european Veterinary Congress on MoVeMent disorders 2015 · 2 stProceedings 28 ESVN-ECVN Congress -...

Congres proCeedings european Veterinary Congress on MoVeMent disorders

2015

number 400 date . september 2015 editors . Mandigers p.J.J. & granger n.

28stesVn-eCVn CongresAmsterdam

18–19 september

Proceedings 28st ESVN-ECVN Congress - Amsterdam 2015 3 2

dear friends and Colleagues,

Dear ESVN/ECVN family,

it is my great honour and pleasure to welcome you at this year’s conference as your current president of eCVn. esVn/eCVn have been shaping the Veterinary neurology community across europe and the World for multiple decades now. the climax of the society’s and the college’s annual cycle is our scientific conference. every year its quality is going from better to better, from strength to strength. the topic of this year’s conference is Movement disorders – “Moving on”. Movement disorders remain an underdeveloped area in our specialism. i am therefore especially grateful to paul Mandiger, chairman of the 28th esVn/eCVn congress, and his colleague niklas Bergknut to have taken on this challenging topic and come up with a stellate scientific programme, which will help us to develop our understanding further. We are very fortunate to have so many outstanding speakers sharing their expertise and knowledge from human and veterinary medicine alike. please make them feel welcomed. please also join me in thanking the scientific committee (rita gonçalves, peter smith, nicholas Jeffery, ane uriarte; headed by nicolas granger) for ensuring the high standard of the scientific programme and thank you to susanne pauwels and her team for the fantastic organisation. i am sure none of us will return home from this year’s conference without having learned something or having an idea for future research questions needing answering. there could have never been a better topic for a conference this year as also as a college and society we are “moving on” creating a five year strategic plan to continue strengthening our mission across europe and the World.

Welcome and enjoy all the scientific and social aspects of this conference. yours as always

Holger VolkECVN President

dear Colleagues and friends,It is a great pleasure to welcome you all to the 28th ESVN-ECVN congress. Theme of this year is the challenging subject of Movement Disorders.

from Vin i copied a text we will all recognise: 7 month old FI pitbull mix presented peracutely with the behavior demonstrated in this video. 2 days prior to onset there was a brief period of diarrhea that resolved spontaneously. The dog has been doing this for an entire week except when she sleeps and for 1 hour when she was at the dog park. Normal CBC, chem, and UA. No meds. No recent vaccines. Have not imaged yet or obtained CSF. Certainly seems behavioral but I have never seen it come on so acutely. Of course could be a structural problem but was just curious what other’s thoughts were before proceeding. Given the history of diarrhea and the cost of imaging the owner prefers empirical medical treatment so I have started Prilosec, Flagyl, Xanax, and oral acepromazine. During the appointment I gave IV acepromazine and she very quickly settled down and the behavior stopped.

as veterinary neurologists we all struggle, like (so i am told) our human counterparts, with the broad clinical presentation in paroxysmal disorders, tremors, and epilepsy. i am convinced that despite the invention of the smart phone, which has made our life much easier, we all see at least once a week a case that’s not that straightforward. not only do they offer an intellectual challenge to us they are excellent examples of the need to constantly strive for the best of ourselves.

We have invited an excellent group of world leading experts, Md’s and dVM’s, actively working in the field of epilepsy and movement disorders to shed their ‘state of the art’ views on movement disorders (and epilepsy). We will discuss movement disorders in humans and how, if possible at all, to differentiate from epilepsy. We will have insights on the disorders we are facing in our animals and discuss how we could diagnose and treat them. and to test ourselves three of the invited speakers will guide us, during a 1.5 hours ‘smart phone film lecture’ through the foggy broad presentations owners can send us. if we succeed we can submit it for publication with the first veterinary publication mentioning all delegates as contributors. it would not be amsterdam if we would not have somebody present to tell you something about the artificially induced movement disorders you can see (and experience) in the city centre.

the venue is the prestigious royal tropical institute (www.royaltropicalinstitute.nl/en/) created in 1926. We will meet each other, in a lecture hall where once the greatest scientists of their time, presented their global explorations. and although the building is old, the lecture room is truly ‘state of the art’.

as far as our socials are concerned we will start of on thursday the 17th in the amsterdam Zoo ‘artis’, next we will have a gala dinner in the city centre and finish it off with one of the best live band with a mixture of (veterinary) musicians. and if you want you can take a boat trip (offered to you by the city of amsterdam) or visit one of the many musea amsterdam has.

good to have you over. please enjoy!

paul MandigersChairman of the 28th esVn-eCVn congress

Holger Volk eCVn president

Paul Mandigers Chairman of the 28th esVn-eCVn congress

4 Proceedings 28st ESVN-ECVN Congress - Amsterdam 2015 5 Proceedings 28st ESVN-ECVN Congress - Amsterdam 2015 5

Holger Volkpresident

executive Committee ESVN-ECVN Congress 2015

Veronika steinsecretary

thomas flegelVice-president

laurent garosipast president

niklas Bergknut susanne pauwelspaul MandigersChairman

Julien guevaresVn representative

sam longHead of education Committee

Valentina lorenzotreasurer

lara MatiasekHead of examination Committee

taBle of CoNtENtS

1. Foreword of the president of the esVn-eCVn College 2

2. Foreword of the chairman of the esVn-eCVn Congress 3

3. Members of the executive Committee and local organizing committee 4

4. table of contents 5

5. platinum sponsors and sponsors of the congress 7

6. Who’s who 9

9. useful information 9 -10

10. layout of the exhibition room 11

12. Congress programme 12-13

13. Invited speakers 15

14. oral abstracts 37

15. Poster abstracts 55

local organisingCommittee


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Proceedings 28st ESVN-ECVN Congress - Amsterdam 2015 9 Proceedings 28st ESVN-ECVN Congress - Amsterdam 2015 9

BOOK

NOW FOR

EARLY BIRD RATESJOIN US IN

EDINBURGH NEXT YEAR!

29th Annual Symposium of the ESVN-ECVN

15 – 17 September 2016Royal College of Surgeons, Edinburgh, UK

Register your attendance at: www.vetneuro2016.com

WHo is WHo?

ESVN-ECVN BoArdHolger Volk (President)thomas flegel (Vice-president)Veronika stein (secretary)Valentina lorenzo (treasurer)lara Matiasek (Examination committee)sam long (Education committee)Julien guevar (ESVN Representative)laurent garosi (past-president)

ExAMINAtIoN CoMMIttEElara Matiasek (chair)Mike targettChristine thomsonsebastien Behrtom Harcourt-Brown (examination observer)tarja Joniken (examination observer)iris Van soens (examination observer)

EduCAtIoN CoMMIttEEsam long (chair)elsa BeltranCaroline Hahnnick JefferyMerav shamirJean laurent thibautandrea tipold

SCIENtIFIC CoMMIttEEnicolas granger (chair)laurent garosipeter smith

SyMPoSIuM CoMMIttEEpaul Mandigers (chair)niklas Bergknut

PCo SyMPoSIuMsusanne pauwels

VENuEthe congress will take place in:the royal tropical Institute (KIt)Mauritskade 63, 1092 ad amsterdamthe netherlandst: +31 20 56 88 711, f: +31 20 66 84 579www.kit.nl, [email protected]

ACCESSIBILIty tHE royAL troPICAL INStItutEBy car leave the ring road a10 via the exit Watergraafsmeer/ diemen (s113): follow the Middenweg (direction Centrum/ Watergraafsmeer), which turns into the linnaeusstraat. Kit is at the corner of the linnaeusstraat and the Mauritskade. there are paid parking facilities in the vicinity.

By public transport– from amsterdam Central station: tram 9– from amsterdam Muiderpoort station:

tram 3 or 7– from dam square: tram 9 or 14 – from leidseplein: tram 7 or 10– from Museumplein: tram 3

PArKINgthere are enough on-street parking area’ s near Kit. please note that all parking in the centre of amsterdam is metered from Monday through saturday, 09.00 to 19.00 hrs. for rates and other parking information, please visit www.bereikbaaramsterdam.nl. parking meters take coins and Chipknip smart cards.

rEgIStrAtIoN dESKthe registration area in the congress centre will be open for registration:thursday 17 september: 16.00 – 18.00 hrs. friday 18 september: 07.30 – 18.00 hrs.saturday 19 september: 07.30 – 18.00 hrs.

CErtIFICAtE oF AttENdANCEall participants will receive a certificate of attendance by email after the congress.

uSEFuL inforMation


LANguAgEthe official language of the congress is english.

CoNgrESS BAdgESall participants, accompanying persons and exhibitors must wear the Congress identification badges. entrance to meeting halls, poster and exhibition area will not be permitted to any person without badge.

CurrENCythe dutch currency is euro. Most hotels, restaurants and shops accept international credit cards.

VENuE WELCoME rECEPtIoN: thursday 17 september 19.00 hrs.Artisnatura artis Magistraplantage Kerklaan 38-40 amsterdam the netherlands

VENuE dINNErnH grand Hotel Krasnapolskydam 9 amsterdamthe [email protected]

VENuE dANCEolofskapelZeedijk 2 amsterdam

MoBILE PHoNE MANNErSas a courtesy to other attendees, please observe good mobile phone manners. When attending sessions, please turn off your mobile phone and other wireless communications or use the silent notifications options. if you must take a call, please step out of the room rather than disrupting the event. thank you for your cooperation.

LIABILItyupon registration, participants agree that neither the organizing Committee nor the Congress secretariat assume any liability. participants should, therefore, organize their own health and travel insurance.

We reject all liability for direct or indirect damages, of whatever nature, resulting from or connected in any way with the use of our website, or from the temporary inability to be able to consult our website. nor are we liable for direct or indirect damages arising from the use of information taken from our website.

