along the midline to determine what asymmetry may be present. I allow the patient to smell my [often peppermint-tainted] hand for introduction and observe the face, particularly eyes and associated structures, for an expressional response. Then I examine the parts of the head and neck for evaluation of cranial nerve function [Table 2]. At this stage I will make sure I have the patient’s attention by tapping lightly once or twice above the eye with my finger tips on a cupped hand to induce a combined visual and facial response of palpebral closure, proceeding to a menace response from nasal and temporal fields. This is followed by observation of eye position and pupil size and symmetry using a bright pen torch from 40-50cm. Swinging the light quickly from the fundus of one eye to the other and pausing for about 3s at each pupillary aperture as the light source is brought closer in front of each eye, allows the immediate pupillary response to be observed, unencumbered by blinking. Any asymmetry or suspected deficit means that a dazzle response must be performed and the tests need to be reperformed in dim and bright light, but not direct sunlight. With practice, the central fundus and optic disc can be directly inspected by looking directly along the shaft of light from a pen torch; otherwise an ophthalmoscope should be used. Evidence of optic atrophy, peripapillary retinal lesions, globe position and trembling and ataxic eye movements and nystagmus all can all be detected. Eyeball position in the bony orbit, along with the size of the palpebral aperture and angle of the dorsal eyelashes then can be determined and both ventral movement and induced, normal, horizontal nystagmus of the globe then can be evaluated by first slowly raising the mandible to horizontal and then rotating the head to both sides through an arc of 60-90 degrees. Facial symmetry, reflexes, movement and especially muscle tone, all can then be observed as well as the bulk of the temporalis, masseter and pterygoid muscles being compared. During facial reflex testing with a blunt pair of needle holders sensation in the form of cerebral perception and resentment is evaluated from the nasal septum on each side. During this testing, any increased temperature and presence of sweat at the base of an ear will be evident. Nasal, oral, laryngeal, pharyngeal and hyoid region inspection and particularly palpation are performed and the thoracolaryngeal responses felt for. 2. Body a. Neck & Thoracic Limbs Attention is immediately moved to the neck where bone and muscle symmetry is assessed by close palpation and the local cervical and cervico-facial responses seen and felt. A solid blunt instrument such as 6-12 inch artery forceps or needle holders are best for performing this and other cutaneous testing although on occasion, with a very frightened patient, the tip of a rigid index finger may have to suffice as being more tolerated. A very firm vertical stimulus is required to be applied over sites at the level of and 10-15cm dorsal to the articular processes of cervical vertebrae.

121

b. Trunk & Pelvic Limbs Testing can continue caudally to transfer to the thorax testing the cutaneous trunci reflex over the mid third of the lateral thorax, again with forceful stimuli. There is a variable region over the point of the shoulder, about the C7-T3 dermatomal region, where neither responses are obtained and the cutaneous trunci reflex usually fades in the caudal thoracic region. Flexion, extension and lateral bending of the thoracolumbosacral vertebral column then is conveniently tested with the instrument used to firmly stroke the lateral dorsum from the withers to the caudal gluteal region. Two-pinch technique is used to test dorsal dermatomes and limb autonomous zones for areas of hypoalgesia if there is any evidence whatsoever of a reflex or lower motor neuron spinal cord lesion. Regional loss of muscle bulk, bony asymmetry and areas of sweating also should invoke detailed scrutiny. c. Rectum, Bladder, Anus, Tail Coccygeal extension and flexion is evaluated during anal reflex and perineal sensory testing. A strong, blunt-probe stimulus applied to the anal ring results in its brisk contraction and flexion [clamping] of the tail, whereas a light stimulus results in an anal reflex and with a stroking stimulus results in tail extension. 3. Gait & Posture The minimal components of evaluation of posture and gait consist of the following. • Walking in straight line viewed from the side as well as from behind and in front. • Pulling laterally on the tail with the patient standing still and while walking forward, assessing stride length and trajectory and placement of all four limbs. • Trotting away from and back toward the examiner. • Watching the patient walking in circles and turning tightly in circles in both directions. • Taking the patient oneself and by walking backwards lead the patient in a serpentine path to observe limb placement and lead in a manner such that the direction of each forefoot in turn is required to change direction during its swing phases. • Leading the patient to walk in circles and to turn tightly in circles in both directions, continuing these maneuvers while pulling on the lead rope and the tail simultaneously assessing strength of resistance. • Releasing the tail abruptly and stopping turning tightly to observe for adoption of and standing with abnormal limb positions. Manually placing the limbs in abnormal positions and placing them with the dorsum of the hoof resting on the ground are not useful in detecting neurologic motor or proprioceptive abnormalities. • Hopping the patient on at least the thoracic limbs. Defining the presence and severity of gait and postural abnormalities [Table 3], along with an interpretation of evidence of upper and lower motor neuron abnormal reflexes and function [Table 4] can assist in determining the site(s) of lesions in the nervous system. A patient that is or can be placed in recumbency can be tested for classical limb reflexes. In practical terms these simply consist of the flexor reflexes in thoracic and pelvic limbs and the extensor or patellar reflex in the pelvic limbs. A reflex is regarded as present or hyperactive in a limb if such a response is detected in the recumbent while the limb is uppermost OR is dependent. All other reflex testing really does not usefully contribute to a neuroanatomic

122

diagnosis and results of such additional limb reflex testing should not be used to alter a neuroanatomic diagnosis achieved by interpretation of the remainder of the examination. At the conclusion of the gait evaluation, any issue that is unclear can be returned to for further evaluation and confirmation, and further testing can be considered as appropriate. This will frequently include reassessing the menace and pupillary responses and nasal septal sensation, observing the patient for facial weakness and head deviation while it is resting quietly and undisturbed, blindfolding and, for the smaller patients, hemi-walking, hoping on pelvic limbs, wheel barrowing on thoracic limbs with head and neck held extended. For documentation, further study and possible consultation purposes, taking a video of any possible neurologic signs displayed by a patient is worth considering. It must be recalled however that a badly produced video clip is likely to be worse than a verbal or written description. At best, video sequences of neurologic movement abnormalities, particularly involving the gait, are less precise and accurate than in real life. Results of the neurologic examination should be documented and not left to memory [Figure 1]. After completion of the neurologic examination, the examiner may be able to decide if and where any possible lesion exists. There certainly are many syndromes described in various detail in which one suspects a neuromuscular lesion to account for the signs but none have been found to date *Table 5+. This may be because we haven’t looked in the right place for the morbid lesion, or there is a functional abnormality [e.g. channelopathy, transmitter defect] or a behavioural derangement. Bibliography Adams R and Mayhew IG. Neurologic diseases. Vet Clin North Am Equine Pract 1985; 1:209-234. Blythe LL and Engel HN. Back problems. Neuroanatomy and neurological examination. Vet Clin North Am Equine Pract 1999; 15:71-85. de Lahunta A, Glass E. Veterinary Neuroanatomy and Clinical Neurology. 3rd ed. W.B. Saunders Company. 2009. Furr M and Reed SM. eds. Equine Neurology. Blackwell. 2008. Lorenz MD, Coates JR, Kent M. Handbook of Veterinary Neurology. 5th ed. Elsevier Saunders. 2011. Mayhew IG. Large Animal Neurology. 2nd ed. Wiley-Blackwell. 2009. Palmer AC. Introduction to Animal Neurology. 2nd Ed ed. Blackwell Scientific Publications. 1976; 91-113. Reed SM, Bayly WM and Sellon DC. Equine Internal Medicine. 2nd ed. W. B. Saunders. 2004. Reed SM, Saville WJ and Schneider RK. Neurologic Disease: Current Topics In-Depth. 49th Ann Conv Amer Assoc Equine Pract; 2003.

123

TABLE 1: OUTLINE OF RECOMMENDED FORMAT FOR THE NEUROLOGIC EXAMINATION

Region Evaluation Division General Comment Neonate

Head Behavior Forebrain History important Seizures; especially mild and focal

Adjustment over 2-7 days

Mentation / Sensorium Thalamus Cerebrum Midbrain

Response to environment

Adjustment - 24 hours

Head Posture & Movement

Physical causes Forebrain – turn Vestibular – tilt Tremor – check eyeballs

Head tilt verses head turn

Flexed head posture Jerky movements

Cranial Nerves CN II - XII Brainstem Cervical sympathetic supply

Evaluate regions of head Subtle asymmetry in menace response & nasal sensation

Menace deficit <7 days Eye posture

Body Neck & Forelimbs C1-T2 Particularly asymmetry Flexor reflex only Hopping

All reflexes Hyperreflexia Crossed extension

Trunk & Hindlimbs T3-S2 L4 – femoral n. L5 – cranial gluteal n.

Particularly asymmetry Flexor & patellar reflexes only

All reflexes Hyperreflexia Crossed extension Extensor thrust

Rectum, Bladder, Anus, Perineum

S1-5 S1-2 is common fracture site

Tail Co1- Extension & flexion

Gait & Posture

ORTHOPEDIC PROBLEMS!

Shoulder & gluteal atrophy common Possible analgesic trial

SEPSIS!

Positional deficits All CNS-PNS Placing feet non-contributory

Prematurity

Extensor weakness Brain stem, spinal cord, PNS

Especially LMN Dominant extensor strength

Flexor weakness Brain stem,

124

spinal cord, PNS

Ataxia Spinal ataxia Irregular position & placement

Cerebellar ataxia

Hypermetria characteristic; F > H

Normal to degree

Vestibular gait Crouched posture Deliberate [predictable] stepping Wide based, staggering gait

Wide based to degree

125

126

127

128

A CLINICAL STUDY OF INDUCED PERENNIAL RYEGRASS [LOLITREM-B] INTOXICATION Joe Mayhew & Laura Johnstone Massey University Aotearoa i.g.mayhew@massey.ac.nz Funding By Equine Trust Massey Partnership for Excellence

Perennial Ryegrass Staggers is caused by mycotoxins from the endophyte Neotyphodium lolii that grows in perennial ryegrass, Lolium perenne. The major toxin is lolitrem-B that acts as a BK potassium channel blocker as shown in Fig 1. We fed 9 horses with known amounts of lolitrem-B contained in perennial ryegrass hay and seed according to Massey University Animal Ethics Committee guidelines. Clinical, neurologic, electrolyte and electrodiagnostic monitoring proceeded for at least 2 weeks before, during, and 2 weeks after feeding the trial feed. All horses showed clinical signs and all recovered. Plasma lolitrem-B levels increased during the trial feeding period but were not correlated with severity of clinical signs. Only minute amounts of lolitrem-B were present in urine. Major neurologic signs documented were: • Muscle tremor • Muscle fasciculation • Vestibulocerebellar ataxia • Eyeball tremor • Behaviour change Heart Rate increase and evidence for the presence of allodynia [excessive response to physiologic, non-painful stimuli] was obtained [see Fig 2]. Possible causes of this include effect via BK channel receptors in adrenal glands, dorsal root ganglia or hypothalamus, or via contaminating ergovaline [dopamine-D2 agonist]. Magnetic motor evoked potentials [mMEPs] were recorded and possibly demonstrated impaired motor conduction [Figure 3] in spite of there being no clinical weakness evident to the examiners. Early change in the fractional excretion of solutes *Δ FEx+ induced by frusemide *frusemide ~ Δ FEx(0 – 15min)] before and at the end of 2 weeks of exposure to lolitrem-B changed [Fig 4]. This parameter reflects how renal BK channels handling electrolytes respond to hi-pressure urine flow. Distal limb edema, superficial dermal necrosis on heels and serous nasal discharge occurred in more severely intoxicated horses that may have been due to ergovaline present in the feed. Body temperature did not change. A clear expression of perennial ryegrass staggers in horses due to lolitrem-B was obtained.

129

130

131

132

133

134

135

136

137

VERTEBRAL CANAL MEASUREMENTS IN ADULT HORSES PRESENTING AS WOBBLERS Joe Mayhew Massey University Aotearoa i.g.mayhew@massey.ac.nz

Abstract An equine wobbler is an ataxic horse, no more, no less. Thus, interpretation of precise neurologic examination findings along with results of ancillary test results – having due respect for accuracy and inaccuracy parameters of these – are relied upon to determine a primary clinical diagnosis and its associated likelihood of being correct. In general the more objective our test parameters are and the more cautious our probability estimates are, the more repeatable and reliable our diagnoses and prognoses are. In Aus, NZ and UK the pre-test probability [incidence] of cervical vertebral malformation [CVM] in a wobbler is likely to be lower than in North America [independent of EPM and WNV]. Thus we should be using tests with high sensitivity at the time of doing the test; which often will be well after the initiation of spinal cord compression, making myelography somewhat less sensitive a test. This talk aims to put the measurement of various clinical, laboratory and imaging test results in perspective with respect to evaluating wobblers in practice. Introduction Once the clinician has defined the presence of ataxia due to spinal cord disease as opposed to peripheral nerve, brainstem or cerebellar syndromes, use of ancillary aids can be useful to distinguish some of the common causes. Many cases of wobblers suffering spinal trauma and those with vertebral malformations such as congenital occipitoatlantoaxial defects in particular breeds are generally well defined with plain lateral radiographs. Spinal cord anomalies on the other hand may or may not be associated with vertebral changes evident with radiographic examinations. Confirmation of specific toxic myelopathies in vivo are often problematic and circumstantial evidence is often all that is available for clinical diagnosis of ataxia due to toxicosis associated with stinging nettle, ear mites, ivermectin, monensin, fluphenazine, swainsonine, vetch and sodium bromide (de Lahunta, 1983; Furr and Reed, 2008; Hahn et al., 1999; Mayhew, 1989, 2008; Woods et al., 1992). Numerous inflammatory and vascular processes result in spinal ataxia without apparent regard for region of the world. These include bacterial osteomyelitis, verminous myelitis, fibrocartilage embolic myelopathy and granulomatous myelitis (de Lahunta, 1983; Furr and Reed, 2008; Hahn et al., 1999; Innes and Saunders, 1962; Jubb and Huxtable, 1993; Mayhew, 1989, 2008; McGavin et al., 2001; Peters et al., 2003; Sullivan, 1985; Summers et al., 1995; Swain et al., 2005). It behooves the equine clinician to complete a thorough neurologic workup as early as possible in the course of all neurologic syndromes. This is particularly so as more is known about various spinal cord diseases and more advanced medical and surgical therapeutic regimens become available. Ancillary aids, such as neuroradiology, advanced computerized imaging techniques, electrodiagnostic testing and spinal fluid analysis can be of tremendous help in developing a