CoNgrESS SECrEtArIAtpauwels Congress organisersalexander Battalaan 7 6221 Ca Maastrichtthe netherlandsContact person: susanne pauwelst +31 (0) 43 321 81 [email protected]

ESVN-ECVN 2015Royal Tropical Institute,

Amsterdam, The Netherlands

Rece

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Toilets

12 Proceedings 28st ESVN-ECVN Congress - Amsterdam 2015 13

18-19 September 2015

the 28th European ESVN-ECVN congress

KIT, Amsterdam The Netherlandswww.ecvn.org

Platinum sponsor of the ESVN-ECVN Congress for 2015-2017

Time table ESVN/ECVN congress

ThurSdAy 17-9-2015 residents and Practioneers day at uu-utrecht (from 10 to 16 hrs)

Welcome party - Artis Zoo with guided tours from 18.30 to ... hrs (registration is required!)

FrIdAy 18-9-2015Chair:

SPEAKEr SubjECT

8.30-8.40 Paul Mandigers Welcome

8.40-9.30 hans Stroink Epilepsy in children, classification and diagnostics, when is it epilepsy?

9.30-9.45 Luisa de risio Epileptoid cramping syndrome in the norwich terrier: clinical characterisation and prevalence in the uk

9.45-10.00 Emi Ngaire barker Degenerative encephalopathy of nova scotia duck tolling retrievers

10.00-10.15 Fiona james Epileptogenic electroencephalographic findings in canine episodic head tremor syndrome

10.15-10.45 Coffeebreak

Chair:

10.45-11.00 Franziska Wieländer* Myoclonic epilepsy with photosensitivity in rhodesian ridgebacks

11.00-11.15 Tarek bouzouraa Long-term treatment of canine paroxysmal dyskinesias with fluoxetine: 6 cases

11.15-11.30 Mihai Musteata Interictal cardiac autonomic nervous system disturbances in dogs with idiopathic epilepsy

11.30-11.45 Mark Lowrie Canine epileptoid cramping syndrome: a gluten sensitive paroxysmal movement disorder – more than a gut feeling

11.45-12.30 ronald Corbee (sponsored by hills)

Influence of supplements, nutrition on epilepsy and movement disorders

12.30-13.45 Lunchbreak

Chair:

13.45-14.00 Sofie bhatti Alternative non-medical treatments vagal stimulation, transcranial magnetic stimulation in epilepsy

14.00-14.15 Kenny bossens* The effect of imepitoin, a recently developed antiepileptic drug, on thyroid function test parameters and fat metabolism in healthy beagle dogs

14.15-14.30 Gualtiero Gandini Efficacy of imepitoin as first choice drug in the treatment of 53 naïve dogs affected by idiopathic epilepsy

14.30-15.30 bas bloem Recognition, classification and treatment of neurological movement disorders in humans

15.30-16.00 Teabreak

Chair:

16.00-16.30 bas bloem Recognition, classification and treatment of neurological movement disorders in humans

16.30-16.45 Ana Maria Tomaz Coelho

Value of cerebrospinal fluid analysis in epileptic dogs that lack interictal neurological abnormalities and have unremarkable magnetic resonance imaging of the brain

16.45-17.30 dennis O'brien Movement disorders in animals: terminology, classification part 1

17.30-19.00 ESVN/ECVN AGM

19.00-22.00 ESVN/ECVN Congressdinner Wintertuin, hotel Krasnapolsky (seated dinner)

22.00-02.00 Live music - band Olofskapel

* young neurologist in training / resident

Invited Speakers:Dr. Hans Stroink (md) Canisius ZKh Nijmegen (nl)

Dr. Ronal Corbee (dvm) utrecht university (nl)

Prof.dr. Bas Bloem (md) radboud university (nl)

Prof.dr. Dennis O’Brien (dvm) university of Missouri (usa)

Prof.dr. Angelika Richter (dvm) university of Leipzig (dui)

Dr. Franziska Richter (dvm) university of Leipzig (dui)

Dr. Caroline Hahn (dvm)Edinburgh (uK)

SATurdAy 19-9-2015 SPEAKEr SubjECT

Chair:

8.30-9.30 dennis O'brien Movement disorders in animals: terminology, classification part 2

9.30-9.45 Catherine Escriou Phenotypic characterization of spinning and tail-chasing in german sheperd and jack russel terrier

9.45-10.00 Andrea Fischer Vldlr-associated cerebellar hypoplasia in eurasier dogs

10.00-10.15 Caroline hahn Movement disorders in large animals

10.15-10.45 Coffeebreak

Chair:

10.45-11.45 Angelika richter & Franziska richter

What can we learn from animal models of dystonia/dyskinesias in veterinary and human neurology

11.45.12.00 Clare rusbridge Mri protocol in epilepsy, md cases and outlook for the future

12.00-12.15 Clare rusbridge Computer simulation of the canine spine: the effects of increased spinal cord motion on the developemnt of syringomyelia

12.15-12.30 Gemma Elizabeth Longson

A preliminary study of the penlight-cover test in differentiating between peripheral and central vestibular disease in dogs and cats

12.30-14.00 Lunchbreak

Chair:

14.00-14.45 hans Stroink & dennis O'brien & Angelika richter

Videosessions with the audience and voting system: how much do we think to know,..

14.45-15.00 jessica Freundt revilla* Interleukin-17 and cd40 ligand in canine steroid-responsive meningitis-arteritis

15.00-15.15 Simone Gross* Morphological reclassification of immune-mediated neuropathies (impn) in dogs and cats: beyond the concept of axonal and demyelinating disease

15.15-15.30 Florian Salger* Immunohistochemical characterization of the anti-inflammatory effect of two treatment protocols in dogs with granulomatous meningoencephalomyelitis or necrotizing (meningo)-encephalitis

Chair:

15.30-16.00 Teabreak

16.00-16.15 Kali Tulle Lazzerini* Clinical, imaging characteristics and long term outcome of dogs with intranasal meningoencephalocele: a case series

16.15-16.30 Sarah hanemann* Multiple thoracolumbar partial lateral corpectomies in 17 dogs

16.30-16.45 Cristoforo Francesco ricco*

Comparison of conventional and high definition video telescope assisted ventral slot decompression for cervical intervertebral disc herniation in 51 dogs

16.45-17.00 Antonella Gallucci* Acquisition of involuntary spinal locomotion (spinal walking) in dogs with irreversible thoraco-lumbar spinal cord lesion: a retrospective study on 81 dogs

17.00-17.15 dominik Faissler Role of therapy with growth factors in the management of pain perception negative dogs caused by thoracolumbar disk extrusions

17.15-17.30 Patricia Montoliu Identification of behavioral states in canine neonates and their influence on neurological examination

17.30-17.45 Paul Mandigers & Niklas bergknut

Mushroom, other drugs and smartshops in Amsterdam and what kind of movements disorders can follow, closing remarks

17.10-18.00 Farewell

* young neurologist in training / resident

Thursday 17 September 2015: welcome partyFrom 19.00 to 21.00 hours in ArTIS, the famous Amsterdam Zoo. The Welcome reception will take place in the ‘Koningszaal’. drinks and small canapés will be served. Without registration no admittance!www.artis.nl/bezoekersinfo/route-parkeren

Friday 18 September 2015: congress dinnerFrom 20.00 to 01.00 hours. during and after the seated dinner live music. Without registration no admittance! Costs € 70 (dinner, drinks during the dinner and admittance to the party are included).

Congress VenueThe Royal Tropical InstituteMauritskade 631092 Ad Amsterdam The Netherlands+31 20 56 88 711 www.kit.nl [email protected]

Venue Welcome ReceptionArtisNatura Artis MagistraPlantage Kerklaan 38-40 Amsterdam, The Netherlands

Venue DinnerNh Grand hotel Krasnapolskydam 9 AmsterdamThe [email protected]

Venue DanceOlofskapelZeedijk 2 Amsterdam

Congress SecretariatPauwels Congress OrganisersAlexander battalaan 7 6221 CA MaastrichtThe NetherlandsContact person: Mrs. Susanne Pauwels31 (0) 43 321 81 [email protected]

Proceedings 28st ESVN-ECVN Congress - Amsterdam 2015 13


inVited speaKers

Introducing PEXION® for canine epilepsy.The � rst and only targeted therapy that lets dogs and their owners live in the moment instead of living with side effects.1 With PEXION®, you can change the conversation about epilepsy without changing your patients’ personalities.

Be a part of the change.

Reference: 1. Rieck S, Rundfeldt C, Tipold A. Anticonvulsant activity and tolerance of ELB138 in dogs with epilepsy: a clinical pilot study. Vet J. 2006;172(1):86–95.

PEXION® is a registered trademark of Boehringer Ingelheim Vetmedica GmbH.© 2015 Boehringer Ingelheim Vetmedica GmbH. 15811

Name: Pexion® 100 mg/400 mg tablets for dogs. Active ingredient: imepitoin 100 mg/400 mg. Indication: For the reduction of the frequency of generalised seizures due to idiopathic epilepsy in dogs for use after careful evaluation of alternative treatment options. Target species: dog. Contraindications: Do not use in case of hypersensitivity to the active substance or any of the excipients. Do not use in dogs with severe hepatic impairment, severe renal or severe cardiovascular disorders. Adverse reactions: The following mild and generally transient adverse reactions have been observed in pre-clinical and clinical studies in order of decreasing frequency: polyphagia at the beginning of the treatment (very common), hyperactivity, polyuria, polydypsia, somnolence, hypersalivation, emesis, ataxia, apathy, diarrhoea, prolapsed nictitating membrane, decreased sight and sensitivity to sound. A mild elevation in plasma creatinine and cholesterol levels has been observed in dogs treated with imepitoin; however these did not exceed the normal reference ranges and were not associated with any clinically signi� cant observations or events. Dosage: Oral administration at a dose range of 10 mg to 30 mg imepitoin per kg bodyweight twice daily, approximately 12 hours apart. The required dose will vary between dogs and will depend on the severity of the disorder. The recommended initial dose of imepitoin is 10 mg per kg bodyweight twice daily.Registration: REG NL 110795 / REG EN 110 796 Sewerage Status: UDA.