138

plan for treatment early in the course of disease, before permanent neurologic signs and the consequent hopeless outlook for return of function arise. A CSF sample is best taken at the lumbosacral space from patients with this syndrome because the fluid sampled is likely to be taken from closest to the lesion. Measurements from Radiographs of Wobblers to help Define CVM Plain radiographs in CVM cases usually indicate combinations of stenosis of the vertebral canal which is often exaggerated by flexion or extension of the vertebrae, and osteoarthrosis of the articular processes (Levine et al., 2007; Rantanen et al., 1981; Rendano and Quick, 1978; Van Biervliet et al., 2006; Whitwell and Dyson, 1987). To obtain true lateral cervical radiographs the horse should be in a sedated, standing position with a handler positioned out of the radiographic beam and pulling forward on the patient’s head collar to put added traction on the cervical vertebral column and thus straightening each vertebra along the median plain giving best alignment of vertebral bodies. Particularly in big sedated horses and especially with patients under general anesthesia, degrees of cervical torticollis result, which are difficult to correct for. Many normal variations and inconsequential findings must be realized in interpreting cervical radiographs (Rantanen et al., 1981; Rendano and Quick, 1978; Whitwell and Dyson, 1987). Thus the frequent finding in circa 5% of thoroughbred and Warmblood horses of transposition of ventral processes of C6 on to C5 and more often on to C7 on one or both sides must be considered when vertebrae are being identified on radiographs (Whitwell and Dyson, 1987) and at the time of any surgery. Other notable though usually inconsequential radiographic findings on equine cervical radiographs include: • variations and asymmetry in the shape of the intervertebral notches or orifices at the cranial border of C2; • irregularities to the dorsal aspect of the caudal physes of C2-C7 projecting into the intervertebral space; • separate ossification of the caudal projection of the transverse processes of C6 *occasionally transferred on to C5 or C7]; • serpentine lucent vascular channels in the spine of C2; • irregular border to the caudal aspect of the spine of C2; • irregular size and contour to the dorsal border of the spines of C3-C6; • circular 3-20mm, cyst-like lucencies of the arches and less often bodies of cervical vertebrae; • large and cranially-projecting, irregularly-mineralized spine of C7 [and T1]. Because narrowing of the cervical vertebral canal and associated spinal cord compressive lesions in horses’ necks are predominantly dorsoventral in orientation, measurements of minimal sagittal diameters [MSDs] have been used to compare a CVM candidate with a control population (Mayhew et al., 1978). These MSD measurements must be taken within a vertebra where the sagittal height of the canal is measured perpendicular to the floor of the canal [Figure 1] at its minimal value. This minimal value most often occurs near the cranial orifice but sometimes will, be near the caudal orifice. Values approaching or lower than those for the control population [Table 1] strongly indicate that compression likely is occurring. Significant angular deformities, severe osteoarthrosis, history or suspicion of trauma and indications that

139

transverse compression could be occurring also can be indications to suspect narrowing of the vertebral canal and to possibly proceed with a contrast myelographic study.

To correct for size of horse and for radiographic enlargement several concurrent radiographic measurements have been used as common denominators for correcting the absolute MSD measurements into corrected MSDs (Van Biervliet et al., 2006). The most favored of these correction factors is the dorsal height of the cranial physeal region at its maximum height, again measured perpendicular to the floor of the vertebral canal within that vertebra [Figure 1]. The

140

ratio of the MSD to the height of the cranial physis of the same body [C3 in the case of the axis] is referred to as the minimal intravertebral sagittal ratio [SR]. As a general rule of thumb horses with signs of cervical spinal cord disease that have SR values below 50% have a greatly increased risk of having cervical vertebral canal stenosis. With such a finding, and if there are other characteristics identified as in Figure 2 then CVM can be diagnosed with some degree of confidence. Of note here is that when developing reference ranges for MSD and SR values and when taking such measurements from radiographs of suspected cases of CVM, it must be clear which measurements are being taken. Firstly the minimal height of the vertebral canal within a vertebra may be anywhere along its length, not only near the cranial orifice. Secondly, with poor quality definition, under-exposed radiographs the MSD often is measured smaller than when measured from high quality radiographs taken of the same vertebrae and when compared to measurements obtained at post mortem examination. This most often occurs because the ventral margins of the pedicles of the articular processes are misinterpreted as the dorsal margin of the vertebral canal itself. In this situation an imaginary line drawn cranially along the lamina of the roof of the canal within the vertebra is extended in a slightly dorsal curvature to mimic the normal contour of the cranial orifice and through the radiodense pedicles to indicate where the height of the MSD will be measured to. Interpretation of such measurements must be predicated by the admission that the radiographic image is of inferior quality. The inclusion of intervertebral measurements for canal diameters [Figure 1] taken from standing lateral survey radiographs is likely to increase the discrimination of Types I and II CVM cases from non-CVM cases. These measurements can be corrected for horse size and radiographic magnification as has been done for the intravertebral sagittal ratios. Reference values can be developed for each diagnostic radiologic facility but as a guide Table 1 gives reference ranges for horses that were or were suspected to be ataxic and did not have cervical spinal cord compression based on full gross pathologic and neurohistologic evaluation. Notably, some of the SR cut-off points for this set of data using either mean less 2 SD or the absolute minimum values are below 50%. Prior to deciding on any surgical interference, myelographic evidence of spinal cord compression is accepted as being mandatory. Positive contrast myelography under general anesthesia is not an innocuous procedure in the horse (Beech, 1979; Nyland et al., 1980). Hemorrhagic, aseptic, neutrophilic meningitis occurs 6 to 48 hours following the procedure, which can be associated with complicated recoveries and often with fever (Nyland et al., 1980; Van Biervliet et al., 2004a). Digital radiographic imaging, experience with the procedure, modern anesthetic protocols and newer nonionic, water-soluble contrast agents such as iopamidol and iohexol have vastly improved the safety of this procedure and quality of resulting radiographic images making even ventrodorsal views through the caudal cervical region quite useful (May et al., 1986; Van Biervliet et al., 2004a; Widmer et al., 1998). Standing myelography in the conscious horse (Foley et al., 1986) is an unnecessarily painful process such that the procedure should only be performed under general anesthesia. Myelography is regarded as clinically necessary to demonstrate impingement on the spinal cord by a stenotic vertebral canal or by exuberant periarticular soft tissue or cyst, and with or without additional dynamic positioning in flexion and extension. Considerable care must be taken to not further compromise the spinal cord with excessive manipulation of the neck under

141

general anesthesia. With manual flexion the dorsal and ventral contrast myelographic columns can be totally obliterated in normal foals. Although unequivocal spinal cord compression can readily be determined with myelography, often subjective evidence of contrast-column compromise exists, which is of questionable significance because of the lack of definitive, objective criteria (Beech, 1979; May et al., 1986; Mayhew et al., 1978; Papageorges et al., 1987; Rantanen et al., 1981; Van Biervliet et al., 2002, 2004b). If a question is raised concerning the presence or not of a myelographic cervical spinal cord compression in a horse, then a degree of objectivity can be introduced by using minimal flexed dural sagittal diameter measurements, dorsal myelographic column reduction ratios and dural diameter reduction ratios (Hudson and Mayhew, 2005; Mayhew et al., 1978; Pujol and Mathon, 2003; Tomizawa et al., 1994c; Van Biervliet, 2004; Van Biervliet et al., 2006; Van Biervliet et al., 2002, 2004b). These measurements are well described and need to be available for specialty practices prepared to undertake invasive cervical vertebral surgery on horses with CVM. The use of 50% reduction of dorsal myelographic contrast column has been purported to be a very good criteria for compressive spinal cord disease and indication for surgery (Grant et al., 1985; Nout and Reed, 2003; Papageorges et al., 1987; Wagner, 1987; Walmsley, 2005). However, it appears that this is not the case and it is agreed that a 50% reduction of the dorsal myelographic column should not be used alone to diagnose CVM, nor used alone to plan surgical treatment at a site of suspected compression (Hudson and Mayhew, 2005; Mayhew and Green, 2002; Van Biervliet et al., 2002, 2004b). Better diagnostic accuracy is achieved by using a 20% reduction of the total dural diameter on neutral myelographic views for midcervical sites, and a 20% reduction of the same measurement at C6-7 with the neck in either neutral or flexed position (Van Biervliet, 2004). In this author’s experience the use of absolute minimal neutral and flexed dural sagittal diameter measurements (Hudson and Mayhew, 2005; Mayhew et al., 1978) still appear to be reasonably precise for defining the sites of spinal cord compression in cases of CVM and further data files should be forthcoming for this (Hahn et al., 2006). A group of workers in Japan have studied detailed relationships between morphologic measurements taken from cervical vertebrae in normal and CVM-affected young Thoroughbred horses (Tomizawa et al., 1994a, b). These workers then correlated their measurements (Mayhew et al., 1978) with histologic lesions and found that the accuracy of radiographically diagnosing CVM was very good but not completely precise (Tomizawa et al., 1994d). Finally, they developed complex measurements of ratios of stenosis from plain survey radiographs [Ss] and from myelograms [Sm] (Tomizawa et al., 1994c). The Ss compared the average sagittal diameter of the vertebral canal measured in the middle of each of two adjacent vertebrae with the extrapolated dural height between these vertebrae as measured from extensions of lines drawn along each dorsal lamina of the vertebral canals in each vertebra. Likewise the Sm compared the average sagittal diameter of the dural space measured in the middle of each of two adjacent vertebrae with the minimal flexed dural sagittal diameter (Mayhew et al., 1978) between these adjacent vertebrae. The conclusions were that Ss and Sm measurements were useful for the clinical diagnosis of CVM (Tomizawa et al., 1994c). In summary, using the various subjective [Figure 2] and semiquantitated measurements [Table 1] and calculations discussed above, the presence or absence of pathologic narrowing of the vertebral canal and consequent spinal cord compression then can be stated with some

142

confidence, backed by sensitivity and specificity accuracy parameters in the region of ~90%. In selecting criteria of high positive predictive value or high negative predictive value it behooves the radiologist and surgeon to decide beforehand whether advisable to err on the side of false positive diagnosis - and perform an occasional unnecessary surgical procedure - or on the side of false negative diagnosis - and leave a possibly surgically amenable compressive site unattended. As indicated, occasionally the compression in both Type I and Type II [arthritic] CVM cases can be transverse rather than dorsoventral. In Type I cases this is usually due to a kyphotic angular deformity [Figure 2] between C2-3, C3-4 or occasionally C4-5 (Hudson and Mayhew, 2005; Pujol and Mathon, 2003; Whitwell and Dyson, 1987). This is associated with ventral positioning of the pedicles and articular processes bringing the latter level with the lateral aspects of the spinal cord (Mayhew et al., 1978; Mayhew and Green, 2002). In horses with CVM, many times the intervertebral SR will still be abnormal even if the intravertebral SR measurement is not. Likewise in Type II cases with transverse compression the sagittal ratios are often small and prominent osteoarthropathy usually is present. On lateral myelography of these cases the dorsal and ventral contrast columns may not appear compressed and the minimal flexed dural sagittal diameter measurement may not be too small. However, a blanching of the overall contrast column, widening of the sagittal shadow of the spinal cord and sometimes the presence of two dorsal borders to the contrast column due to asymmetric dorsolateral intrusion of articular tissues, indicates spinal cord compression. This occurs most often at C6-7 and C7-T1 (Mayhew et al., 1978; Mayhew and Green, 2002). Thus, measurements taken from high quality, true lateral, standing radiographs of the neck from the base of the skull to T1 can be used to predict reasonably well the presence of current or recent spinal cord compression in a wobbler. If surgery is an option in an individual case then myelography is to be recommended to help confirm current compression of the spinal cord at a particular site or sites, or to attempt to negate this possibility. If no compression is deemed to be present and surgery is not thus an option then a decision is required as to whether to euthanize the patient under anesthesia or to progress to specific therapy for another disease. In conclusion, when evaluating wobblers suspected to suffer from CVM, clinicians, radiologists and surgeons must be aware that, although use of measurements taken from radiographs can improve the accuracy of diagnosis of CVM, there are no infallible, premortem diagnostic tests for the presence and absence of previous and current compression of the spinal cord. A decision must be made as to whether one minimizes the chance of recommending surgery on a horse [vertebral site] that does not require it OR minimizing the chance of failing to give the best chance of stopping progression of spinal cord compression. The attitude to performance horses undergoing surgical fusion of cervical vertebrae varies in different countries and such an atmosphere must be considered when advising on outcomes for wobblers suspected of having cervical spinal cord compression due to CVM. Bibliography Beech, J., 1979, Metrizamide myelography in the horse. J Am Vet Rad Soc 20, 22-31. de Lahunta, A., 1983, Veterinary Neuroanatomy and Clinical Neurology, 2nd Edition. W.B. Saunders Company, Philadelphia. Foley, J.P., Gatlin, S.J., Selcer, B.A., 1986, Standing myelography in six adult horses. Vet Radiol