There are a million reasons why owners love their dogs

NONE OF THEM ARE WORTH GIVING UP

Reason 16: Duets are always more fun.


EPILEPSy IN CHILdrEN, CLASSIFICAtIoN ANd dIAgNoStICS, WHEN IS It EPILEPSy?

Hans Stroink (MD, PhD), Canisius Hospital, Nijmegen, The Netherlands

in childhood many non-epileptic paroxysmal events occur making a correct diagnosis difficult. the first question is: are the events epileptic or not? an eyewitness account is important, but not always clear. a home video may be helpful. the eeg can be misleading. 3.5% of healthy children, who will never develop epilepsy, show epileptiform discharges during a standard eeg. in children with for example adHd or autism the incidence is even much higher. artefacts and normal variants can simulate epileptiform discharges in all ages. this may result in a misdiagnosis. Moreover, many epilepsy patients don’t show epileptiform discharges.in humans the onset of idiopathic (genetic) epilepsy is almost always before the age of 20. Most human idiopathic epilepsy syndromes are not diagnosed by excluding a cause. they are clinically easily recognisable, characterised by specific age of onset, semiology (generalised as well as focal) and moment of time of the seizures, and eventually the eeg. for example rolandic epilepsy with centrotemporal spikes starts during school age with specific partial seizures during sleep; juvenile myoclonic epilepsy and awakening epilepsy start between 10-20 years with generalised seizures shortly after awakening. during the presentation diagnosis and classification will be discussed extensively.

INFLuENCE oF SuPPLEMENtS / NutrItIoN oN EPILEPSy ANd MoVEMENt dISordErS

Ronald Jan Corbee, DVM, PhD, Dipl. ECVCN. Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands.

Introductionnutrition affects health and disease, and nutritional therapy is common practice for many years. as Hippocrates stated: let thy food be thy medicine and medicine be thy food. nutritionists deal with nutrition induced disorders (i.e. disorders caused by nutrient deficiencies) and with nutrition related disorders (i.e. disorders that are affected by nutrition like the beneficial effect of phosphorus restriction on the progression of renal failure).

Nutrition induced disorders regarding epilepsy and movement disordersnutrition induced disorders regarding epilepsy and movement disorders are: deficiencies in nutrients that are needed for development of brain tissue and myelin sheaths, deficiencies in minerals and electrolytes interfering with neurotransmission, hypoglycemia, hypocalcemia, arginine deficiency in cats causing hepatic encephalopathy, and thiamine deficiency. Most of these deficiencies are seldom seen due to the fact that most cat and dog owners are feeding complete and balanced diets. the effects of several nutrient deficiencies are described in nrC 2006 (1). toxicities that can cause epilepsy and movement disorders are: protein excess causing hepatic encephalopathy, lead poisoning, pathogens from raw food, and contaminants like salinomycine (2,3) and mycotoxins (4). guidelines for early diagnosis and treatment are given in the article by Barker et al. 2013 (5).

Nutrition related disorders regarding epilepsythe ketogenic diet has been effective in cases of epilepsy in young children (6), however, dogs do not get ketotic so this is not an effective treatment option for dogs (7). Because no studies have been done in cats,

Introducing PEXION® for canine epilepsy.The � rst and only targeted therapy that lets dogs and their owners live in the moment instead of living with side effects.1 With PEXION®, you can change the conversation about epilepsy without changing your patients’ personalities.

Be a part of the change.

Reference: 1. Rieck S, Rundfeldt C, Tipold A. Anticonvulsant activity and tolerance of ELB138 in dogs with epilepsy: a clinical pilot study. Vet J. 2006;172(1):86–95.

PEXION® is a registered trademark of Boehringer Ingelheim Vetmedica GmbH.© 2015 Boehringer Ingelheim Vetmedica GmbH. 15811

Name: Pexion® 100 mg/400 mg tablets for dogs. Active ingredient: imepitoin 100 mg/400 mg. Indication: For the reduction of the frequency of generalised seizures due to idiopathic epilepsy in dogs for use after careful evaluation of alternative treatment options. Target species: dog. Contraindications: Do not use in case of hypersensitivity to the active substance or any of the excipients. Do not use in dogs with severe hepatic impairment, severe renal or severe cardiovascular disorders. Adverse reactions: The following mild and generally transient adverse reactions have been observed in pre-clinical and clinical studies in order of decreasing frequency: polyphagia at the beginning of the treatment (very common), hyperactivity, polyuria, polydypsia, somnolence, hypersalivation, emesis, ataxia, apathy, diarrhoea, prolapsed nictitating membrane, decreased sight and sensitivity to sound. A mild elevation in plasma creatinine and cholesterol levels has been observed in dogs treated with imepitoin; however these did not exceed the normal reference ranges and were not associated with any clinically signi� cant observations or events. Dosage: Oral administration at a dose range of 10 mg to 30 mg imepitoin per kg bodyweight twice daily, approximately 12 hours apart. The required dose will vary between dogs and will depend on the severity of the disorder. The recommended initial dose of imepitoin is 10 mg per kg bodyweight twice daily.Registration: REG NL 110795 / REG EN 110 796 Sewerage Status: UDA.

Reason 125: His nose gets into everything.

There are a million reasons why owners love their dogs

NONE OF THEM ARE WORTH GIVING UP


Brain diet: effects of nutrition on cognitionthe effects of antioxidants and l-carnitine on cognition in dogs have been studied (25,26). the effects were demonstrated on the long-term (2 years) in 48 Beagle dogs, and the dogs that received additional environmental enrichment performed best, indicating that a multimodal treatment (including diet fortification) is the best approach (26).

references1. National Research Council 2006. Nutrient Requirements of Dogs and Cats.

2. Linde-Sipman, J.S. van der, Ingh, T.S.G.A.M. van den, Nes, J.J. van, Verhagen, H., Kersten J.G.T.M., Beynen, A.C., Plekkringa, R.

Salinomycin-induced Polyneuropathy in Cats: Morphologic and Epidemiologic Data. Vet Pathol 1999 36: 152-156

3. Peixoto, P.V., Nogueira, V.A., Gonzaléz, A.P., Tokarnia, C.H., França, T.N. Accidental and experimental salinomycin poisoning in

rabbits. Pesq Vet Bras 2009 29 no.9 Rio de Janeiro

4. Puschner, B. Mycotoxins. Vet Clin North Am Small Anim Pract 2002 32 409-419

5. Barker, A.K., Stahl, C., Ensley, S.M., Jeffery N.D. Tremorgenic mycotoxicosis in dogs. Vetlearn.com 2013

6. Levy, R.G., Cooper, P.N., Giri, P. Ketogenic diet and other dietary treatments for epilepsy. Cochrane Database Syst Rev. 2012 Mar

14;3:CD001903

7. Naoum, H., Nes, J.J. van, Kappert, H.J., Beynen, A.C. Effect of acetic acid consumption on clinical laboratory values in the dog.

Journal of An Phys An Nutr 2002 86, 105-110

8. Maguire, P.J., Fettman, M.J., Smith, M.O., Greco, D.S., Turner, A.S., Walton, J.A., Ogilvie, G.K. Effects of diet on pharmacokinetics of

phenobarbital in healthy dogs. J Am Vet Med Assoc. 2000 15;217(6):847-852

9. Fukunaga K., Saito, M., Muto, M., Mishima, K., Fujiwara, M., Orito, K. Effects of urine pH modification on pharmacokinetics of

phenobarbital in healthy dogs. J Vet Pharmacol Ther. 2008 31(5):431-436

10. Frenia, M.L., Schauben, J.L., Wears, R.L., Karlix, J.L., Tucker, C.A., Kunisaki, T.A. Multiple-dose activated charcoal compared to

urinary alkalinization for the enhancement of phenobarbital elimination. J Toxicol Clin Toxicol. 1996 34(2):169-175

11. Pusch, M., Jordt, S.E., Stein, V., Jentsch, T.J. Chloride dependence of hyperpolarization-activated chloride channel gates.

J Physiol. 1999 1 515:341-353

12. Larsen, J.A., Owens, T.J., Fascetti, A.J. Nutritional management of idiopathic epilepsy in dogs. J Am Vet Med Assoc. 2014

245(5):504-508

13. Tanizawa, K., Mizuno, T., Ueda, K., Koyama, I. Taurine treatment for spontaneous epilepsy in the cat. Nihon Juigaku Zasshi. 1986

48(5):1041-1043

14. Gelder, N.M. van, Koyama, I., Jasper, H.H. Taurine treatment of spontaneous chronic epilepsy in a cat. Epilepsia. 1977 18(1):45-54

15. Scorza, F.A., Lopes, A.C., Cysneiros, R.M., Arida, R.M., Silva, M.R. The promise of omega-3 against sudden unexpected death in

epilepsy: until further notice, it remains innocent, until proven guilty. Arq Neuropsiquiatr. 2013 Jan;71(1):51-54

16. Matthews, H., Granger, N., Wood, J., Skelly, B. Effects of essential fatty acid supplementation in dogs with idiopathic epilepsy:

a clinical trial. Vet J. 2012 Mar;191(3):396-398

17. McDonald, T.S., Tan, K.N., Hodson, M.P., Borges, K. Alterations of hippocampal glucose metabolism by even versus uneven

medium chain triglycerides. J Cereb Blood Flow Metab. 2014 34(1):153-160

18. Law, T.H., Yuanlon, P., Zanghi, B., Want, E., Volk, H. The effects of a medium chain triglycerides diet trial on dogs with idiopathic

epilepsy. In Proceedings: ACVIM 2015.

19. Lutz, S., Sewell, A.C., Reusch, C.E., Kook, P.H. Clinical and laboratory findings in border collies with presumed hereditary juvenile

cobalamin deficiency. J Am Anim Hosp Assoc. 2013 49(3):197-203

20. Takeda, A., Nyssen, O.P., Syed, A., Jansen, E., Bueno-de-Mesquita, B., Gallo, V. Vitamin A and carotenoids and the risk of Parkinson‘s

disease: a systematic review and meta-analysis. Neuroepidemiology. 2014;42(1):25-38

21. Black, V., Garosi, L., Lowrie, M., Harvey, R.J., Gale, J. Phenotypic characterisation of canine epileptoid cramping syndrome in the

Border terrier. J Small Anim Pract. 2014 55(2):102-107

22. Park, H.J., Seo, D.K., Song, K.H., Seo, K.W. Paroxysmal dyskinesia suspected as canine epileptoid cramping syndrome in a young

Yorkshire terrier dog. J Vet Med Sci. 2014 76(8):1129-1132

23. Ribaldone, D.G., Astegiano, M., Fagoonee, S., Rizzetto, M., Pellicano, R. Epilepsy and celiac disease: review of literature. Panminerva

Med. 2011 53(4):213-216

it should not be recommended in cats until these diets have been demonstrated to be effective and safe. diet change may affect phenobarbital treatment. a low protein diet (less than 17% of protein on a dry matter basis) lowers the half-life of phenobarbital by 7-9 hours compared to a normal protein diet (22% of protein on a dry matter basis) in dogs (8). urine alkalizing diets, that are used in cases of renal failure, calciumoxalate urolithiasis, cysteine urolithiasis, and urate urolithiasis promotes the excretion of phenobarbital (9,10). therefore, it is recommended to check plasma phenobarbital levels after a diet change.potassium-bromide is used as mono-treatment and in multimodal-treatment of epilepsy. the working mechanism is well described in the article by pusch et al. 1999 (11). Because bromide acts on chloride channels, there are several interactions with dietary chloride. it is important to keep dietary chloride intake as constant as possible during potassium-bromide treatment as increased intake of chloride (common source are human foods and treats) decreases the elimination half-life of bromide, whereas a decreased intake of chloride may lead to bromism (12).several micro-nutrients have been mentioned to play a role in epilepsy. taurine (100-500mg per cat per day) has been reported to reduce seizure frequency in a small number (n=6) of cats (13,14) and (relative) deficiencies of several micronutrients have been reported to increase seizure frequency in humans (15). dietary long-chain polyunsaturated fatty acids eicosapentaenoic acid and docosahexaenoic acid (epa+dHa 106mg per kg of metabolic body weight) have been reported to reduce seizure frequency in a great dane (15), however a clinical trial of epa+dHa (115mg per kg metabolic body weight) in 15 dogs failed to demonstrate an effect (16). the authors explained this difference due to the fact that early onset of treatment may be effective, whereas initiation of treatment in refractory cases is not (16). Medium chain triglycerides (MCt) have been reported to be effective in mice (17). a recent study in 21 dogs demonstrated a reduction in seizure frequency on a MCt supplemented diet compared to a control diet, but unfortunately the diet composition was not given (18).

Nutrition related disorders regarding movement disordersMovement disorders may alter energy requirements. furthermore, the medication used in movement disorders can affect taste and smell. in some movement disorders the gastrointestinal tract is involved and may require alterations in feeding management (i.e. megoaesophagus requires feeding from a height, swallowing disorders may require a different texture of the food). Movement disorders are associated with cobalamin deficiency (19). evidence for nutritional therapy for movement disorders in dogs and cats is lacking, and in humans there is a lot of conflicting data (20).Movement disorders can be associated with mycotoxicosis as described earlier (4,5), however these cases are usually self-limiting (4,5). there is some evidence that supports nutritional therapy in dogs with canine epileptoid cramping syndrome (CeCs) (21,22). one study on the phenotypic characterization of CeCs in 29 Border terriers reported that in 14 out of 26 dogs that switched from their own diet to a “hypoallergenic diet” there was a reduction in frequency of episodes (21). one case report in a 9 month old yorkshire terrier reported marked improvement when the dog was switched to a commercially available renal diet (22). the authors did not explain the mechanism behind the nutritional therapy and also gave no information about the previous diet. the typical aspects of the diet they chose are: low protein, low sodium, alkalizing, added epa+dHa and antioxidants, and egg as the sole protein source. theoretically this could also be a “hypoallergenic diet”.the effects of “hypoallergenic” diets on epilepsy have also been studied. in humans, epilepsy is associated with several systemic (auto)immune disorders, including celiac disease (23). Marked improvement was demonstrated after switching to a gluten-free diet (24). the mechanism is unknown, and in dogs and cats to date no studies have been performed. it is, however, not harmful to put dogs with epilepsy on a “hypoallergenic” diet to monitor the effects, especially when other signs of adverse reactions to food are present.


type of movement disorder has been defined properly, because the approach to each type of movement disorder is more focused. for example, the work-up for dystonia is very different from that for, say, chorea. second, adequate classification – as a means to establish the correct diagnosis – often has prognostic implications. for example, essential tremor is sometimes mistaken for early pd, but the prognosis is clearly different. furthermore, since several movement disorders are genetically determined (for example, Huntington’s disease), accurate classification leading to the proper diagnosis may also have implications for the patient’s family. finally, differentiating between the different types of movement disorder can have important consequences for treatment.

unfortunately, the diagnostic process is commonly perceived as being difficult, is frequently protracted, and misdiagnoses are common. Because of their unusual presentation, patients with movement disorders may be diagnosed as having a psychogenic disease (although the converse is also true).

Here, we provide a viewpoint, as a practical approach to help clinicians in the “pattern recognition” of movement disorders, and in the process of translating a particular movement disorder syndrome – once it has been classified clinically – into an etiological diagnosis. this is not a review of the literature, is not meant to be exhaustive, and will only briefly touch upon ancillary investigations, which are not within its scope. What we concentrate on is the most important step in the diagnostic process, i.e. the clinical approach. an unambiguous diagnostic process begins with the recognition of the type(s) of movement disorder present in the patient as the first crucial step. in the remainder of this viewpoint, we first highlight the salient features of these different types of movement disorder, attaching to each of them one or more specific keywords for ease of recognition. We then propose a practical approach, using the identified movement disorder(s) as the starting point for a stepwise diagnostic work-up.

general classification principles & phenomenology generally speaking, two main categories of movement disorder phenomena can be distinguished, with several specific subdivisions (table 1). the first category corresponds broadly to akinetic-rigid disorders, the second to hyperkinetic disorders. the hyperkinetic disorders are usually perceived as being more difficult diagnostically. it helps tremendously to separate this group into two main subdivisions: one where the movements have a jerky character, and a second where this jerky character is absent. not that many disorders feature a combination of both categories.

Akinetic-rigid syndromesthe literature uses the terms akinesia, bradykinesia and hypokinesia inconsistently. We define akinesia as an umbrella term for a symptom complex that can include bradykinesia (slowness of movement) and hypokinesia (poverty of movement, and movements that are smaller than intended), but also – crucially and fundamentally – the progressive fatiguing and decrement of repetitive alternating movements seen during finger or foot tapping. We ask the patient to make large, regular repetitive alternating movements of each extremity in turn: opposition of the thumb to the crease between the terminal phalanges of the index and third fingers, and repeatedly tapping the forefoot on the floor, keeping the heel on the ground. it is easy to see early progressive reduction in amplitude or speed of the movements (or, at the ankle, to hear it). sometimes, however, the clinical question is not whether akinesia/bradykinesia is present, but whether it is absent. this takes a bit more time to demonstrate, and in order to be certain of this we recommend asking the patient to do up to 64 repetitions in each extremity, if necessary. sometimes severe tremor can intervene to “hijack” the movements, and make this assessment difficult or impossible. in the widely used Queen square Brain Bank Criteria7 for the diagnosis of parkinsonism, bradykinesia is defined as including these last two elements, which we would consider under the broader rubric of akinesia. this variability in terminology is not in itself important as long as, whatever name one gives, fatiguing and decrement are defining features for (untreated) parkinsonism. note that signs of

24. Freeman, H.J. Neurological disorders in adult celiac disease. Can J Gastroenterol. 2008 22(11):909-911

25. Araujo, J.A., Studzinski, C.M., Head, E., Cotman, C.W., Milgram, N.W. Assessment of nutritional interventions for modification

of age-associated cognitive decline using a canine model of human aging. Age (Dordr). 2005 27(1):27-37

26. Milgram, N.W., Head, E., Zicker, S.C., Ikeda-Douglas, C.J., Murphey, H., Muggenburg, B., Siwak, C., Tapp, D., Cotman, C.W. Learning

ability in aged beagle dogs is preserved by behavioral enrichment and dietary fortification: a two-year longitudinal study.

Neuro biol Aging. 2005 26(1):77-90

tHE CLINICAL APProACH to MoVEMENt dISordErS

Wilson F. Abdo1, Bart P.C. van de Warrenburg1, David J. Burn2, Niall P. Quinn3 and Bastiaan R. Bloem1

1Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre; 2Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne, United Kingdom; and 3Institute of Neurology, London, United Kingdom

SummaryMovement disorders are common. in this viewpoint, aimed at trainees and general neurologists, we provide a practical step-by-step approach to help clinicians in their “pattern recognition” of movement disorders, as a process that ultimately leads to the diagnosis. the key to success is to establish the phenomenology of the clinical syndrome. this is determined from the specific combination of the dominant movement disorder, often combined with other abnormal movements in patients presenting with a mixed movement disorder, plus a set of associated neurological and non-neurological abnormalities. the clinical syndrome so defined should, in turn, lead to a differential diagnosis. sometimes simple pattern recognition will suffice and lead directly to the diagnosis, but often ancillary investigations, guided by the dominant movement disorder, are required. We illustrate this diagnostic process for the most common types of movement disorder: akinetic-rigid syndromes, and for the various types of hyperkinetic disorders (myoclonus, chorea, tics, dystonia, and tremor).