143

Ultrasound 27, 54-57. Furr, M., Reed, S.M. 2008. Equine Neurology (Ames, Iowa, Blackwell), p. 412. Grant, B.D., Barbee, D.D., Wagner, P.C., al., e., 1985. Long term results of surgery for cervical vertebral malformation. In: 31st Ann Conv Am Assoc Equine Pract, pp. 91-96. Hahn, C.N., Handel, I., Bronsvoort, B.M., Green, S.L., Mayhew, I.G. 2006. Assessment of intra- and inter-vertebral minimum sagittal diameter ratios in the diagnosis of cervical vertebral malformation in horses. Hahn, C.N., Mayhew, I.G., MacKay, R.J., 1999, The Nervous System, In: Collahan, P.T., Mayhew, I.G., Merritt, A.M., Moore, J.M. (Eds.) Equine Medicine and Surgery. Mosby-Year Book Inc., St Louis, MO, pp. 863-996. Hudson, N.P.H., Mayhew, I.G., 2005, Radiographic and myelographic assessment of the equine cervical vertebral column and spinal cord. Eq Vet Edu 17, 34-38. Innes, J.R.M., Saunders, L.Z., 1962, Comparative Neuropathology. Academic Press, London. Jubb, K.V.F., Huxtable, C.R., 1993, The Nervous System, In: Jubb, K.V.F., Kennedy, P.C., Palmer, N. (Eds.) Pathology of Domestic Animals. Elsevier, p. 780. Levine, J.M., Adam, E., MacKay, R.J., Walker, M.A., Cohen, N.D., 2007, Confirmed and Presumptive Cervical Vertebral Compressive Myelopathy in Older Horses: a Multicenter Retrospective Study (1992-2004). J Vet Int Med 21, In Press. May, S.A., Wyn-Jones, G., Church, S., Brouwer, G.J., Jones, R.S., 1986, Iopamidol myelography in the horse. Equine veterinary journal 18, 199-202. Mayhew, I.G., 1989, Large Animal Neurology. Lea & Febiger, Philadelphia, PA, 380 p. Mayhew, I.G., 2008, Large Animal Neurology, 2nd. Edition. Wiley - Blackwell, Oxford. Mayhew, I.G., deLahunta, A., Whitlock, R.H., Krook, L., Tasker, J.B., 1978, Spinal cord disease in the horse. Cornell Vet 68 Suppl 6, 1-207. Mayhew, I.G., Green, S.L., 2002. Radiographic diagnosis of equine cervical vertebral malformation. In: Am Col Vet Int Med Forum. McGavin, M., Carlton, W., Zachary, J., 2001, Thomson's Special Veterinary Pathology, 3rd Edition. Mosby, St. Louis, MO. Nout, Y.S., Reed, S.M., 2003, Cervical vertebral stenotic myelopathy. Eq Vet Edu 15, 212-223. Nyland, T.G., Blythe, L.L., Pool, R.R., Helphrey, M.G., O'Brien, T.R., 1980, Metrizamide myelography in the horse: clinical, radiographic, and pathologic changes. American journal of veterinary research 41, 204-211. Papageorges, M., Gavin, P.R., Sande, R.D., Barbee, D.D., Grant, B.D., 1987, Radiographic and myelographic examination of the cervical vertebral column in 306 ataxic horses. Vet Radiol Ultrasound 28, 53-59. Peters, M., Graf, G., Pohlenz, J., 2003, Idiopathic systemic granulomatous disease with encephalitis in a horse. J Vet Med A Physiol Pathol Clin Med 50, 108-112. Pujol, B., Mathon, D., 2003, Wobbler syndrome in horses, cervical stenotic myelopathy. A review. Revue Méd. Vét 154, 289-306. Rantanen, N.W., Gavin, P.R., Barbee, D.D., Sande, R.D., 1981, Ataxia and paresis in horses. Part II. Radiographic and myelographic examination of the cervical vertebral column. Comp Cont Ed Pract Vet 3, S161-S171. Rendano, V.T., Quick, C.B., 1978, Equine radiology-the cervical spine. Mod Vet Pract 53, 921-929.

144

Sullivan, N.D., 1985, The nervous system, In: Jubb, K.V.F., Kennedy, P.C., Palmer, N. (Eds.) Pathology of Domestic Animals. Academic Press, Orlando. Summers, B.A., Cummings, J.F., de Lahunta, A., 1995, Veterinary Neuropathology. Mosby, St. Louis, MO., 527 p. Swain, J.M., Hudson, N.P., Rhind, S.M., Baird, P.M., Mayhew, I.G., 2005, A novel, progressive, sclerosing panencephalitis in a horse. Equine veterinary journal 37, 276-280. Tomizawa, N., Nishimura, R., Sasaki, N., Hayashi, Y., Senba, H., Hara, S., Kadosawa, T., Takeuchi, A., 1994a, Morphological analysis of cervical vertebrae in ataxic foals. The Journal of veterinary medical science / the Japanese Society of Veterinary Science 56, 1081-1085. Tomizawa, N., Nishimura, R., Sasaki, N., Hayashi, Y., Senba, H., Hara, S., Kadosawa, T., Takeuchi, A., 1994b, Morphometrical analysis of the cervical vertebrae of Thoroughbred foals. J Equine Vet Sci 5, 95-99. Tomizawa, N., Nishimura, R., Sasaki, N., Kadosawa, T., Senba, H., Hara, S., Takeuchi, A., 1994c, Efficacy of the new radiographic measurement method for cervical vertebral instability in wobbling foals. The Journal of veterinary medical science / the Japanese Society of Veterinary Science 56, 1119-1122. Tomizawa, N., Nishimura, R., Sasaki, N., Nakayama, H., Kadosawa, T., Senba, H., Takeuchi, A., 1994d, Relationships between radiography of cervical vertebrae and histopathology of the cervical cord in wobbling 19 foals. The Journal of veterinary medical science / the Japanese Society of Veterinary Science 56, 227-233. Van Biervliet, J., 2004. Value of contrast radiography in the assessment of cervical spinal lesions. In: Brit Eq Vet Assoc Congress, pp. 278-279. Van Biervliet, J., Flaminio, J., Divers, T., Nixon, A., Summers, B., Nydam, D., 2004a. The febrile response after cervical myelography in the horse: a retrospective analysis and experimental study. In: Am Col Vet Int Med Forum. Van Biervliet, J., Mayhew, J., de Lahunta, A., 2006, Cervical vertebral compressive myelopathy. Clin Tech Eq Pract 5, 54-59. Van Biervliet, J., Scrivani, P.V., Divers, T.J., Erb, H.N., de Lahunta, A., Nixon, A., 2002. Evaluation of a diagnostic criterion for spinal cord compression during cervical myelography in horses. In: Am Col Vet Int Med Forum. Van Biervliet, J., Scrivani, P.V., Divers, T.J., Erb, H.N., de Lahunta, A., Nixon, A., 2004b, Evaluation of decision criteria for detection of spinal cord compression based on cervical myelography in horses: 38 cases (1981-2001). Equine veterinary journal 36, 14-20. Wagner, P.C., 1987, Large Animal Vertebral and Spinal Cord Surgery, In: Oliver, J.E., Hoerlein, B.F., Mayhew, I.G. (Eds.) Veterinary Neurology. WB Saunders, Philadelphia, pp. 459-469. Walmsley, J.P., 2005, Surgical treatment of cervical spinal cord compression in horses: a European experience. Eq Vet Edu 17, 39-43. Whitwell, K.E., Dyson, S., 1987, Interpreting radiographs. 8: Equine cervical vertebrae. Equine veterinary journal 19, 8-14. Widmer, W.R., Blevins, W.E., Jakovljevic, S., Levy, M., Teclaw, R.F., Han, C.M., Hurd, C.D., 1998, A prospective clinical trial comparing metrizamide and iohexol for equine myelography. Vet Radiol Ultrasound 39, 106-109. Woods, L.W., Johnson, B., Hietala, S.K., Galey, F.D., Gillen, D., 1992, Systemic granulomatous disease in a horse grazing pasture containing vetch (Vicia sp.). J Vet Diagn Invest 4, 356-360.

145

SEIZURES, SYNCOPE AND SLEEP ATTACKS Joe Mayhew Massey University Aotearoa i.g.mayhew@massey.ac.nz

True episodic events wherein the horse is totally normal between events are not so common in equine practice, and, because they are often not witnessed by veterinarians, they conjure up hobgoblin and wacky diagnoses – strokes and brain tumors in particular. The principal disorders covered here will be epilepsy [recurrent seizures] and sleep disorders in horses. As with other species, video capture of events is a powerful tool in making the diagnosis. Therapies are available but should only be undertaken after careful considerations. The potential confounding influences of third parties such as Insurance Companies on clinical management must not be underestimated. INTRODUCTION Seizures, abnormal sleep patterns and syncope, can be difficult to distinguish apart. The last of these, occurring in the absence of heart failure, is incredibly rare but the first 2 are quite distinguishable if observed. A [24-hour] video recording can be useful to capture suspected episodes of sleep and seizures when they are not overt. SLEEP DISORDERS Sleep disorders can be divided into narcolepsy [pathologic sleep patterns] with cataplexy [somatic motor paralysis], narcolepsy without cataplexy and idiopathic hypersomnia [excessive sleepiness]. Narcolepsy occurs in 0.02 - 0.15% of the human population and patients typically demonstrate excessive diurnal sleep, flaccid paralysis with somatic areflexia [cataplexy], sleep paralysis, sleep-onset hallucinations and nocturnal disrupted sleep. Strict EEG and EOG criteria, including the early onset of rapid eye movement (REM) at the beginning instead of the middle of a sleep cycle, are in place for confirming the diagnosis and distinguishing narcolepsy from narcolepsy without cataplexy and from idiopathic hypersomnia. A familial form occurs in dogs and humans and in the latter it is associated with the genetic allele HLA-DQβ1-0602. Narcolepsy without cataplexy shares the same electrophysiological abnormalities and associated signs but there is no demonstrable cataplexy. Purely excessive daytime sleep attacks [wittingly referred to as unwanted siestas] occur in idiopathic hypersomnia. Regarding the pathophysiology, 2 novel neuropeptides, hypocretins [orexins] 1 and 2, were found to be specifically expressed in certain hypothalamic neurons and defective hypocretin signaling was related to both familial and sporadic narcolepsy. A mutation in the hypocretin receptor-2 gene was present in dogs with familial narcolepsy although they had normal levels of hypocretins in their CSF and hypothalamus. Neurotransmission through hypocretin-1 was likely to be intact indicating that defective hypocretin-2 function is more important in producing narcolepsy in that model. In contrast, dogs with sporadic narcolepsy had no expressed hypocretins in the CSF or brain tissue. In the sporadic and some familial forms of the disease various pieces of evidence indicate that there may be an autoimmune attack on hypocretin-producing neurons and decreased

146

hypocretin-expressing neurons in the hypothalamus have been reported. Attempts to identify a neural autoantibody in canine and human narcolepsy have been unsuccessful. Also, evidence for the presence of a functional, IgG autoantibody, that upregulates cholinergic activity [being a characteristic of narcolepsy], being present in serum of narcoleptic humans and not in controls, has been presented. Further evidence that the immune system plays a role in canine genetically dependant narcolepsy has been published. This study found that immunosuppressive and anti-inflammatory drugs delayed the onset and severity of narcolepsy and cataplexy in treated dogs compared to controls. Results of attempts at treating narcolepsy in dogs with prednisolone and systemic and intrathecal hypocretin-1 have been poor, perhaps because of depleted hypothalamic neurons. Using imipramine for the narcolepsy and yohimbine *an α-2 antagonist to activate adrenergic transmission] for the cataplexy showed promise. Sleep Disorders in Foals Many normal newborn foals can be induced into a cataplectic state by firm, whole-body restraint *‘cuddling’+ to sometimes even lie still on the ground when released. This response wanes rapidly over a few days. It has been postulated that this phenomenon is a persistence of a protective mechanism that stops violent reflex movement occurring in utero. An early onset, probably familial form of narcolepsy with cataplexy *“fainting foals”+ has been seen in at least Suffolk, Shetland Pony, Fell Pony, Warmblood and Miniature Horse foals. Signs of daytime sleepiness and episodes of partial to total cataplexy [flaccid paralysis with limb areflexia] begin at several weeks of age. Some form of stimulation, such as grooming or petting or feeding, may induce episodes. Between attacks there is no neurologic abnormality. Pharmacologic testing has helped confirm the diagnosis and some foals have shown improvement while on imipramine given at 1-2mg.kg-1, bid to qid. Although it has been difficult to document REM sleep at the onset of a full attack, this syndrome almost certainly is true familial narcolepsy with cataplexy. Affected foals remain affected though some have had a decrease in severity, duration and frequency of episodes with time. Sleep Disorders in Adult Horses Although some syndromes of adult onset sleep attacks may well be true narcolepsy, complete cataplexy with limb atonia and areflexia, as well as REM sleep at the onset of an episode, do not appear to have been documented. Thus, it is most likely that at least some of these cases are examples of sporadic idiopathic hypersomnia. Many breeds and crossbreeds have been affected and there is a wide range in the age at onset of signs. Signs range from drowsiness with hanging of the head and buckling at the knees, to sudden and total collapse with the horse mostly awakening before becoming recumbent. Some horses will fall and may injure their lips, face, or dorsal fetlocks or knees, but usually get up quietly within seconds to a minute or so. Chronic traumatic lesions at these sites can be the client’s primary complaint. Periodicity varies from one attack every few weeks to more than 10 per day. When forced to walk, horses having a sleep attack may appear incoordinated. Some form of pleasurable stimulation, such as grooming, petting, washing down, or leading the horse out of a stall or into a pasture, may in a few cases precipitate an attack. Some horses learn to rest their mandibles on a half door or sit back on a manger while in a sleepy state to appear to help prevent collapsing. This can result in chronic scarring under the mandibles or on the points of