BackgroundMovement disorders such as parkinson’s disease (pd), tremor, tics and dystonia are common. for example, the overall prevalence of pd is 1% in people in the ages 65-85 years, and this increases to 4.3% above the age of 85 years.1 the prevalence of essential tremor – the most common form of tremor – is 4% in the ages >40 years, and increases up to 14% in people over the age of 65 years.2, 3 the prevalence of tics in school aged children and adolescents is as high as 21%.4

the clinical presentation of movement disorders is complex, often variable, and sometimes even bizarre. establishing the correct diagnosis can therefore be difficult, even in the hands of experienced movement disorder specialists. However, accurate recognition based on clinical acumen is important, for several reasons.

first, a correct classification of the type of movement disorder(s) forms the basis for the subsequent diagnostic process. for most disorders, there is no specific biological marker that can unambiguously diagnose the underlying disease. Many diagnostic tests are available,5, 6 but these are often expensive, time-consuming and sometimes invasive. Moreover, their diagnostic value (over and above clinical judgement) is often limited, especially in early stages of the disease. Hiding clinical uncertainty behind a broad battery of ancillary studies (the “scatter gun” approach) is generally unrewarding, because of the large range of potential diagnoses. the investigational work-up can be greatly simplified once the


moments of occurrence for myoclonus. thus, myoclonus can occur spontaneously (at rest), but is also often present, and usually worsened, during movement (action myoclonus) or provoked by external tactile or acoustic stimuli (reflex myoclonus). Cortical myoclonus is more often action – or stimulus-sensitive, mostly to distal touch or stretch, and occasionally to visual stimuli. Brainstem myoclonus is more commonly provoked by auditory stimuli, or tactile stimuli around the face or snout. it is therefore important to look for stimulus sensitivity when assessing suspected myoclonus. Cortical myoclonus is often more focal, and subcortical myoclonus more often generalised. Certain types of myoclonus have different neurophysiological characteristics.10

a clinically difficult category is propriospinal myoclonus, i.e. myoclonus generated within the spinal cord with subsequent upward and downward spread, as these movements are perceived as being too slow and lacking the jerky character.11 often polymyographic recordings are needed to prove the myoclonic nature of these axial movements. in some cases spinal pathology can be demonstrated, but in most it is not. a proportion of this latter group are psychogenic, but their semiology and physiology can mimic organic cases, so diagnosis of pathogenesis is difficult.

startle reactions, which are part of the spectrum of myoclonus, are also provoked by external stimuli, most often by auditory triggers, but also by surprise, alarm or acute pain. the startle reaction is characterised by a bilaterally synchronous shock-like set of movements.12

ChoreaChorea is perhaps not immediately appreciated as being a “jerky” movement disorder, perhaps because the word Chorea (greek for dance) suggests a certain grace rather than abrupt, jerky movements. However, if one carefully observes a patient with chorea, it immediately becomes evident that the “choreography” includes a constellation of randomly flowing movements, which are, individually, jerky in nature. thus, chorea can be defined as involuntary movements that are abrupt, unpredictable and non-rhythmic, resulting from a continuous random flow of muscle contractions. a key difference from myoclonus is that the pattern of movements randomly changes from one body part to another, conveying the impression of “fidgeting” to the observer. so if we were to attach a key description to chorea, it would be randomly flowing jerks. other typical signs of chorea are the motor impersistence, such as seen in the fluctuating strength of the grip (so-called ‘milkmaid’s grip’), or hung-up reflexes (sustained contractions and choreatic movements of the leg after the knee jerk reflex).13 some patients with chorea, e.g. in Huntington’s disease, may have additional brief (<100 msec) muscle jerks that are myoclonic, and/or longer (>500 msec) co-contracting muscle spasms that are dystonic.

Mild chorea may be subtle, but can usually be detected if the clinician carefully observes the patient with this possibility in mind. finger chorea is best brought out by the subject counting backwards with eyes closed and arms outstretched, or when walking. identifying chorea is sometimes hampered by the fact that patients frequently try to mask their chorea by incorporating the jerks into voluntary movements. another pitfall is that choreatic patients themselves often have relatively few subjective complaints, certainly in early stages, when it is usually the partner who complains about the movements. this is not uncommon in for example Huntington’s disease.

Ballism is typically considered under the rubric of chorea because it shares the same pathophysiology and treatment. Ballistic movements are uncontrollable, severe, mainly proximal, large amplitude chorea. they are usually unilateral (hemiballism) and are classically described after an acute lesion in the region of the contralateral subthalamic nucleus.14 the term hemichorea can also be used when the amplitude of the movement is small. sometimes the movements involve only one limb (monoballism). Bilateral ballistic movements are rare and mostly due to metabolic abnormalities.

akinesia may be masked in treated patients. it is also important to recognise that slowness of movement, without fatiguing and decrement, is seen with pyramidal and cerebellar dysfunction (often with additional clumsiness or irregularity). this may explain why patients with an upper motor neurone presentation of amyotrophic lateral sclerosis (with pyramidal slowing, and increased tone due to spasticity) are rarely misdiagnosed as having parkinsonism.8

an additional component of akinesia is absence or poverty of automatic movements (we refer to this as hypokinesia), manifested by, for example, hypomimia, with reduced blinking, or a reduced arm swing during walking. Care should be taken not to mistake depression for a masked face, and to recognise other possible causes for reduced arm swing, since this can be seen in subjects who are unsteady for any cause, in patients with dystonia, and with musculoskeletal problems such as frozen shoulder (although the latter not uncommonly precedes the diagnosis of pd).

increased muscle tone across a joint due to rigidity or spasticity can be differentiated while examining the full range of motion of a joint with varying speeds. in rigidity the resistance is more or less stable, and equal between flexion and extension movements, during the whole trajectory. in spasticity the tone is preferentially increased in arm flexors and leg extensors, and sudden decreases of muscle resistance (‘clasp knife phenomenon’) may be felt.

“Jerky” hyperkinetic syndromesthis category includes myoclonus (together with excessive startle), chorea and tics. Jerky movements may be seen in isolation or in combination with non-jerky movements.

MyoclonusMyoclonic movements are sudden, brief, shock-like involuntary movements caused by muscular contractions, which are usually positive, but sometimes negative (due to brief loss, or inhibition of muscular tonus, as in “liver flap” or “asterixis” in hepatic or uremic encephalopathy). negative myoclonus can also be seen while walking, producing a typical veering gait pattern, or the sudden postural lapses (“bouncy gait”) seen in post-anoxic myoclonus. Myoclonic muscle contractions are mostly accompanied by some movement of the affected body segment, in contrast to, for example, fasciculations or myokymia, where the twitches remain within the affected body segment. Myoclonus is best likened to the effect seen after stimulating the nerve supplying the muscle with a single electric shock (or with a train of shocks, because the myoclonic jerks may occur repetitively within the same muscle). so the keyword in identifying myoclonus is shock-like movements.

When myoclonus occurs in series, the timing of the jerks can be either rhythmic or irregular. sometimes rhythmic myoclonus may be mistaken for tremor (e.g. spinal segmental myoclonus; or hereditary cortical myoclonus, which has also been erroneously labelled “cortical tremor”). if myoclonus is repetitive but more arrhythmic (as in “polyminimyoclonus”, which consists of fine myoclonic individual finger jerks seen in the outstretched hands in, for example, patients with multiple system atrophy), the movements can be mistaken for irregular tremor. However, isolated tremor lacks the defining abrupt and shock-like character of myoclonus. What was called palatal myoclonus is now termed palatal tremor because of its rhythmic nature and lack of abrupt jerky movements.

there are several ways to describe and classify myoclonus. the distribution of myoclonus can be focal, multifocal, segmental or generalized. Etiologically myoclonus can be subdivided into physiological myoclonus (e.g. hypnic jerks), essential myoclonus (idiopathic or hereditary), epileptic myoclonus, or symptomatic myoclonus in case of an underlying disorder. Physiologically myoclonus is subdivided into cortical, subcortical, spinal and peripheral.9 finally, it is important to carefully look for the specific


may begin in a single digit. a diagnostic pitfall is failure to recognize that resting tremors can occur in any position assumed by the affected body part, even when this involves a posture that is actively maintained against gravity (and thereby mimic a postural tremor). for example, the typical resting tremor in the hands of patients with pd can also be observed when the arms are stretched out in front. in this case, the distinction between postural tremor (as in essential tremor) and true resting tremor is possible by carefully examining how rapidly the tremor becomes manifest after the new posture has been assumed: immediately in case of postural tremor, but after a delay of several seconds in case of resting tremor (a phenomenon termed “resetting” or “re-emergent tremor”). also, the frequency of a resetting tremor is the same as that in rest position.18

Kinetic tremors occur during volitional movements. a distinction is made between simple/action tremor (evident during a target-directed movement), terminal tremor (evident at the end of a target-directed movement) and intention tremor (which increases progressively in amplitude throughout the movement until it reaches the intended target). Isometric tremor occurs when muscles forcefully contract without shortening, e.g. while pushing against a wall. finally, psychogenic tremor is characterized by a variable frequency, direction and amplitude, as well as by distractibility.19

attempts have been made to classify tremor according to its frequency. However, it is rarely possible to establish a diagnosis based purely on this parameter, for two reasons: it is difficult to accurately assess the tremor frequency in the clinic, without neurophysiological equipment; and the frequency spectrum between different tremor types overlaps considerably. an exception is primary orthostatic tremor, a leg tremor that is present during standing, and which is characterised by an unusually high and pathognomonic tremor frequency of 14–18 Hz.20 this particular tremor is barely visible to the naked eye, although patients may manifest a discernable leg or trunk tremor with a lower frequency. although commonly said to be mainly present during standing, eMg studies have shown that the high-frequency orthostatic tremor persists in the trunk and weight bearing leg during walking, and that this tremor can also arise in the upper extremities when patients support their weight with the arms.21

Many disorders are characterised by the presence of “mixed” tremors. thus, pd patients not only have resting tremor, but commonly also a postural tremor with a higher frequency. another example is Holmes tremor (also known as midbrain or rubral tremor), which typically has resting, postural and intention components, often at an unusually low frequency of around 2 to 3 Hz.

When tremor involves a body part already affected by dystonia (see below - most commonly this association is seen in patients with spasmodic torticollis), it is classified according to the Mds Consensus statement as “dystonic tremor”. Many patients with spasmodic torticollis also have a postural tremor of one or both arms.22 in the Consensus statement this is called “tremor associated with dystonia”. However, this term is a bit of a mouthful, and since most believe that this tremor is in fact part of the patient’s dystonia, we personally prefer to also call this “dystonic tremor”, provided no other cause is identified. dystonic tremor can mimic the tremor of pd, especially when it precedes overt dystonia or when the dystonia is subtle, leading to a misdiagnosis of pd. to confuse matters further, arm swing is often reduced in patients with dystonia, even in torticollis patients with no other arm involvement. However, people with dystonic tremor do not have true akinesia, and also have normal dopamine transporter imaging, in contrast to patients with pd.23 Many dystonic tremors are also misclassified as essential tremor.24 to complicate matters further, postural tremors similar to essential tremor are frequently present in patients with dystonia. the presence of (often subtle) dystonic postures should distinguish between these two diagnoses (for example, “dinner-forking” posture of the outstretched hand, or a tendency for the ulnar fingers or thumb to point downwards with the arms held out).

Ticstics are the third category of sudden and jerky movements, but now the keyword for recognition is the stereotyped character of the recurrent movements. another fundamental difference from myoclonus and chorea is that patients report that their tics are preceded by rising discomfort or urge (“sensory tic”) that is relieved by the actual movement (“itch and scratch” analogy). another important feature is that tics can usually be largely suppressed for short periods by an effort of will. However, suppression of tics typically comes at the expense of mounting inner tension, leading to a “rebound” of tics afterwards. Because of their stereotyped character, tics can usually be mimicked easily.

tics usually predominate in the face, upper arms and neck. they can be divided into simple tics (e.g. eye blinking, nose wrinkling, shoulder shrugging, throat clearing) or complex tics (e.g. touching things, smelling objects, echopraxia, jumping). another subdivision is into motor tics (such as stereotyped head jerks) or phonic tics (repetitive sniffs or sounds, words or even sentences). a notorious diagnostic pitfall is that tics are often less prominent or even absent in the clinical examination room, apparently because the anxiety associated with being examined suppresses the phenomenon. Videotaping the patient, without an examiner present, can therefore be very helpful. occasionally, a motor tic can have an abrupt onset but the subsequent movement or posture might be slow or prolonged rather than jerky. this is referred to as a dystonic tic, but the suppressibility and stereotyped nature are the clinical clues to classifying such movements as a tic. dystonic tics can occur in conjunction with other non-dystonic tics.

stereotypic movements are like tics, but the actions consist of a complex set of movements that are longer lasting, patterned, repetitive, purposeless or ritualistic. these stereotypies are less paroxysmal than tics, but occur over and over again in a more continuous fashion. the movements may be simple (composed of a few manoeuvres, e.g. rocking or head banging) or more complex (composed of multiple simple manoeuvres performed together or in sequence). stereotypies are typically seen in patients with autism, mental retardation, rett syndrome, psychosis, or congenital blindness and deafness.15 16

“Non-jerky” hyperkinetic syndromesthis category includes tremor and dystonia. although dystonia can have a jerky nature, its core feature is prolonged muscle spasms. therefore, dystonia is placed here in the non-jerky category.

TremorBy definition, tremor is characterised by involuntary, rhythmic and sinusoidal alternating movements of one or more body parts. this does not necessarily involve a limb, as tremor can affect almost any body part (e.g. the head, chin or soft palate). the keyword in identifying tremor is rhythmicity, i.e. the oscillations occur at a regular frequency. However, identifying rhythmicity with the naked eye is not always easy, because tremors – despite having a fixed frequency – often have a variable amplitude. such changes in amplitude with time can occur spontaneously, but may also result from movements or changes in posture assumed by the patient, or from emotions and fatigue. despite the amplitude change, tremor frequency remains unchanged. in such patients, objective and quantitative tremor registration, using electromyography and accelerometry, can confirm rhythmicity.

tremors can be classified in various ways. one important classification system is according to the characteristic moment or situation of occurrence (table 2).17 a resting tremor can only be definitively identified when the affected body part is not actively moving, and when the effect of gravity is removed completely. resting tremor usually disappears during voluntary actions. sometimes eye closure or distraction is needed to provoke the resting tremor (for example, asking the patient to count backwards whilst sitting with the arms resting on the arms of a chair). occasionally it is only seen in the arm when the subject is walking (“dependent tremor”). the rest tremor may be very focal. for example, tremor in pd


of musician’s dystonia. the task-specificity may lead to diagnostic confusion, for example in patients with leg dystonia who may have severe difficulty walking forward, but can walk backwards or run normally. if no problem is apparent and the complaint is highly task-specific, it can be helpful to ask the person to bring along the relevant musical instrument or golf club, to demonstrate the problem. failing this, asking the patient to bring in a home video segment to highlight the symptom can also be very revealing.

“Lookalikes” of movement disordersa range of conditions, both neurological and non-neurological, can mimic various movement disorders. it is obviously important not to miss these lookalikes, and several common examples are shown in table 3.

diagnostic levelsa systematic approach is recommended when clinicians see patients who present with one or more types of movement disorder (flow diagram). the work-up we use in every patient consists of four key questions that need to be addressed consecutively in order to establish the correct diagnosis. of course, not every question can always be answered unambiguously in each patient.

1. Which different types of movement disorder are present in this patient?some movement disorders can occur almost in pure isolation. one example is essential tremor, where affected patients typically present with a symmetrical action and postural tremor in the arms but, by definition, without other neurological abnormalities,30 except for perhaps a mildly unsteady gait that might only become apparent during the tandem walk test.31 However, many clinical syndromes are characterised by the presence of several different types of movement disorders that occur in the same patient: the “mixed movement disorder”. for example, a patient with multiple system atrophy can present with a combination of akinesia, rigidity, tremor, ataxia, and fine polyminimyoclonus in the outstretched hands.32, 33 if one looks carefully, such overlap is more often the rule than the exception in patients with movement disorders. the nature of this overlap differs between different disorders, between individual patients with the same disorder, and even within a given patient depending on their disease stage.

in order to differentiate between clinical syndromes (which relies heavily upon pattern recognition, i.e. specific combinations of symptoms and signs), it is important to precisely classify the type of movement disorder that occurs in individual patients. some combinations immediately raise a specific diagnostic suspicion, such as the combination of dystonia and “lightning” myoclonic jerks which are characteristic of myoclonus dystonia (dyt-11). importantly, whenever patients present with a mixed movement disorder, one should always consider the possibility of adverse effects of medication (most commonly dopamine d2 receptor blocking agents such as neuroleptics). drug induced movement disorders are frequently encountered in patients with a known movement disorder, but also in patients without a history of movement disorders. for example, the presence of chorea in a patient with a previous diagnosis of primary dystonia could be due to the use of anticholinergics, and should not lead to an extensive work-up for secondary dystonia. patients without a known history of movement disorders and who use antipsychotics can develop tremor, a hypokinetic rigid syndrome, or orofacial dyskinesias. the risk increases with prolonged medication use, but even single doses can be responsible. it may be necessary to request a comprehensive list of previous medications from the general practitioner, as the effects of an offending agent can persist for months following discontinuation.

2. What is the dominant type of movement disorder?even when the clinical syndrome is characterized by the simultaneous presence of different types of movement disorder, usually one type will dominate. for example, most adult patients with Huntington’s disease not only have the characteristic chorea, but also display bradykinesia when this is carefully

some tremors are easier to feel than to observe. superficial palpation of involved muscles can suffice, sometimes at rest, but in particular during passive movements of the affected muscles. “Cogwheeling” simply reflects the sensation of feeling an underlying tremor, irrespective of its cause. it can be felt in patients with essential or dystonic tremor, and in patients with pd. However, in the first two examples there is no additional rigidity (in which case one speaks of “cogwheel rigidity”) or akinesia, whereas these are present in pd. orthostatic tremor can also be palpated as a kind of ‘rhythmical shivering’ of the legs, or heard through the stethoscope (thumping sound like a helicopter) in cases where it is not obviously visible.25

Dystoniaone definition is “an involuntary abnormal co-contraction of antagonistic muscles, which may cause sustained abnormal postures or twisting and repetitive movements”. another definition is “abnormal characteristic postures and movements, produced by slow sustained muscle contraction which distort limbs, trunk, neck, face or mouth.” Both definitions underscore that an important keyword in identifying dystonia is abnormal posture. as such, dystonia is the only movement disorder that can be visualised in a static image, even though additional rhythmic, irregular or paroxysmal jerky involuntary movements frequently can accompany the abnormal postures. an example of such involuntary associated movements is athetosis, defined as “distal mobile dystonia”: slow, writhing and irregular movements of the distal extremities, with abnormal posturing.26 the term choreoathetosis used to be applied to describe a mixture of chorea and dystonia (as in l-dopa induced dyskinesias in some pd patients), but today we tend to call these mobile choreodystonic movements.

dystonias can be classified in several ways, based on their distribution (focal, segmental, multifocal, generalized, or hemi-dystonia), age at onset (early, i.e. ≤ 26 years; or late, i.e. ≥ 26 years), or based on cause (primary, dystonia-plus, degenerative or secondary).27

Clinical features are helpful in distinguishing primary from secondary dystonia. primary dystonia is characterized by the presence of dystonia only (except for tremor). dystonia-plus syndromes present with a second and relevant neurological feature, such as parkinsonism (as in dopa-responsive dystonia) or sometimes – as has recently become apparent – ataxia.28 the term “myoclonus dystonia” crept into usage in relation to the very brisk, brusque, lightning-like tic-tac jerks that are typical of patients with hereditary alcohol-responsive myoclonus with dystonia (dyt-11); this syndrome is often due to an epsilon-sarcoglycan mutations. in secondary dystonias, other clinical features are usually associated, and an identifiable cause can often be found. these secondary dystonias are mostly associated with additional clinical features.