147

the hocks. Narcoleptic attacks while under saddle have been reported in three horses to my knowledge, indicating that riding may present a significant safety risk. The condition usually does not worsen; although some affected aged mares have relentless progression of signs to the point of frequent and abrupt periods of collapse, resulting in severe knee and face trauma. Attacks can be induced with the cholinesterase inhibitor, physostigmine (0.06 to 0.08 IV mg.kg-1), although lack of a positive response to physostigmine does not rule out a diagnosis of narcolepsy, and side effects, particularly diarrhea, can accompany its use. Narcolepsy is induced within minutes of physostigmine administration. Caution is required in carrying out the provocative test because the drug can cause colic. Atropine 0.08 mg.kg-1 IV resolves signs of narcolepsy and cataplexy for up to 30 hours after administration. For longer-term control, the tricyclic antidepressant drug, imipramine, may be useful. This can be given at 1-2 mg.kg-1 1M or IV 2 or 3 times daily. Signs may be relieved for 5 to 10 hours without side effects. Unfortunately, oral administration of imipramine is not reliable in adult horses. Unfortunately, such responses to drugs do not help differentiate the various forms of seep attacks. As suggested above it is likely that some of these cases are examples of sporadic idiopathic hypersomnia and may represent “not a pathologic entity in itself, but rather the consequence of chronic sleep deprivation in very long sleepers”. In fact a few horses have responded to long term NSAID therapy by not only reducing the daytime sleepiness and partial collapsing episodes, but have begun to lay down more. This suggests that the horse not lying down due to a painful condition such as bilateral spavin or discospondylosis caused added sleep deprivation. SEIZURES AND EPILEPSY Fortunately, horses have a relatively high seizure threshold, as it seems to take a considerable insult to the forebrain to precipitate convulsions. Younger animals, particularly neonatal foals, convulse more readily than adults do. Foals frequently demonstrate mild generalised seizures seen as periods of jaw chomping ("chewing-gum fits"), tachypnea, tremor of facial muscles and jerky head movements. The post-ictal phase of depression and temporary blindness lasts for minutes or even for days following one or more generalised seizure, particularly in foals. The seizure threshold tends to be lowered at quiet or pleasurable times. Thus seizures often occur at night and are not witnessed. Epilepsy may occur in conjunction with other signs of forebrain disease persistent during the inter-ictal period. These may be quite subtle and consist of degrees of blindness seen as an asymmetric menace response, asymmetric hypoalgesia from the nasal septum, an asymmetric hopping response on the thoracic limbs and a tendency to drift to one side when blindfolded and asked [not led] to walk straight forward. Epilepsy in Foals Repeated seizures in neonatal foals usually indicate sepsis and/or hypoxic/ischemic encephalopathy. Adolescent foals, especially Arabians, can suffer from epilepsy that is probably of genetic origin. The seizures usually are symmetrical and generalised and the first seizure may follow an episode of sepsis or other acquired disease. Control of the seizures with medication usually is successful and the patients appear to grow out of the condition. Finally, although not true epilepsy foals with severe cerebellar disease have been seen to have ‘convulsive episodes’ regarded as ‘cerebellar fits’ but they are aware of their environment during these attacks.

148

Epilepsy in Adult Horses Repeated generalized seizures, with no active underlying disease process and occurring in families of purebred animals [ie true or idiopathic epilepsy] does not appear to have been demonstrated in adult horses. Thus, epilepsy in adult horses can be regarded as acquired until proven otherwise. Any morbid or biochemical forebrain lesion potentially can act as a seizure focus and the resulting epileptic syndrome may begin days to years after the initial lesion. Also, a non-progressive cerebral lesion such as an old glial scar may result in epilepsy that resolves progresses or remains stable. If the horse is essentially healthy with minimal [see above] or no neurologic signs evident between seizures then most possible causes of cerebral disease including viral encephalitis, hepatoencephalopathy, leukoencephalomalacia [Fusarium sp. mycotoxicosis] and other toxicities are exceedingly unlikely to be causes of epilepsy. Three diseases at least should however be given consideration as underlying specific causes. In horses that have been on the American Continent, equine protozoal myeloencephalitis [EPM] caused by Sarcosystis neurona must be considered and serum and cerebrospinal immunoassay tests be performed so that appropriate treatment can be initiated if the tests are positive. In most countries consideration should be given to treatment for thromboembolic and migratory verminous encephalitis at the beginning of an epileptic syndrome using larvacidal doses of anthelmintics and NSAID and/or glucocorticosteroids. Cases with bacterial granulomatous ependymitis/choroiditis and true brain abscesses can be insidious in there clinical progression and one or more seizures may be the initial overt sign. Most times inter-ictal signs including those indicated above will be detected on a full neurologic examination. Surgical and antibacterial therapy is feasible but heroic. IF AND WHEN TO START ANTICONVULSANT THERAPY To begin with it must be reported to the owner that a patient with epilepsy is unsafe to ride until seizure-free and not on anticonvulsant medication for at least 6 months. Also, if the horse injures itself to require veterinary attention [to document the injury for the record] then euthanasia must be considered. With respect to this decision and in reporting to an Insurance Company, it is reassuring to have a video of one of the seizures and to have some, albeit subtle, inter-ictal sign to document that the horse has epilepsy associated with an acquired intracranial disease. On the other hand, a sensible owner can be advised that the vast majority of seizures will occur at quiet times and not while working; the written report however must state that the horse is unsafe. The client should be encouraged to keep an accurate diary of known and suspected seizure episodes particularly noting pre-ictal signs, site on the body where the seizures begin and the severity and timed duration of seizures. This will allow a best prediction, as to whether the epilepsy is stable, resolving or progressing, to be made. Should individual seizures be occurring say less than one every month and the patient does not injure itself to require veterinary attention then medication probably is not indicated. If there are cluster seizures, or status epilepticus, or more than one seizure a month, or the patient injures itself to require veterinary attention and the client does not accept euthanasia as an option, then anticonvulsant therapy must be considered.

149

A GUIDE TO ANTICONVULSANT THERAPY IN HORSES For acute control of seizures in adult horses 50mg IV doses of diazepam should be used. If this is not available then standard doses of α-2 agonist drugs can be used. If these are ineffective then general anaesthesia is indicated and at this stage euthanasia must be strongly recommended. The following is a guide to maintenance anticonvulsant therapy to help control seizures in epileptic adult horses:- • Have the owner keep a diary of seizure activity and all medication given. • Administer phenobarbitone at 5 mg/kg-1 SID, PO. • Increase the dose 20% every 2 weeks until seizures are controlled to a tolerable level. • If the side effect of unacceptable sleepiness occurs and seizures are not controlled, reduce dose 20% and add KBr at 25 mg/kg-1 SID, PO. • Consider loading dose of ~8 times the normal dose for KBr given over the first 24 hours. • After control, monitor serum concentrations and aim to keep them in the therapeutic ranges:- phenobarbitone, 15-40 μg/ml-1; bromide, 1000-4000 μg/ml-1. • If the patient is completely seizure free for 6 months then slowly wean the patient off one drug at a time over 3 months. If seizures begin, raise the dose(s) again. • Ivermectin, a potentiator of inhibitory GABA-ergic synapses [and probably all the avermectins], should not be given to horses on anticonvulsant therapy because of the risk of breaks in seizure control that have occurred following its use. • Other drugs can be expected to change anticonvulsant drug pharmacodynamics. REFERENCES ON REQUEST

150

HYPONATRAEMIC SEIZURES IN FOALS JE Axon, JB Carrick, CM Russell, NM Collins Scone Equine Hospital, Scone NSW 2337

Hyponatraemia is a commonly reported biochemical abnormality in foals and when severe

(<122mmol/L), it has been associated with subtle to severe neurological deficits (Green and

Mayhew 1990; Hurcombe 2008). Severe hyponatraemia has been described in foals with

diarrhoea, uroperitoneum, acute renal failure, inappropriate antidiuretic hormone (ADH)

release, hydroureter syndrome, rhabdomyolysis, pseudohypoaldosteronism and overzealous

administration of water enemas or excessive water intake (Green and Mayhew 1990; Perkins,

Valberg et al 1998; Hurcombe 2008; Divers 2011). There are however only limited reports

published on foals with neurological deficits associated with severe hyponatraemia (Lakritz,

Madigan et al 1992; Wong, Sponseller et al 2007).

The following study reports on the clinical findings, treatment and outcome of foals presenting

to SEH Clovelly Intensive Care Unit with neurological deficits attributed to hyponatraemia.

Material and methods

Medical records from January 2002 to December 2010 for foals (<6mths of age) that were

admitted to Clovelly Intensive Care Unit, Scone Equine Hospital with a serum sodium

concentration less than 122 mmol/L on admission were retrieved. Those with abnormal

neurological signs were identified. Information obtained from the medical records included

signalment, history, presenting clinical signs, clinicopathologic data, treatment and short- and

long-term survival.

Results

Sixty foals were identified with serum sodium concentrations < 122 mmol/L. The serum sodium

concentrations ranged from 98 mmol/L to 121 mmol/L. Of the 60 foals, 12 (20%) presented

with abnormal neurological signs, five of these were admitted with grand mal seizures. The

abnormal neurological signs included ataxia, head pressing, facial grimacing, apparent

blindness, muscle fasciculations, hypermetria, and aimless wandering. The abnormal

neurological signs in 11 of the 12 foals were attributed to severe hyponatraemia. The clinical

cause of the hyponatraemia in these foals was identified as renal dysfunction in nine cases,

diarrhoea in two cases and multiorgan dysfunction in a critically ill neonate. One case with

diarrhoea also had renal dysfunction. Foals with renal dysfunction had abnormal fractional

excretion of electrolytes, azotaemia (not associated with dehydration), casts and renal tubular

epithelial cells on urinalysis, and/or low creatinine clearance times.

151

Serum sodium concentrations of the 12 foals with neurological signs ranged from 99 mmol/L to

121mmol/L. The foal with the serum sodium concentration of 121mmol/L was admitted at 6hrs

of age with grand mal seizures and was diagnosed with neonatal syndrome and sepsis thus the

seizure activity was attributed to neonatal encephalopathy, not hyponatraemia. The other 11

foals’ serum sodium concentration ranged from 99 to 114 mmol/L. Their calculated osmolalities

ranged from 209.2 to 258.33 mOsm/kg (reference range: 275 to 312 mOsm/kg).

Treatment consisted of therapy aimed at the primary disease and correction of the

hyponatraemia. No complications were reported following correction of the serum sodium

concentrations.

Two cases died, one could be attributed to the hyponatraemic seizures causing upper airway

obstruction; the other was due to the primary diseases (neonatal syndrome and sepsis). Of the

ten surviving cases, two died after discharge of unknown causes and eight continued onto to be

verified, named and/or raced.

Conclusion

Renal dysfunction was the most common cause of severe hyponatraemia in the foals

presenting with neurological signs. The favourable outcome in this group of foals should

encourage practitioners to pursue the appropriate treatment of foals presented with

neurological dysfunction due to hyponatraemia.

References

Divers, TJ (2011). Disorders of the bladder, ureters and urethra. In McKinnon AO, Squires EL,

Vaala WE, Varner DD editors: Equine Reproduction. Ed 2, West Sussex, Wiley-Blackwell. Vol 1:

625-631.

Green, SL, Mayhew IG (1990). Neurological disorders. In Koterba AM, Drummond WH, Kosch

PC, editors: Equine Clinical Neonatology. Philadelphia, Lea & Febiger: 496-530.

Hurcombe S (2008). Electrolytes and neurological dysfunction in horses. In Furr, M Reed S

editors: Equine Neurology. Iowa, Blackwell Publishing: 269-282.

Lakritz, J, Madigan JE, Carlson GP (1992). Hypovolemic hyponatremia and signs of neurological

disease associated with diarrhea in a foal. JAVMA 200: 1114-1116.

Perkins, GA, Valberg, SJ, Madigan, JE, Carlson, GP, Jones, SL (1998). Electrolyte disturbances in

foals with severe rhabdomyolysis. J Vet Intern Med 12 173-177.

Wong, DM, Sponseller BY, Brokus C, Fales-Williams AJ. (2007). Neurologic deficits associated

with severe hyponatremia in 2 foals. JVECC 17: 275-285.

152

NEUROSTEROID: KEY REGULATORS AND PROTECTORS OF THE FETAL BRAIN

JONATHAN J. HIRST1,2, MEREDITH A. KELLEHER1,2, DAVID W. WALKER3, HANNAH K. PALLISER1,2 1Mothers and Babies Research Centre, John Hunter Hospital, Newcastle,

2School of Biomedical Science, University

of Newcastle, Newcastle. 3Monash Institute for Medical Research, Monash University, Melbourne. Email:

jon.hirst@newcastle.edu.au.

Neurosteroids are synthesized in the CNS from peripheral precursors or directly from

cholesterol and have a key role regulating behavioral state and excitability. The most important

-reduced metabolites of progesterone including allopregnanolone.

These steroids exert their action by modulation of GABAergic transmission in addition to

potential actions via steroid receptors. During pregnancy allopregnanolone is synthesized from

placental progesterone and concentrations in the fetal blood and brain are remarkably high

compared to the adult. These concentrations fall dramatically following the removal of the

placenta at birth. In previous studies we have shown that fetal 5α-reductases are rate-limiting

in controlling allopregnanolone levels in the fetal brain (Yawno, Walker, Hirst et al., 2007).

Moreover this production exerts a major control over fetal CNS excitability. We used a sheep

model of perinatal hypoxaemia that involves a 10min occlusion of the umbilical cord (UCO) to

examine the role of allopregnanolone in fetal compromise. We found that inhibition of

allopregnanolone synthesis, using the 5 -reductase inhibitor finasteride, markedly exacerbated

brain injury induced by transient UCO. These findings showed that allopregnanolone reduced

excitotoxicity and by doing so acts to reduce brain injury. During these studies we showed that

allopregnanolone levels in the brain rise after UCO suggesting that increased allopregnanolone

production represents an endogenous mechanism to protect the fetal brain (Nguyen, Yan,

Castillo-Melendez, et al., 2004). In addition, we showed that normal levels of allopregnanolone

have a role in regulating late gestation cell proliferation in the fetal hippocampus suggesting

this steroid has a role in late gestation development, and potentially in repair processes,

following hypoxic/ischaemia brain injury (Yawno, Walker, Hirst et al., 2007).