several characteristics support the presence of dystonia. the following features are especially applicable for primary dystonias. the abnormal posturing typically has a consistent directionality (a torticollis with rightward head rotation will not usually suddenly change to a leftward torticollis). the abnormal movements are patterned and repeatedly involve the same muscle groups. in early stages, the dystonia is typically “mobile” (i.e. the patient can still actively or passively move the affected body part), but the dystonia might become more fixed with further disease progression. note that fixed dystonia may be a relatively early feature in patients with corticobasal degeneration, while fixed posturing that is present immediately at onset of the disease is often felt to reflect a psychogenic cause.29 a further typical feature of dystonia is the presence of a sensory trick or “geste antagoniste”, which is a mechanism (usually identified and used by the patient) to reduce dystonia, for example, gently touching the cheek to correct torticollis, or chewing gum to reduce oromandibular dystonia. dystonia is commonly brought out by action or activity (note that this is not the same thing as paroxysmal dystonia). often this may take the form of an element of task-specificity, i.e. the movements or postures are predominantly or even exclusively present under specific circumstances. examples include writer’s cramp or the various forms


note that some specific types of movement disorder always influence clinical decision-making, even when present in a subtle way and not as the “dominant” movement disorder. for example, when patients present with predominant dystonia but also with mild signs of ataxia, the work-up should include, and perhaps even primarily focus on, a search for causes of (hereditary) ataxia.37

details of the diagnostic work-up largely depend on the dominant type of movement disorder and the residual clinical uncertainties with respect to the differential diagnosis. for example, in patients with unexplained chorea that looks like Huntington’s disease, the initial diagnostic step may often simply involve genetic testing for Huntington’s disease, after appropriate counselling. When this is negative, the diagnostic work-up may then be expanded.38 each movement disorder and each clinical syndrome thus has its own specific diagnostic approach. a detailed discussion of these diagnostic trajectories themselves is not within the scope of this review.

ConclusionWe have outlined a suggested clinical approach to the patient with a movement disorder. as supplementary Material, we provide examples of how this method might work for patients presenting predominantly with myoclonus (table 5), chorea (table 6) or dystonia (table 7). We hope that application of the proposed serial diagnostic steps may help clinicians to identifying overall clinical syndromes, which in turn will help to guide the diagnostic process.

Acknowledgementthis clinical approach was handed down to us by the late prof. david Marsden.

Conflict of interest statementthis work was supported by nWo Vidi research grant #016.076.352 to professor B.r. Bloem. dr. W.f. abdo was supported by a research grant from the stichting internationaal parkinson fonds. dr. B.p.C. van de Warrenburg, professors d.J. Burn and n.p. Quinn have no conflict of interest to declare regarding the submission of this manuscript.

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sought. However, in the typical early-to-middle stage case the clinician will usually have little difficulty in identifying chorea as the dominant type of movement disorder. this distinction is important because the specific diagnostic work-up for chorea is different from that for bradykinesia. thus, determining the dominant movement disorder syndrome is an essential step, as it steers the differential diagnosis and determines the subsequent diagnostic trajectory.

recognising the dominant type of movement disorder is often easier in earlier stages of the disease. in patients with more advanced disease, the originally dominant signs may become masked due to secondary disease complications or newly emerging movement disorders. for example, in advanced stages of Huntington’s disease, chorea is often no longer prominent, but akinesia, rigidity and dystonia may predominate. another example includes levodopa induced dyskinesias in patients with pd. sometimes parkinsonian patients can simultaneously have tremor in some part of the body and levodopa induced dyskinesias-dystonia in other body parts. However, levodopa induced dyskinesias can also dominate the clinical picture and overshadow tremor and clinically resemble choreoathethosis. the solution in such cases lies in a detailed medical history, and familiarity with all stages of the disease.

1. What are the associated features?the complexity of the clinical picture increases when patients exhibit additional neurological or non-neurological symptoms or signs. Clinicians can, however, take advantage of this, as these associated features may provide important clues about the underlying aetiology. for example, examining the eyes for oculomotor apraxia and telangiectasia in patients with chorea and ataxia may lead to a diagnosis of autosomal recessive ataxia telangiectasia. similarly, finding Kayser-fleischer rings in the cornea in a patient with dystonia would indicate a diagnosis of Wilson’s disease, while early and prominent autonomic dysfunction in a patient with parkinsonism should raise the possibility of multiple system atrophy.32, 33

sometimes, elements of the history provide important clues, such as specific factors that exacerbate or relieve the abnormal movements. for example, involuntary movements that present in frequent, brief attacks that are induced by sudden movements (such as rising from a chair) suggest a diagnosis of paroxysmal kinesigenic dyskinesias.34,35 When patients with torticollis report that their head jerks improve dramatically with alcohol, a diagnosis of myoclonus dystonia (dyt-11) should be suspected.36 associated non-neurological clues are important, e.g. chorea in a woman with migraine, recurrent venous thrombosis or multiple spontaneous abortions suggests antiphospholipid syndrome. the presence of associated neurological and non-neurological features can thus help to narrow the differential diagnosis that was initially based on the dominant movement disorder syndrome.

family history and ethnicity may also be critical for the diagnosis. parental consanguinity, a positive family history and ethnicity in otherwise classical idiopathic parkinsonism may raise the possibility a monogenic cause of pd. a dominant family history of tremor in patients with a postural tremor suggests essential tremor or dystonic tremor. in dystonia, many inherited forms are known. a positive family history of dystonia combined with filipino ethnicity raises the possibility of the X-linked dyt-3 (“lubag”).

2. What is the differential diagnosis and diagnostic work-up?taken together, an overall clinical syndrome is determined from the specific combination of one (dominant) movement disorder, plus perhaps several concurrent types of movement disorder, plus a set of associated neurological and non-neurological abnormalities. this clinical syndrome should in turn lead to a differential diagnosis. sometimes simple pattern recognition will suffice and lead directly to the diagnosis, but often ancillary investigations are required. in such cases, the diagnostic process will be guided by the dominant movement disorder.


disorders and seizure disorders are often unclear. diseases that cause visible contractions of muscle fibers, such as fasciculations, but do not cause movement of the body part are not classified as movement disorders.

trEMorStremor is defined as a rhythmic, oscillatory movement of body parts. they are further broken down by the frequency of the oscillations and when the tremors occur. feedback systems have a natural tendency to oscillate and in muscles such feedback systems produce a physiologic tremor. under most conditions, physiologic tremor is barely perceptible, but stress, fear, fatigue, weakness, and drugs such as caffeine can produce an exaggerated physiologic tremor. these tremors are typically fast and small amplitude and tend to occur when standing still, diminishing with movement. disease processes such peripheral nerve disease, pheochromocytoma, hypoglycemia will exaggerate physiologic tremors. tremor can also be incidental in aged dogs.orthostatic tremors occur when standing and affect primarily the hind limbs. they tend to be a little bit slower and coarser than physiologic tremor. the dogs often hesitant to sit or stand, and thus appear weak. When the dog walks, however, the movements show no evidence of weakness and the tremors resolve. they also resolve when the dog is sitting or lying down. the cause is not known but they have been reported most commonly in great danes1. Bulldogs and doberman pincers show benign head tremors that appear to be hereditary2,3. these may be a variation on orthostatic tremors since the head must also be supported against gravity. Both appear to be benign conditions. intention tremors are a hallmark of cerebellar disease of any cause. the term intention tremor may not be appropriate for animals since we cannot know what they intend to do, but it captures the key feature of the tremor so the term is still used. these tremors only occur when the animal is making a goal directed movement. they disappear completely at rest. they are most apparent in the head but can involve the entire body or limbs. the head tremors can become dramatic when the animal eats and the limb tremors when they try to walk down stairs. the tremor is very slow and coarse.

MyoCLoNuS Myoclonus is a very brief, sharp contraction of a muscle, group of muscles or the entire body. it can be single or repeated rhythmically. rhythmic myoclonus lacks the smooth, oscillatory character of a tremor. focal myoclonus is a common sequelae to canine distemper infections. generalized myoclonus is often a sign of a more generalized neurodegenerative disease4,5. sometimes myoclonus can be elicited by stimulation. a hereditary myoclonus in irish Wolfhounds called startle disease or hyperekplexia is caused by a dysfunction of the inhibitory neurotransmitter glycine6. Without this inhibition, the normal startle response is exaggerated. in other conditions the jerks occur spontaneously. the latter is sometimes call myoclonic epilepsy but is often not clear if the cortical epileptic discharges that would classify it as a seizure disorder are present or not. negative myoclonus looks similar clinically, but is actually caused by brief loss of tone in a muscle followed by a jerk as the animal catches itself. opsoclonus-myoclonus is an unusual form of myoclonus affecting the eyes as well as the body. the body appears more like a generalized tremor, but the eyes make very rapid, uncontrollable darting movements. it is thought to be an autoimmune disease.

CErEBELLAr AtAxIACerebellar ataxia is the most common movement disorder diagnosed in veterinary practice. the cerebellum is responsible for the fine-tuning of movement. When an animal is learning to walk or perform any motor task, the cerebellum monitors commands coming from the forebrain motor systems and receives feedback from the vestibular system and proprioception sensors in muscles about balance and execution of the movement respectively. Motor learning occurs in the cerebellum as synapses are strengthened or weakened to perfect the movement. Coton de tulears with Bandera’s neonatal ataxia

12. Bakker,M.J., van Dijk,J.G., van den Maagdenberg,A.M., & Tijssen,M.A. Startle syndromes. Lancet Neurol. 5, 513-524 (2006).

13. Hallett,M. & Kaufman,C. Physiological observations in Sydenham’s chorea. J. Neurol. Neurosurg. Psychiatry 44, 829-832 (1981).

14. Postuma,R.B. & Lang,A.E. Hemiballism: revisiting a classic disorder. Lancet Neurol. 2, 661-668 (2003).

15. Muthugovindan,D. & Singer,H. Motor stereotypy disorders. Curr. Opin. Neurol. 22, 131-136 (2009).

16. Shprecher,D. & Kurlan,R. The management of tics. Mov Disord. 24, 15-24 (2009).

17. Deuschl,G., Bain,P., & Brin,M. Consensus statement of the Movement Disorder Society on Tremor. Ad Hoc Scientific Committee.