These findings led us to develop a guinea pig model of placental insufficiency to examine the

role of allopregnanolone in chronic compromise during late gestation. In these studies we

ablated 50% of the uterine artery branches supplying each placenta during mid-gestation (35

days; term = 70 days). This procedure resulted in asymmetric fetal growth restriction with a

~35% reduction in body weight. The fetuses from these pregnancies exhibited significantly

-reductase-2 enzyme expression in the fetal brain and allopregnanolone levels were

suppressed (Kelleher, Palliser, Walker et al. 2011). This work suggested that reduced

availability of neurosteroids in the growth restricted fetus may contribute to vulnerability to

brain injury, particularly an increased susceptibility to hypoxia/ischaemia-induced damage

around the time of birth. The finding that there was an associated reduction in myelin basic

153

protein (MBP) expression in these fetuses further indicates that a deficiency in neurosteroid

production may account for the reduced myelination seen after delivery of growth restricted

neonates.

The observations from this work indicated that adequate exposure to the normal gestational

neurosteroid environment is essential not only for protecting the fetal brain from adverse

events, but also for the appropriate late gestation neurodevelopment. This suggested the

premature decline in neurosteroid levels in the brain that occurs following preterm birth may

contribute to the poor neurodevelopmental outcomes in these pregnancies. Furthermore

neurosteroid supplementation of neonates following preterm birth may be of value in

improving outcome. To investigate these proposals we examined outcome following preterm

birth in guinea pigs. For these studies guinea pig neonates were delivered by c-section at 62-63

days gestation (preterm) or at 69 days (~term). Preterm neonates were managed with

surfactant treatment, received ventilatory support, assisted feeding and were maintained in an

incubator. Groups of neonates received twice daily progesterone treatment or vehicle from

postnatal day 1 until term equivalence (8 days postnatal). Both the term and untreated

preterm neonates exhibited a significant decrease in brain allopregnanolone concentrations

after birth. The preterm neonates also had markedly reduced expression of MBP, glial fibrillary

acidic protein (GFAP) and 5α-reductase-2 when compared to levels seen in term neonates. In

preterm animals, MBP expression in the hippocampus (CA1 region) remained reduced at

postnatal day 8. This suggests at term equivalent age late developmental processes in these

preterm neonates have not completely caught up to term levels. Progesterone treatment

successfully increased salivary progesterone and allopregnanolone concentrations in the brain

and so supplemented brain levels to those that would have been present had the neonates

remained in utero. In conclusion, the progesterone therapy used in these studies successfully

increased brain allopregnanolone levels, suggesting that the immature neurosteroid system in

the preterm brain is sufficient for allopregnanolone synthesis if precursors are made available.

These findings support the potential of progesterone replacement in preterm neonates as a

possible therapeutic avenue to improve brain development and neurological outcomes.

Kelleher MA, Palliser HK, Walker DW, Hirst JJ. (2011) Sex-dependent effect of a low

neurosteroid environment and intrauterine growth restriction on foetal guinea pig brain

development. Journal of Endocrinology 208:301-9

Nguyen PN, Yan EB, Castillo-Melendez M, Walker DW, Hirst JJ. (2004) Increased

allopregnanolone levels in the fetal sheep brain following umbilical cord occlusion. Journal of

Physiology 560: 593-602

Yawno T, Yan EB, Walker DW, Hirst JJ. (2007) Inhibition of neurosteroid synthesis increases

asphyxia-induced brain injury in the late gestation fetal sheep. Neuroscience 146: 1726-1733

154

HORNER’S SYNDROME VERSES FACIAL PARESIS Joe Mayhew Massey University Aotearoa i.g.mayhew@massey.ac.nz

Total facial paralysis involving all three components, the auricular, palpebral and buccal branches, of cranial nerve seven [the facial nerve, CNVII] is easily identified. Also, with damage to the sympathetic supply to the face and subsequent eye signs of Horner’s syndrome and sweating over the whole side of the face extending a variable distance down the neck, also is readily identified. However, paresis of facial muscles, especially involving just the palpebral branch can result in a syndrome quite similar to that seen with the mild *eye+ signs of Horner’s syndrome when the tatter is due to an incomplete lesion or to involvement just of the sympathetic supply to the eye and not to the whole face. In an attempt to clarify this clinical dilemma, it will be worth reviewing the anatomy and physiology of autonomic and somatic control of the face and its associated structures (Mayhew, 2009; Mayhew, 2010). Sympathetic Innervation to the Eyes and Head Nuclei within the brain that control sympathetic motor function are located in the hypothalamus, midbrain, pons and medulla oblongata. First order neuronal fibers descend through the midbrain, medulla and cervical spinal cord to synapse on cell bodies in the lateral intermediate gray columns in the thoracolumbar spinal cord. The preganglionic, second-order, sympathetic cell bodies supplying the head and neck are situated in this position in the cranial thoracic segments, T1-T3. Axons leave these segments of the spinal cord, traverse the cranial thorax, ascend the neck in the cervical sympathetic trunk adjacent to the vagus nerve and pass to the cranial cervical ganglion that lies under the cranial part of the atlas. In the horse, this ganglion is on the caudodorsal wall of the medial compartment of the guttural pouch. Postganglionic, third-order, sympathetic fibers leave the cranial cervical ganglion to innervate the glands, smooth muscles and blood vessels of the eyeball, head and cranial cervical area down to ~C2 [Figure 1]. Sympathetic fibers supplying skin of the neck from C2-C8 leave the parent bundles in the thorax and pass cranially with the vertebral vessels running in the lateral vertebral foramina to segmentally join the vertebral nerves supplying each cervical dermatome. Damage to the sympathetic supply to the eye and its associated structures results in slight ptosis of the upper lid, a miosis or constriction of the pupil, slight enophthalmos and a slight protrusion of the nictitating membrane [Figure 2]. Vision and the pupillary light responses are unaffected. In most species this is referred to as Horner’s syndrome. The degree of miosis seen in sympathetic denervation of the eye *Horner’s syndrome+ is not dramatic in horses. Horner’s syndrome alone can be seen with retrobulbar lesions involving postganglionic sympathetic fibers. In addition, hyperemic mucous membranes of the head [Figure 10-3], hyperthermia of the face and in horses sweating of the face and cranial neck are evident with more proximal sympathetic lesions [Figure2]. These latter findings are caused by the interruption of sympathetic fibers to the blood vessels and sweat glands of the head and neck (Smith and Mayhew, 1977). With cutaneous vasodilation more circulating adrenalin is brought to the sweat glands and this neurohormone has powerful sudomotor effects in horses (Jenkinson et al.,

155

2006). If the sympathetic fibers are affected at the level of, or distal to, the cranial cervical ganglion in the wall of the guttural pouch, sweating over the head projects caudal only to the level of about the atlas. Preganglionic lesions proximal to this level, as in the neck, result in sweating further down the neck to about the level of C2 to C3 (Usenik, 1957). Cranial thoracic lesions can affect the sympathetic fibers not only in the cervical sympathetic trunk but also those innervating the skin of the remainder of the neck travelling with the vertebral nerve and segmental dorsal spinal nerve roots. There then is sweating over the whole neck and head. A first order sympathetic neuronal lesion in the descending, tectotegmentospinal tract in the brainstem or cervical spinal cord, results in sweating on the whole side of the trunk, neck and head as well as the eye signs of Horner’s syndrome (Mayhew, 1980). Of some diagnostic interest is that at least horses with acute sympathetic lesions and distributions of sweating, administration of α-2 agonist sedative drugs will result in expected sweating over normal skin of the body but often reverses the vasodilation and sweating over the sympathetically denervated skin such that it becomes dry. Muscles [and their innervation] of the upper eyelid that when paralyzed may result in ptosis of the upper eyelids are the levator palpebrae superioris [CN III], the levator anguli oculi medialis *CN VII+ and Müller’s tarsal smooth muscle *sympathetic+ (Hahn and Mayhew, 2000b). The ptosis resulting from sympathetic lesions can be readily reversed using a low dose of topical α-1 adrenergic agonist [0.5ml of 0.5% phenylephrine eye drops]. Not only does the upper eyelid ptosis resolve within 10-30 minutes but the lowered angle of the upper eye lashes [i.e. pointing towards the ground] also resolves and often quite impressively. This phenylephrine eye drop test is thus useful to assist in diagnosis of Horner’s syndrome in horses (Hahn and Mayhew, 2000a). Third order sympathetic neuronal fibers do not pass through the petrosal bone as in small animal species therefore Horner’s syndrome usually is not recognized with otitis media in large animals or with petrosal bone fractures. In horses the sympathetic fibers innervating the eye are more often damaged in and around the guttural pouch. Facial Nerve - CN VII. This is predominantly a motor nerve innervating the muscles of facial expression, as well as the lachrymal and certain salivary glands. It contains the lower motor neurons for movement of the ears, eyelids, lips and nostrils, in addition to the motor pathways of the menace, palpebral and corneal reflexes. Unilateral facial paralysis is generally seen as drooping of an ear, ptosis of an upper eyelid, drooping of the upper lip and pulling of the affected nostril toward the unaffected side [Figure 3]. Some normal horses have asymmetric contour of the external nares and slight deviation of the nostrils to one side. Comparison of tone in the ears, eyelids and lips on each side helps to detect mild facial weakness, especially when the patient is relaxed. Occasionally a small amount of food may remain in the cheeks on an affected side. This must not be confused with the dysphagia that results from sensory and/or motor trigeminal paralysis. Because of lack of muscle tone, saliva may drool from the commissure of the lips with facial paralysis. If only weakness of the lips and a deviated nasal philtrum without a drooped ear and ptosis occur, probably only the buccal branches along the side of the face are involved. Mild weakness of facial muscles can often be felt rather than seen and will also become more evident when the patient is resting quietly or has been tranquilized.

156

Ptosis seen with CN VII lesions is due to paralysis of the strong levator anguli oculi medialis muscle in horses that is innervated by the facial nerve. It is possible that the bulk of atonic supraorbital muscles and paralysis of the frontalis muscle contribute to the ptosis also. Unfortunately, when upper eyelid ptosis is seen in horses the immediate thought is one of it being due to Horner’s syndrome. However, facial paralysis is vastly more common than sympathetic denervation of the eyelids and always must be considered the most likely cause. Damage to the upper motor pathways, which control the facial nucleus and nerve, and which are in the frontal cortex, internal capsule, crus cerebri and brainstem, can result in abnormal facial expression. This occurs without flaccid facial paralysis or facial areflexia. There is still tone in the muscles of facial expression and facial reflexes [CN V sensory CN VII motor] are present, but the expression may be bland or grimacing on one or both sides. Needle electromyographic examination of the facial muscles does not reveal denervation because lower motor neuron disease has not occurred. Large, focal cerebral lesions such as hematomas, S. neurona encephalitis and abscess have produced such signs of supranuclear facial motor dysfunction that appear to be ipsilesional. With distal, peripheral, facial nerve involvement usually one or two branches of the nerve, not all three nerve branches (auricular, palpebral, buccal), are involved. Pressure on the side of the face as a result of a tight halter or recumbency damages buccal branches, paralyzing just the nares and lips; however, the ear and upper eyelid may droop because of direct auricular and palpebral nerve trauma. Brainstem lesions, particularly those caused by equine protozoal myeloencephalitis and listeriosis, can selectively involve the facial nucleus in the brainstem and can mimic a peripheral lesion by producing a selective, partial, facial paresis, at least to the muzzle and lips of the distal face. Horses accommodate to unilateral facial paralysis very well but bilateral facial paralysis results in difficulty prehending and chewing food and horses in particular do sequester food in the flaccid cheek pouches and drop a lot while eating. Permanent facial paralysis may necessitate enucleation of the eyeball because of keratitis sicca and exposure ophthalmitis. Exercising horses may require false nostril surgery as a result of an obstruction to inspiratory airflow (Torre, 2003). Chronic paralysis with muscle atrophy and fibrous contracture of the face can cause twisting of the muzzle and nares back across the midline towards the paralyzed side. In the early phase of irritative lesions such as meningitis, neuritis and focal trauma involving the facial nerve, facial muscles can twitch and even remain in spasm prior to paresis or paralysis that often ensues. As occurs in many other regional muscle groups (Beech, 1982), facial muscles occasionally are seen to undergo repetitive contraction described as facial tic. Some of these syndromes wax and wane and one facial tic in a horse has been seen to become almost violent in when hypocalcemia occurred and to quieten with calcium treatment. The underlying cause is notoriously not found (Beech, 1982; de Lahunta et al., 2006; Kerby, 2006). Common clinical causes The commonest cause of facial paresis or paralysis in horses in AUS and NZ would be facial trauma. Injury to the side of the face causing damage to buccal branches can also damage palpebral and auricular branches to give full facial weakness. Particularly with a horse falling over backwards and striking the poll, damage to the temporal bones and middle and inner ears occurs which often causes combinations of peripheral vestibular signs and facial paralysis.

157

Again, in AUZ and NZ trauma would be the commonest cause of Horner’s syndrome, this time to the neck. The most frequent type of trauma would be a misplaced injection that deposits a compound adjacent to the vagosympathetic trunk lying next to the common carotid artery in the neck. With α-2 agonist and local anesthetic agents’ signs of Horner’s syndrome and sweating of the face and cranial third to half of the neck will be temporary. With suspensions and insoluble drugs signs from a resulting entrapment neuropathy can be permanent. Guttural pouch mycosis also causes Horner’s syndrome in this part of the world. If a horse in AUZ or NZ with facial paresis or Horner’s syndrome has spent any time in North, Central or South America, then S. neurona protozoal myeloencephalitis should be considered a possible cause. Bibliography Beech, J., 1982, Forelimb tic in a horse. Journal of the American Veterinary Medical Association 180, 258-260. de Lahunta, A., Glass, E.N., Kent, M., 2006, Classifying involuntary muscle contractions. Comp Cont Ed Pract Vet 28, 516-529. Hahn, C.N., Mayhew, I.G., 2000a, Phenylephrine eyedrops as a diagnostic test in equine grass sickness. The Veterinary record 147, 603-606. Hahn, C.N., Mayhew, I.G., 2000b, Studies on the experimental induction of ptosis in horses. Vet J 160, 220-224. Jenkinson, D.M., Elder, H.Y., Bovell, D.L., 2006, Equine sweating and anhidrosis Part 1 - equine sweating. Vet Dermatol 17, 361-392. Kerby, M.J., 2006, Repetitive facial nerve stimulation in a cow. The Veterinary record 158, 420. Mayhew, I.G., 1980, Horner's syndrome and lesions involving the sympathetic nervous system. Equine Practice 2, 44-47. Mayhew, I.G., 2009, Large Animal Neurology, 2nd. Edition. Wiley - Blackwell, Oxford. Mayhew, I.G.J., 2010, Neuro-ophthalmology: A review. Equine veterinary journal Suppl 37, 80-88. Smith, J.S., Mayhew, I.G., 1977, Horner's syndrome in large animals. Cornell Vet 67, 529-542. Torre, F., 2003, Use of autogenous cartilage graft from auricular cartilage in treatment of unilateral paralysis of nostril in racing Standardbred horse. Equine Vet Educ 15, 10-14. Usenik, E.A., 1957. Sympathetic innervation of the head and neck of the horse:

neuropharmacological studies of sweating in the horse. PhD. University of Minnesota.

158

159

160

OVERVIEW OF HOW HORSES LEARN AMANDA WARREN-SMITH Honorary Lecturer University of Sydney, Owner Millthorpe Equine Research Centre, Phone 0419 235 785, Email danzcay@gmail.com

Abstract Learning theory describes the ways in which animals learn. It establishes clear guidelines and

training protocols for correct training practices and methods of behaviour modification. Horse

training deals with the modification of behaviour and almost all of the principles of learning

theory that apply to other species also apply to horses (Potter and Yeates 1990). One of the

main principles of learning theory used with horses is operant conditioning whereby horses are

trained to respond consistently to signals through reinforcement and punishment (Skinner

1938).

Reinforcement is the process in which a reinforcer follows a particular behaviour so that the

frequency (or probability) of that behaviour increases (Wolpe, 1958). Negative reinforcement is

the subtraction of something aversive (such as pressure) to reward the desired response and

thus lower the motivational drive (Skinner, 1953). Positive reinforcement is the addition of

something pleasant (a reinforcer) to reward the desired response and thus lower the

motivational drive for that reinforcer (Skinner, 1953).

Punishment is the procedure of providing consequences that reduce the occurrence of a

response (Skinner, 1953). Negative punishment is the subtraction of something attractive (such

as food or company) to punish the targeted response (Skinner, 1953). Positive punishment is

the addition of an aversive stimulus immediately after an undesired response (Skinner, 1953).

To assess the knowledge of learning theory among accredited equestrian coaches in Australia, a

20-item questionnaire was distributed to all coaches registered with the National Coaches

Accreditation Scheme in Australia (n = 830). Of the 206 respondents, 79.5% considered positive

reinforcement to be "very useful", yet only 2.8% correctly explained its use in horse training.

When asked about the usefulness of negative reinforcement, 19.3% of coaches considered it

"very useful" with 11.9% correctly explaining its use. Punishment was rated "very useful" by

5.2% of respondents, although only eight coaches (5.4%) explained punishment correctly.

Release of pressure was considered the most effective reward for horses among respondents

(78.2%). These results indicate that many equestrian coaches lack a correct understanding of

positive and negative reinforcement as they apply to horse training. Given that qualified

coaches play a significant role in the dissemination of information on training practices, this

highlights the need for improved education of equestrian coaches. Education to remedy this

situation has the potential to enhance the welfare of horses through reduced behavioral

conflict and improve training outcomes1.

161

The need for precise definitions is accepted in human psychiatry (DSM-IV, 1994) and is

increasingly called for in veterinary behaviour medicine (Overall, 1997; 2005). In contrast, the

use of non-scientific terms is customary in equestrian circles and is added to by contemporary

trainers and self-styled horse whisperers. Data suggest that qualified equestrian instructors

frequently confuse the meaning of terms that originated in behavioural science (Warren- Smith

and McGreevy, in prep). Several descriptors may be used for the same behaviour, depending on

the observer (Mills, 1998). The use of such terms may encourage imprecise and inappropriate

interpretations of equine behaviour. For example, many layman’s terms imply subjective

mental states in the horse and that horses are culpable participants in the training process.

These assumptions can have negative welfare implications for the domestic horse and safety

implications for riders and handlers (McLean, 2004)2.

References Potter GD, Yeates BF (1990) Behavioural principles of training and management. In Evans JW,

Borton A, Hintz HF, Vleck LD, editors The horse New York, WH Freeman and Co.

Skinner BF (1938) The behavior of organisms, New York, Appleton-Century. Skinner BF (1953) Science and human behaviour, New York, Macmillan.

Wolpe J (1958) Psychotherapy by reciprocal inhibition, Palo Alto, Stanford University Press.

Citations 1Warren-Smith AK, McGreevy PD (2008) Equestrian coaches’ understanding and application of

learning theory in horse training Anthrozoös 21:153 2McGreevy PD, McLean AN, Warren-Smith AK, Waran N, Goodwin D (2005) Defining the terms

and processes associated with equitation Proceedings of the 1st International Equitation

Science Symposium, Melbourne 1:10

162

WELFARE (AND SAFETY) IMPLICATIONS FOR APPLYING LEARNING THEORY IN HORSE TRAINING Lesley Hawson PhD candidate, University of Sydney, Associate Australian Equine Behaviour Centre, Phone: 0422 558 001 Email: lhawson@gmail.com

Most horse training relies on the principle of negative reinforcement. It is the removal of

pressure from rein, leg and lead rein that rewards the desired response. When the pressure

from rein, spurs, whip, noseband etc is not released at the correct moment unwanted

behaviours are inadvertently reinforced (McGreevy and McLean, 2010). If the pressure release

inconsistently rewards variable behaviours or the release does not occur the horse will become

confused and display conflict behaviours. The horse characteristically becomes more hyper-

reactive and tense. If the horse cannot control the stimulus through inducing pressure release

via its response then ultimately it will cease offering responses and become dull. These errors

in training can lead to chronic stress, learned helplessness and ultimately wastage due to

“behaviour problems”.

Slaughter data indicate that catastrophic outcomes may be the case for many horses.

European research reports that 66.4% of a 3,100 sample of non-racing horses were slaughtered

between 2 and 7 years of age. The authors (Ödberg and Bouissou, 1999) suggest that this high

wastage rate could be due in large part to behavioural issues. Doughty (2009) found a similar

figure of 59.8% of the horses processed through the two horse meat abattoirs in Australia were

under seven years of age. Sixty percent of these were wastage from the racing industry, 10 %

were feral horses and the remainder was from the pleasure industry. Again, no real

conclusions could be made on why these horses were presented for slaughter but behavioural

issues must be on the list.

Recent review of the literature showed that increased risk of serious injury from a horse arises

from cumulative exposure. Age and gender distribution of horse-related injuries follow

participation related activities in Australia. Horse behaviour is implicated in up to 61% of

incidents. If serious injury is a likely result of exposure to horses, then the centuries of horse

management, training and education to date appear to have done little to prevent injuries to

human beings in their interactions with equids (Hawson et al., 2010).

While the basic principles of learning theory are well elucidated their application in the real

world of horse training remains poor, even at the elite level, as evidenced by the recent furors

over the “blue tongue” incident (http://www.youtube.com/watch?v=8hIXGiV4N4k) and

expose of training practices at the 2011 World Reining Final

(http://www.youtube.com/watch?v=en_90D5TOKA). The price horses and people pay for

inadequate application of learning theory can be high.

REFERENCES

163

Doughty A., Cross N., Robins A., Phillips C.J.C. (2009) The origin and foot condition of horses slaughtered in Australia for the human consumption market. Equine Veterinary Journal 41:808-811.

Hawson L.A., McLean, A.N., Mc Greevy, P.D. (2010) The roles of equine ethology and applied learning theory in horse-related human injuries. Journal of Veterinary Behavior: Clinical Applications and Research 5:324-338.

McGreevy P., McLean A. (2010) Equitation Science Wiley-Blackwell. Ödberg F.O., Bouissou M.F. (1999) The development of equestrianism from the baroque period

to the present day and its consequences for the welfare of horses. Equine Vet J Suppl:26-30.

164

INTERPRETATION OF HORSE'S RESPONSES Amanda Warren-Smith Honorary Lecturer University of Sydney, Owner Millthorpe Equine Research Centre, Phone 0419 235 785, Email danzcay@gmail.com

Round-yard studies Part 1 Recently, training horses within round-pens has increased in popularity. Practitioners often

maintain that the responses they elicit from horses are similar to signals used with senior

conspecifics. To audit the responses of horses to conspecifics, 6 mare-young-horse dyads were

introduced to each other in a round-yard and videoed for 8 min. These dyads spent more time

greater than 10 m apart than less than 1 m apart (P<0.001). The time they spent less than 1 m

apart decreased over the 8 min (P= 0.018). Mares occupied the centre of the round-yard and

chased youngsters for 0.73% of the test period (P<0.001). All agonistic approaches were made

by mares (P<0.001) and all investigative approaches by youngsters (P=0.018). Head-lowering

and licking-and-chewing were exhibited most when the youngsters were facing away from the

mares (P<0.001). The frequency of head-lowering increased during the test period (P=0.027)

while the frequency of licking-and-chewing did not change. The current results bring into

question the popular interpretation and ethological relevance of equine responses commonly

described in round-yard training and show that mares did not condition young horses to remain

in close proximity to them.

Part 2 Practitioners often claim that during round-yard training the responses they elicit from horses are similar to signals used between young horses and mares. Preliminary research revealed that when mare-colt dyads (n=12) were placed in a round-yard, mares occupied the centre of the round-yard and chased youngsters for 0.73% of the total test period. The aim of this study was to record the behavioural interactions using a continuous sampling method during a longer time period (15 min per dyad), using a larger sample (n=90) comprising colts and fillies. Analysis of variance revealed that mares exhibited more agonistic interactions (P<0.001) and vocalisations (P=0.028) than youngsters while youngsters exhibited more interaction with a foreign object, snapping, investigative approaches and head lowering than mares (P<0.001). Fillies showed more agonistic reactions (P=0.050), interaction with a foreign object (P=0.009) and investigative approaches (P=0.048) than colts. Colts exhibited more snorting (P=0.033) and maintained greater distances away from the mare (P=0.016) than fillies. Mares occupied the centre of the round-yard and chased youngsters for 0.27% of the test period and this was most likely to occur with colts (P=0.001). Practical applications The aim of training methods is to have at least some influence over the horses to which they

are applied; clearly a thorough understanding of such methods is required. The results of this

and other studies have shown that the responses elicited from human-horse interactions in

165

round-yards are not reflected in horse-horse interactions. The welfare of horses being

subjected to round-yard training methods may often be jeopardised by trainers having

unrealistic expectations based on incorrect assumptions that the behaviour exhibited mimics

that of the horse-horse interactions in more natural environments.

Citations Part 1: Warren-Smith AK, McGreevy PD (2008) Preliminary investigations into the ethological

relevance of round-pen (round-yard) training of horses Journal of Applied Animal Welfare

Science, 11:285

Part 2: Koster D, Wegert AC, Bronicki BB, Warren-Smith AK (2009) Further investigations into

the ethological relevance of round-yard training of horses Proceedings of the 5th International

Society for Equitation Science Conference, Sydney 2009 5:35

Recognition of their related fellow horses Horses in groups form dominance hierarchies. Within these, pair bonds also commonly arise. In

domestic situations, mares and foals will usually be weaned. The behavioural responses

exhibited by both mares and foals at weaning suggest that separation anxiety may be

experienced by each. What happens to the mare-foal bond after this separation is unknown.

Anecdotal reports suggest that related horses will recognise each other when reunited after a

prolonged period of separation. This could facilitate herd management of horses when they are

subsequently housed together by having pair bonds form more rapidly and with less agonistic

interactions. Therefore this study aimed to determine whether or not mares and young horses

(< 3 yrs) appear to recognise each other after a period of prolonged separation (17.23 ± 1.50

months). Ninety mare-young horse dyads (70 unrelated; 20 related) were each placed into a

round-yard and their interactions video-taped for 15 min. One-way analysis of variance

indicated that the distance between the dyads immediately prior to agonistic interactions was

greater for related than non-related dyads (8.25 and 5.70 ± 1.16 m respectively; P=0.030).

Investigative approaches occurred more within related than unrelated dyads (P=0.018).

Youngsters of related dyads were more likely to exhibit snapping than those of unrelated dyads

(P=0.001). There was no difference between the related and unrelated dyads for the responses

of head lowering, head shaking, licking the lips, snorting, vocalising and yawning. Being related

had no influence on whether or not agonistic interactions were exhibited, the time the dyads

spent in close proximity or which member of the dyad made the initial approach to the other.

Practical applications Given that related dyads were more likely to exhibit investigative approaches it would seem

that related horses do recognise each other after a prolonged period of separation. Therefore

management of groups of horses could be improved when related horses are subsequently

housed together. While agonistic encounters occurred in all dyads, unrelated dyads had less

166

distance between them than related dyads prior to their occurrence. This could suggest that

members of related dyads may be less likely to suffer injury than those of non-related dyads.

Citation McDonald BJ, Warren-Smith AK (2010) Mare and foal recognition after a prolonged period of

separation Journal of Veterinary Behavior: Clinical Applications and Research 5: 215

Human influence for calming During studies of the effects of head-lowering achieved via negative reinforcement, the

influence of a handler being near the horses was not measured. This potential operator effect

may have confounded results; therefore this study investigated behavioural and physiological

effects of the presence of a familiar handler (handled regularly for previous week) on horses

after arousal. Four groups of 7 horses were used. Group A were not aroused then left alone; B

were aroused then left alone; C were not aroused then given free interaction with a familiar

handler and D were aroused then given free interaction with a familiar handler. Pre-test heart

rates were recorded in the test area, then those in Groups B and D were subjected to arousal

(the handler jumping up and down and waving a hat beside the horse) such that the horse’s

heart rate exceeded 100 beats per minute. The halter and lead rope were then removed and

the handler departed. For the following 300 s, the horses in Groups A and B were left alone

whereas for Groups C and D, another handler with whom the horses were familiar entered the

round-yard and stood still in the centre and looked at the ground. Repeated measures analysis

showed that the heart-rate of the horses was greatest during the first 0-60 s and 150-180 s

post-arousal in Groups B and D and lowest in Groups A and C (P<0.001). The interaction of

treatment-and-time showed that Group B had the highest heart-rate during the test period

(P=0.022). Latencies to approach the handler did not differ between groups. The horses in

Group D took fewer steps (P<0.001), were least likely to sniff the ground (P<0.015) or look out

of the arena (P=0.028) and those in Group A were most likely to exhibit head lowering

spontaneously (P=0.016).

Practical applications These results suggest that allowing an aroused horse free interaction with a familiar handler

has more of a calming influence than leaving the horse alone. For equitation to be ethical and

sustainable, having a familiar handler present when a horse is stirred up will help calm the

horse. This is important as research has shown that horses' ability to learn is enhanced by

calmness.

Citation Warren-Smith AK, Greetham L, McGreevy PD (2009) The influence of human presence on

calming aroused horses Proceedings of the 5th International Society for Equitation Science

Conference, Sydney 2009 5:22

167

Conflicts Oversimplification of the definition of ‘normal behaviour’ has resulted in a broad

misunderstanding of some aspects of equine behaviour. These behaviours have been labelled

'abnormal behaviours', 'misbehaviours' or 'problem behaviours' and it is often implied that the

horse is to blame. In reality, they are merely various expressions of the flight response and are

normal, adaptive, behaviours that have evolved to ensure the survival of the domestic horse.

This study was performed to identify the most frequently expressed conflict responses and was

conducted on dressage horses as the desire for these horses to perform ‘willingly’ and

‘cooperatively’ with the rider is emphasised more than any other equestrian discipline. Data

were collected at the Dressage NSW Clarendon Event, held at Hawkesbury Showground,

Clarendon on Saturday 9th and Sunday 10th August 2008. The event program consisted of nine

levels of competition from which eight riders from each level were selected at random, giving a

total of 72 horse/rider combinations. Conflict responses were shown at all levels of dressage

competition. One way analysis of variance showed that tail swishing was the most frequently

exhibited conflict response, followed by ears back, being above the bit, tenseness, teeth

visibility, pulling, hollowing of the back and short stiff striding respectively (P=<0.001). Horses at

Preliminary level were more likely to be above the bit while those at advanced level were least

likely (P=0.003). Horses at Prix St. Georges and Grand Prix put their ears back and swished their

tails most frequently while those at Novice level showed these responses least (P=0.041 and

P=0.007 respectively). Horses at Preliminary showed more shortening and stiffening of the

stride than horses at any other level (P=0.004).

Practical applications The identification of these most frequently exhibited conflict responses should prompt

equestrians to recognise, appreciate and address these behaviours before they progress into

more severe expressions of conflict behaviours. Training programs should place strong

emphasis on behaviours as a means of communication and this in turn should contribute to

improved sustainability of the equine athlete.

Citation Williams LR, Warren-Smith AK (2010) Conflict responses exhibited by dressage horses during

competition Journal of Veterinary Behavior: Clinical Applications and Research 5:215

168

BRIDLES, NOSEBANDS AND HALTERS Amanda Warren-Smith Honorary Lecturer University of Sydney, Owner Millthorpe Equine Research Centre, Phone 0419 235 785, Email

danzcay@gmail.com

Bridles Throughout equitation history, bitted bridles have been the primary method of controlling the

ridden horse. In response to health and behavioural concerns arising from the use of bitted

bridles, bitless bridles offer new methods of steering and control. However, the effectiveness

of bitless bridles on horses had not been previously examined scientifically. Therefore, the

current study measured behavioural and cardiac responses of horses undergoing foundation

training (bridling, long-reining and riding) wearing either a bitted or bitless bridle. The horses

wearing the bitted bridle exhibited more chewing, opening of the mouth, pawing the ground

and tail swishing than those in the bitless bridle. The horses wearing the bitless bridle exhibited

more head lowering during long-reining compared to those in the bitted bridle. The frequency

of chewing, opening the mouth and head raising decreased as training progressed. The number

of steps taken after the application of the halt stimulus was greatest for the horses in the bitted

bridle during long-reining compared with those in the bitless bridle. During long-reining, the

heart rate and heart rate variability of the horses were higher for those in a bitted bridle

compared with a bitless bridle.

Practical application The results of this study suggest that horses wearing bitless bridles performed at least as well

as, if not better than, those in bitted bridles. If the use of bitted bridles does cause discomfort

to horses as suggested by some, then the use of bitless bridles could be beneficial and certainly

warrants further investigation.

Citation Quick JS, Warren-Smith AK (2009) Preliminary investigations of horses’ (Equus caballus)

responses to different bridles during foundation training Journal of Veterinary Behavior: Clinical

Applications and Research 4:169

Nosebands Any apparatus that restricts a horse’s movement can compromise welfare but the intentional

restriction caused by some nosebands seems to be too often overlooked as a cause of

discomfort and pain. In a bid to safeguard horse welfare, some equestrian manuals and

competition rule books propose that ‘two-fingers’ be used as a spacer to guard against over-

tightening of nosebands but fail to specify where this gauge should be applied. The vagueness

of this directive prompted us to undertake a small random survey of the finger dimensions of

adult men (n=10) and women (n=10). There were significant gender differences in the

measurements of fingers of adults (P <0.001) illustrating that the ‘two-finger rule’ is not a

169

reliable guide for standardized noseband fastening. Infra-red thermograph was used to

measure the temperature of the facial skin and the eye of adult horses (n=5) wearing a double

bridle with and without a cavesson noseband. Based on the mean circumference of adult index

and middle fingers (9.89cm ± 0.21), a taper gauge was developed for use as a spacer at the

nasal planum (NP) or beside the mandible (M) when tightening the noseband. The nosebands

could be fastened significantly tighter when the taper gauge was used at M than at NP (P=0.02).

Wearing double bridles and nosebands that had been tightened with and without the taper

gauge caused an increase in eye temperature compared with baseline values (P=0.012). The

tighter the noseband was fastened, the cooler the facial skin of the horse (and presumably the

greater the impairment of vascular perfusion) when compared with baseline values (P=0.016).

Practical Application This study suggests that horses wearing double bridles and nosebands undergo a physiological

stress response and may have compromised blood flow to the skin in the vicinity of the

noseband. Consequently, on welfare grounds, the use of nosebands that cause any constriction

of jaw movement should be reviewed as a matter of priority.

Citation Paul McGreevy PD, Warren-Smith AK, Guisard Y (nd) The effect of double bridles and crank

nosebands on facial cutaneous and ocular temperature in horses Journal of Veterinary

Behavior: Clinical Applications and Research accepted

Halters The success of interactions between humans and horses is determined by the effectiveness of

the communication from handler to horse. Many pieces of equipment are utilised on horses,

one such piece is the halter or headcollar, of which there are two main types; the web halter

and the rope halter. Anecdotally, there is debate as to which halter type is the most effective

for controlling horses. Given that halters are the main form of horse control in unridden

activities, it is important to establish which type of halter is most effective for training purposes.

Therefore, the current study investigated the effectiveness of the different halter types on

horses (n=10) while being led. The horses were paired and one from each pair placed into

Group 1 (web) and the other from each pair placed into Group 2 (rope). Each horse was led a

10 m distance on 5 consecutive occasions with a 30 s rest between each. The time taken for

each horse to respond to the leading stimulus as well as to complete the distance was recorded

and analysed using one-way ANOVA. There was no difference between the groups for the time

taken to lead forward, although there was a trend for the horses wearing the rope halter to

complete the distance in less time than those wearing the web halter (P=0.079).

170

Practical application While the results herein show that there was no difference between the two halter types, given

the low number of horses used in this trial, further work should be conducted using greater

numbers of horses as well as horses with different handling experience.

Citation McDonald BJ, Warren-Smith AK (2008) A preliminary investigation into the effectiveness of

different halter types used on horses Proceedings of the 4th International Society for Equitation

Science Conference, Dublin 4:80

171

REIN TENSION WITH ACCELEROMETRY – OBJECTIVELY MEASURING HORSE PERFORMANCE Warren-Smith AK1, Bronicki BB2, Evans D3, Curtis R4, Marsh D4 1Honorary Lecturer University of Sydney, Owner Millthorpe Equine Research Centre, Phone 0419 235 785, Email

danzcay@gmail.com 2Millthorpe Equine Research Centre

3Equine Health and Fitness, Phone 0411 289 212, Email equinehealthfitness@gmail.com

4Crafted Technology, Phone 02 4757 4876, Email robac@ieee.org

Abstract

In most equestrian disciplines, the horse's head position whilst performing will influence results. Dressage horses are required to be 'on the vertical' such that their nasal plane is perpendicular (or within 6 degrees) to the ground. This head carriage should be maintained with lightness i.e. minimal tension in the reins. Judging of dressage is subjective and previous research has shown that accredited dressage judges are not always able to assess lightness; a problem that could be overcome with the implementation of objective measures.

Additionally, the position of the horses head and the rein tension applied will influence the horse's strides. For example, maintaining excessive rein tension while executing an extended trot will result in diagonal displacement. Using objective measures can accurately assess this common fault.

Using the Rein Check® with a tri-axial accelerometer, the rein tensions and head movements of horses can be assessed and it can be clearly determine whether or not the head position conforms to that specified in the FEI rule book. Furthermore, with minimal equipment placed on the horse, for example a GPS, heart rate monitor and accelerometers on the legs, most of a horse's performance can be objectively assessed and this eliminates the subjectivity that underpins judging of most horse competitions today.

Practical application If the progressive training of a horse is correct, self carriage will develop naturally and the horse

will be able to maintain the 'on the vertical' posture with ‘lightness’ and importantly, without

the rider forcing the head position of the horse. Unfortunately this is rarely the case in modern

day competition and the welfare of horses in this situation is severely compromised. If horse

training is to be ethical and the career of a performance horse is to be sustainable, objective

measures of parameters such as lightness and the position of the nasal plane are required to

overcome problems associated with the subjective nature of judging. This can be achieved with

the use of equipment such as accelerometers and tensiometers which are unobtrusive and

simple to use.

Citation Warren-Smith AK, Bronicki BB, Evans D, Curtis R, Marsh D (2009) The use of accelerometry and

rein tension to objectively assess the performance of horses Proceedings of the 5th International

Society for Equitation Science Conference, Sydney 5:16

LATERALITY IN HORSES

172

Amanda Warren-Smith Honorary Lecturer, University of Sydney, Owner, Millthorpe Equine Research Centre Phone: 0419 235 785 Email: danzcay@gmail.com Lesley Hawson PhD candidate, University of Sydney, Associate Australian Equine Behaviour Centre Phone: 0422 558 001 Email: lhawson@gmail.com

Despite the fact that humans have ridden and driven horses for many centuries, very little is understood about the motor and sensory processes operating in these large, mobile and reactive mammals. While laterality and handedness were previously thought to occur only in humans they are is now well recognised in a wide variety of species (Austin and Rogers, 2007; Lazenby, 2002). Laterality is thought to arise from an interaction of genetically controlled conformational asymmetry, innate motor preference and learned behaviour (Pearce et al., 2005). Horses in dressage and jumping are reported to have a preference to the left (Pearce et al., 2005) while there is compelling evidence in the racing population, that there is a right lead preference both at the individual and population level (Williams and Norris, 2007).

McGreevy and Thomson (2006) suggest that laterality may have been selected for in performance horses. They chose to examine horses that moving without human prompting or interference. In the breeds they studied, Thoroughbreds and to a lesser extent Standardbreds were most often left leg preferent (i.e. placing their left fore leg forward while grazing), whereas Quarter Horses bred for cutting displaying the least bias. The strength of the preferences was shown to increase with age. Warren-Smith and McGreevy’s (2010) innovative use of pedometers in grazing horses may provide a simple means by which to evaluate innate motor laterality, again without any possible operator effect.

Apparent sensory preferences provide fascinating insight into brain hemisphere dominance in the horse and may provide information on the emotionality of the horse. The latter is important as emotional state in the horse has been shown to influence eating, drinking, defaecation, sociability and learning ability (McCann et al., 1988; Visser et al., 2003). Although the tradition of leading and mounting the horse from the left has usually been attributed to former military uses, it may be that the left side of the horse is preferred by both horse and rider for information processing (Larose et al., 2006). Several studies have shown that horses are more likely to regard objects and humans that have high emotional salience with their left eye (Austin and Rogers, 2007; De Boyer Des Roches et al., 2008; Larose et al., 2006). It is hypothesised that, in keeping with results from other species, utilising the left eye engages the right cerebral hemisphere which is predominantly associated with emotional evaluation and escape behaviours (Vallortigara and Rogers, 2005). This finding has implications for training and handling, some of which have been tested in recent experiments (Austin and Rogers, 2007; Sankey et al. in press).

The right hemisphere dominance may also apply to olfactory and auditory stimuli. McGreevy and Rogers (2005) report a right nostril bias to olfactory stimulus in young horses. As the olfactory system does not decussate, this suggests an important information processing role in the right hemisphere. This right hemisphere dominance was also shown in Basile et al’s 2009

173

study of auditory function for calls from unfamiliar conspecifics whereas calls from familiar conspecifics appeared to be processed by the left hemisphere (right ear attention).

Laterality in horses has considerable implications for veterinarians, riders and owners as it may both help and hinder our management of these animals. This presentation will review the literature available on laterality and asymmetry in horses. Both sensory and motor systems will be explored with an emphasis on what current research implies for brain hemisphere functioning and consequent application of this knowledge to the ridden horse.

REFERENCES: Austin N.P., Rogers L.J. (2007) Asymmetry of flight and escape turning responses in horses.

Laterality: Asymmetries of Body, Brain and Cognition 12:464 - 474. Basile M., Boivin S., Boutin A., Blois-Heulin C., Hausberger M., Lemasson A. (2009) Socially

dependent auditory laterality in domestic horses (Equus caballus). Animal Cognition 12:611-619.

Davies H.M.S., Watson K.M. (2005) Third metacarpal bone laterality asymmetry and midshaft dimensions in Thoroughbred racehorses. Australian Veterinary Journal 83:224-226.

De Boyer Des Roches A., Richard-Yris M.A., Henry S., Ezzaouïa M., Hausberger M. (2008) Laterality and emotions: Visual laterality in the domestic horse (Equus caballus) differs with objects' emotional value. Physiology and Behavior 94:487-490.

Larose C., Richard-Yris M.A., Hausberger M., Rogers L.J. (2006) Laterality of horses associated with emotionality in novel situations. Laterality 11:355-367.

Lazenby R.A. (2002) Skeletal Biology, Functional Asymmetry and the Origins of "Handedness". Journal of Theoretical Biology 218:129-138.

McCann J.S., Heird J.C., Bell R.W., Lutherer L.O. (1988) Normal and more highly reactive horses. I. Heart rate, respiration rate and behavioral observations. Applied Animal Behaviour Science 19:201-214.

McGreevy P.D., Rogers L.J. (2005) Motor and sensory laterality in thoroughbred horses. Applied Animal Behaviour Science 92:337-352.

McGreevy P.D., Thomson P.C. (2006) Differences in motor laterality between breeds of performance horse. Applied Animal Behaviour Science 99:183-190.

Pearce G.P., May-Davis S., Greaves D. (2005) Femoral asymmetry in the Thoroughbred racehorse. Australian Veterinary Journal 83:367-370.

Sankey C., Henry S., Clouard C., Richard-Yris M.-A., Hausberger M. Asymmetry of behavioral responses to a human approach in young naive vs. trained horses. Physiology & Behavior In Press, Corrected Proof.

Vallortigara G., Rogers L.J. (2005) Survival with an asymmetrical brain: Advantages and disadvantages of cerebral lateralization. Behavioral and Brain Sciences 28:575

Visser E.K., Van Reenen C.G., Engel B., Schilder M.B.H., Barneveld A., Blokhuis H.J. (2003) The association between performance in show-jumping and personality traits earlier in life. Applied Animal Behaviour Science 82:279-295.

Warren-Smith A., McGreevy P. (2010) The use of pedometers to estimate motor laterality in grazing horses. Journal of Veterinary Behavior: Clinical Applications and Research 5:177-179.

174

Williams D.E., Norris B.J. (2007) Laterality in stride pattern preferences in racehorses. Animal Behaviour 74:941-950.

175

RIDER ASYMMETRY AND HANDEDNESS Lesley Hawson PhD candidate, University of Sydney, Associate Australian Equine Behaviour Centre Phone: 0422 558 001 Email: lhawson@gmail.com

One of the major challenges in equitation science is that it involves the unique combination of two different species. Although balance and symmetry are important in most elite equestrian activities, little research has been conducted into rider asymmetry. Humans have a clear population bias for one hand versus the other, with nine out of ten individuals being right-handed. The preferred thoracic limb can produce forces approximately 10% larger than the non-preferred limb as well as manifesting faster and more accurate fine motor control. The non-preferred thoracic limb may have a separate role in positional control via sensory mediated error correction (2008). Similarly, most humans also appear to be right-footed in that most people will use the right foot to mobilize or manipulate and use the left leg for postural support (Gabbard and Hart, 1996; Hardt et al., 2009). Motor bias may be accompanied by morphological asymmetries. For example, between 70 and 90% of humans are afflicted with a functional leg length inequality (LLI)(Gurney, 2002; Knutson, 2005; Symes and Ellis, 2009). Knutson (2005) showed that the right leg is shorter than the left in 53 – 73% of people. LLI is believed to cause both pelvic and thoracic girdle rotation so that the right hemi pelvis is rotated anterior and ventral while the left hemi pelvis rotates posterior and dorsal. Such rotation can create asymmetry in horse-riders. Symes and Ellis (2009) found that right handed riders (n=17) commonly sit with the thoracic girdle rotated to the right and that there is axial rotation to the left and anti-clockwise for all gaits except right lead canter. This is unsurprisingly since the cue for canter is asymmetric and so an asymmetric rider may deliver it with more flaws than an asymmetric one. In the Symes and Ellis study, the general clockwise direction of the right lead canter appeared to in conflict with the preferred axial rotation of the rider, resulting in asynchrony between rider and horse. Pugh and Bolin (2004) suggest that riders shorten the stirrup leather on the side that has the short leg to promote a more balanced seat. However, this advice runs counter to most equestrian doctrine and may be insufficient if the rotation resulting from the LLI is well established. The asymmetry of the rider may have an effect on stride biomechanics. Roepstorff et al (2009) found that, in mounted trotting horses, the left fore/right hind sitting diagonal is more loaded than its opposite which would be consistent with Symes and Ellis’ (2009) findings. Handedness of the rider could play a role in rein cue effectiveness. In Kuhnke et al’s (2010) study of right-handed well trained riders (n=11), regardless of either gait, direction or particular rider, continuous tension was most commonly applied to the rein of the horses’ preferred side while contact with the opposite rein was non-continuous. That said, more even contact was found if the rein of the horse’s preferred side was in the rider’s dominant hand. In contrast,

176

more tension was applied if the rein in the non-dominant hand. Overall, more tension was applied to the left rein of the left lateralized horses than to any rein of the right lateralized horses. These results suggest that right-handed riders may be better suited to right lateralised horses as the common axial rotation in right LLI of these riders could act to support a right lateralised horse on its non-preferred side while hindering a left lateralised horse on its non-preferred side. It should be noted that these findings run counter to accepted riding theory and illustrate how equitation science can elucidate more effective rider/horse communication processes that ultimately result in better performance. SADDLE FIT Horse laterality (and especially fore limb inequality that may also be also linked to truncal asymmetry) and rider asymmetry place enormous challenges on the role of the saddle. Exploration of this aspect of the horse/rider dyad is in its infancy. As balance and position of the rider can exert various effects from improving the biomechanical efficiency of the horse’s stride to detraining learned responses, it is paramount that the saddle promotes stability in the coupling system between horse and rider (Lagarde et al., 2005; McGreevy and McLean, 2010; Peham et al., 2004). New technologies such as saddle pressure pads, adjustable panels and new construction materials may assist this process. APPLIED LEARNING THEORY Most horse people remain unaware of learning theory in horse training. Horse riding and training remain a trial-and-error process or are regarded as some sort of vicarious process undertaken by successful riders and trainers. This has led to a focus on rider position for centuries in the mistaken belief that this is the main means to effect good performance (McGreevy and McLean, 2010). In fact, the process of training a horse can be understood by applying a set of eight principles. These are:

1. Train easy-to- discriminate signals. 2. Reduce negative reinforcement pressure (reins and legs) to very light versions of

pressure (light signals). 3. Shape the components of responses progressively. 4. Train and subsequently elicit responses singularly. 5. Train only one response per signal. 6. Train all responses to be initiated and subsequently completed within a consistent

composition and time frame. 7. Train persistence of elicited responses. 8. Avoid and dissociate flight responses.

REFERENCES Gabbard C., Hart S. (1996) A question of foot dominance. Journal of General Psychology

123:289-296. Goble D.J., Brown S.H. (2008) The biological and behavioral basis of upper limb asymmetries in

sensorimotor performance. Neuroscience and Biobehavioral Reviews 32:598-610. Gurney B. (2002) Leg length discrepancy. Gait & Posture 15:195-206.

177

Hardt J., Benjanuvatra N., Blanksby B. (2009) Do footedness and strength asymmetry relate to the dominant stance in swimming track start? Journal of Sports Sciences 27:1221-1227.

Knutson G.A. (2005) Anatomic and functional leg-length inequality: a review and recommendation for clinical decision-making. Part I, anatomic leg-length inequality: prevalence, magnitude, effects and clinical significance. Chiropr Osteopat 13:11.

Kuhnke S., Dumbell L., Gauly M., Johnson J.L., McDonald K., König von Borstel U. (2010) A comparison of rein tension of the rider's dominant and non-dominant hand and the influence of the horse's laterality. Comparative Exercise Physiology 7:57-63.

Lagarde J., Kelso J.A.S., Peham C., Licka T. (2005) Coordination dynamics of the horse-rider system. Journal of Motor Behavior 37:418-424.

McGreevy P., McLean A. (2010) Equitation Science Wiley-Blackwell. Peham C., Licka T., Schobesberger H., Meschan E. (2004) Influence of the rider on the variability

of the equine gait. Human Movement Science 23:663-671. Pugh T.J., Bolin D. (2004) Overuse injuries in equestrian athletes. Curr Sports Med Rep 3:297-

303. Roepstorff L., Egenvall A., Rhodin M., Bystr, m A., Johnston C., van Weeren P.R., Weishaupt M.

(2009) Kinetics and kinematics of the horse comparing left and right rising trot. Equine Veterinary Journal 41:292-296.

Symes D., Ellis R. (2009) A preliminary study into rider asymmetry within equitation. The Veterinary Journal 181:34-37.

178

POSITIVE AND NEGATIVE REINFORCEMENT Amanda Warren-Smith1, McGreevy PD2 1Honorary Lecturer University of Sydney, Owner Millthorpe Equine Research Centre, Phone 0419 235 785, Email

danzcay@gmail.com 2Faculty of Veterinary Science University of Sydney, Phone 02 9351 2810, Email paul.mcgreevy@sydney.edu.au

Abstract Twenty horses were paired for age, sex and breed and placed into one of two groups. The horses in Group A (control) were reinforced using only negative reinforcement (NR) while those in group B (treatment) were reinforced with both positive reinforcement (PR) and NR concurrently. All horses were shaped for the halt response while being driven in long-reins over a period of 5 consecutive days. On day 1, all horses were given a baseline test of 20 random halts while being long-reined in an indoor arena. On days 2–4, the shaping of the halt response continued with horses being reinforced according to the group to which they had been allocated. On day 5 of testing the baseline test was repeated (final test). During the baseline and final tests, behavioural responses and accuracy of completion of the halt response were recorded. Heart rates were recorded continuously during testing. One-way analysis of variance in randomised blocks and analysis of covariance using baseline data as a covariate showed no effect on latency to halt. However, horses reinforced with both NR and PR shook their heads vertically less and were more likely to lick their lips than those reinforced with NR only. There was also a trend for an increase in roundness of outline of the horses that were reinforced with both PR and NR. Practical application These results suggest that the implementation of PR effectively into equitation training may improve the welfare of the horse. Citation Warren-Smith AK, McGreevy PD (2007) The use of blended positive and negative reinforcement in shaping the halt response of horses (Equus caballus) Animal Welfare 16:481

179

TIMING OF REINFORCEMENT Amanda Warren-Smith1, McLean AN2, Nicol HI3, McGreevy PD4 1Honorary Lecturer University of Sydney, Owner Millthorpe Equine Research Centre, Phone 0419 235 785, Email

danzcay@gmail.com 2Australian Equine Behaviour Centre, 730 Clonbinane Rd, Broadford, Vic, 3658.

3Faculty of Rural Management, University of Sydney, PO Box 883, Orange, NSW, 2800

4Faculty of Veterinary Science, University of Sydney, NSW, 2006.

Abstract Horses are used worldwide for a range of activities. Their usefulness and welfare in these pursuits are strongly influenced by their trainability which may in turn be influenced by learning ability. Handling and riding horses can expose both handler and horse to a considerable risk of injury. This risk can be reduced by employing correct handling procedures that can facilitate learning in horses. As with all training, efficacy is influenced by consistency and timing. To determine the optimum timing of reinforcement, sixteen unweaned naïve foals that had previously undergone minimal human-animal interaction (i.e. not had a headcollar previously applied) of Warmblood (WB; n = 6), Thoroughbred (TB; n = 5) or Warmblood x Thoroughbred (WB x TB; n = 6) breeding were randomly assigned to three treatment groups for testing on ten training days at approximately 14-day intervals. Pressure applied to a headcollar via a lead rope was used as the stimulus for each foal to walk forward and this was repeated until the foal had walked a distance of 8 m. The effects of three different latencies of negative reinforcement were evaluated by releasing the pressure either immediately as the first foreleg step commenced (Treatment 1); when the second step of the forelegs was completed (Treatment 2) or when the fourth step of the forelegs was completed (Treatment 3). Each foal’s rate of learning was measured by the proportion of correct responses relative to the total number of responses performed. Behavioural responses exhibited (rears, strikes, head shakes, falls, sideways movement and hops) and the steps taken over the distance were also recorded. Initially the foals undergoing Treatment 1 appeared to learn more quickly than those foals undergoing Treatments 2 and 3, suggesting that Treatment 1 was associated with the greatest compliance and the quickest learning. However, the foals undergoing Treatment 3 ultimately achieved significantly (P<0.001) more correct responses, suggesting that the longer delay of reinforcement (i.e., the longer duration of aversive stimulus) may enhance learning via the negative reinforcement inherent in lead training in foals. While some conflict behaviours were shown in all treatment groups, most were exhibited on training day 2. This was reflected in the analysis of composite behaviours performed, with training days 1 and 2 being different (P<0.001) from training day 3 and training days 1 - 3 being different (P<0.001) from training days 4 – 10. These changes indicate that learning occurred in all treatment groups. The foals used in this study were sired by five different stallions. While the foals sired by stallion 2 (WB) performed significantly (P<0.001) more correct responses, those foals sired by Warmblood stallions were significantly (P<0.001) less likely to perform correct responses when compared with those foals of TB or WB x TB breeding. Colts were significantly (P<0.001) more likely to perform correct responses than were fillies.

180

Citation Warren-Smith AK, McLean AN, Nicol HI, McGreevy PD (2005) Variations in the timing of reinforcement as a training technique for foals (Equus caballus) Anthrozoös 18:255