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18. Jankovic,J., Schwartz,K.S., & Ondo,W. Re-emergent tremor of Parkinson’s disease. J. Neurol. Neurosurg. Psychiatry 67, 646-650 (1999).

19. Bhatia,K.P. & Schneider,S.A. Psychogenic tremor and related disorders. J. Neurol. 254, 569-574 (2007).

20. Gerschlager,W. et al. Natural history and syndromic associations of orthostatic tremor: a review of 41 patients. Mov Disord. 19,

788-795 (2004).

21. Britton,T.C. et al. Primary orthostatic tremor: further observations in six cases. J. Neurol. 239, 209-217 (1992).

22. Munchau,A. et al. Arm tremor in cervical dystonia differs from essential tremor and can be classified by onset age and spread of

symptoms. Brain 124, 1765-1776 (2001).

23. Schneider,S.A. et al. Patients with adult-onset dystonic tremor resembling parkinsonian tremor have scans without evidence of

dopaminergic deficit (SWEDDs). Mov Disord. 22, 2210-2215 (2007).

24. Jain,S., Lo,S.E., & Louis,E.D. Common misdiagnosis of a common neurological disorder: how are we misdiagnosing essential

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26. Morris,J.G. et al. Athetosis II: the syndrome of mild athetoid cerebral palsy. Mov Disord. 17, 1281-1287 (2002).

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distinct but heterogeneous entity. J. Neurol. Neurosurg. Psychiatry 78, 774-775 (2007).

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MoVEMENt dISordErS

Dennis P. O’Brien DVM PhD DACVIM-Neurology, Columbia, Missouri

Movement disorders are a group of condition characterized by involuntary movements. seizures would technically fall under this definition, but they are classified separately. seizures are characterized by abnormal electrical activity in the cerebral cortex seen on eeg, and are typically accompanied by loss of consciousness and post-ictal behavior changes. focal seizures, however, may not affect consciousness, and some movement disorders are also episodic. thus the border between episodic movement


the cerebellum is the first to degenerate and the dogs have classic cerebellar ataxia. affected dogs have tremors, but they are intention tremors associated with movement in contrast to the tremors of parkinsonism which occur at rest. except for primates, none of the experimental or hereditary forms of parkinsonism in animals show a resting tremor. Beginning at about 6-8 months of age, affected dogs begin having difficulty initiating movement. they shift their weight forward until they finally propel themselves forward in a gait called festination. With further progression of the disease, they are unable to initiate voluntary movements. they adopt a hunched-up posture when they try to walk and rock until they lose their balance and fall. in addition to degeneration of the cerebellum, affected dog have degeneration of the substantia nigra and basal nuclei.

dySKINESIA ANd dyStoNIAparkinsonism is considered a hypokinetic disease of the basal nuclei because there is difficulty initiating movement. another group of diseases are called hyperkinetic movement disorders because the basal nuclei are unable to stop movements. involuntary movements, (dyskinesia) or abnormal muscle tone (dystonia) then occur. dyskinesias can be focal or generalized. focal dyskinesia can involve the facial muscles or single limbs. in the limbs, proximal or distal muscles may be preferentially affected. the movements can either be slow or rapid and they may be continuous or episodic (paroxysmal). in humans, dyskinesias are divided into three general categories; athetosis, chorea, and ballism. athetosis is a slow, continuous, writhing movement involving primarily the distal arm. the movements may be somewhat purposeful. Chorea (from the greek “to dance”) also affects predominantly distal limb muscles, but the movements are totally involuntary. they are more rapid and fragmented. Ballism is also a rapid movement, but it affects predominantly proximal muscles. the result is a flailing or flinging movement. dystonia is a sustained contraction of muscles. the axial muscle or limb muscles can be affected. the limbs can either be held in flexion or extension and sometimes a tremor of the affected muscles accompanies dystonia. as with dyskinesias, the episodes can last from minutes to hours but tend to be more infrequent. often a mix of different dyskinesias and dystonia will occur in the same patient. acquired dyskinesias can be drug induce or secondary to basal nuclei lesions from infections or stroke. the best characterized dyskinesias in veterinary medicine are paroxysmal and appear to be hereditary. like seizures, the animals are normal between episodes. in contrast to generalized seizures, animals remain conscious during paroxysmal dyskinesias and they do not have the life threatening complications sometimes seen in seizures. some dyskinesias have clear triggers such as stress or excitement while others do not. the episodes can occur infrequently to multiple times per day and they can last minutes to hours. the episodes can vary from simple flexion of one limb while walking which looks like a lameness, to frantic, alternating flexion and extension of multiple limbs. the paroxysmal dyskinesias will sometimes respond to antiepileptic drugs or the carbonic anhydrase inhibitor acetazolamide. Chinook dogs have a paroxysmal dyskinesia with primarily dystonia that appears to be inherited as an autosomal recessive trait15. affected dogs have episodes of dystonia and tremors lasting up to an hour. they are conscious during the episodes and appear perfectly normal on recovery. occasional flailing movements of a limb can occur also. in Cavalier King Charles spaniels with episodic falling syndrome, a mutation has been identified in BCan, a gene involved in connections between cells and fiber guidance in the brain development in dogs16. although the dogs do collapse during these episodes, they do not lose consciousness and they have increased tone in the limbs resulting in them adopting a “deer stalking” posture. a similar syndrome, scottie cramp, has been recognized in scottish terriers since the 1940s but sequencing the BCan gene did not reveal any mutations.17 Canine epileptoid cramping syndrome or spike’s disease is a movement disorder that affects Border terriers. as the name implies, the episodes resemble seizures, but the dog remains conscious throughout. Most episode last from 2-30 minutes but may last for hours. the episodes consist primarily of tremors and dystonia affecting the head and body. excessive intestinal noise and vomiting or diarrhea may accompany the episodes leading some owners to suspect a dietary link18. finally a paroxysmal dyskinesia has recently be recognized in soft Coated Wheaten terriers.

have a glutamate in the gene for the metabotropic glutamate receptor 1 (Mglur1), the neurotransmitter receptor that mediates the weakening of synaptic connections on purkinje cells in the cerebellum. as a result, motor learning is abolished and they can never walk7. interestingly, the menace response is also a learned motor response and not a reflex. thus it does not develop until after weaning age and it is often lost in cerebellar disease. once the movement has been learned, the cerebellum utilizes what has been learned to adjust the motor program in real time in response to sensory feedback so that movements are smooth. animals with cerebellar ataxia are not weak and have no proprioception deficits. instead the range and force of movement are not regulated properly, the result is an exaggerated, goose-stepping gait. this is most apparent when the animal is moving quickly or trying to do a more skilled movement like walking down stairs. in severe cases, the animal may have all four feet off the ground simultaneously or flip over backwards. Because the cerebellum works intimately with the vestibular system, affected animals may lose their balance with sudden movements or develop nystagmus which may be vertical. occasionally, affected dogs will fall and adopt a contorted posture which is sometimes mistaken for a seizure.Many acquired diseases including infections such as neospora caninum encephalitis, tumors, and strokes commonly affect the cerebellum and produce cerebellar ataxia and intention tremors. an idiopathic tremor syndrome called idiopathic tremors or idiopathic cerebellitis has been recognized. it is thought to be an immune mediated disease. affected dogs develop an acute onset of severe generalized tremors and cerebellar ataxia. Most dogs improve with anti-inflammatory drugs and diazepam. Maltese and other white dogs are most commonly affected and the condition was originally called “little white shakers”, but we now know it can affect any breed. developing the circuitry of the cerebellum requires interaction of a variety of developmental signals and the process of regulating movement in real time once the cerebellum has developed is very complex. thus mutations in a variety of genes can disrupt cerebellar development or function, and hereditary cerebellar ataxias are common. developmental disorders are typically apparent a neonates. for example, in eurasier dogs, mutations in a gene that is part of the signaling pathway that regulates brain development cause dandy-Walker syndrome, a failure of the midline of the cerebellum to develop, and cerebellar ataxia8. functional disruptions will also cause cerebellar ataxia. potassium channels are critical for regulating neuronal excitability. Jack russell terriers with mutations in one of these channels that is found in high density in the cerebellum have severe spinocerebellar ataxia because the increased excitability disrupts the timing of impulses essential for coordinating movement. the dogs show other signs of excessive excitability of neurons such as seizures and myokymia, uncontrollable, rippling contractions of the muscles at rest9. Hereditary ataxia in other breeds have been associated with genes involved in a variety of processes including autophagy (atg4d in old english sheepdog)10, degradation of proteins in the endoplasmic reticulum (sel1 in finnish Hounds)11 and structural proteins (sptBn2 in beagles)12.

PArKINSoNISMparkinson’s disease is a common neurodegenerative disease of older people. it is caused by degeneration of the substantia nigra. neurons in this area that use dopamine as a neurotransmitter project forward to synapse on the basal nuclei. this system functions the gate-keeper for movement. dopamine is an important component of the “reward system” in the brain. Based on past experience, this system gives either a “go” or a “no-go” signal to the motor programs. Without the dopamine input, the system is stuck in “no-go” and movement cannot be initiated. although the resting tremor is the sign of parkinson’s disease that everyone recognizes, it is the inability to initiate movement that devastates patients with parkinson’s’ disease. these signs of difficulty initiating movement and resting tremors are called parkinsonism and can occur in other hereditary, toxic, and degenerative diseases in people.parkinson’s disease per se has not be identified in dogs or cats, but the signs of parkinsonism are seen in some hereditary movement disorders of dogs. Chinese Crested dogs and Kerry Blue terriers have a juvenile-onset, hereditary disease called canine multiple system degeneration13,14. as the name implies, multiple parts of the motor system in the brain degenerate beginning about 4 months of age.


WHAt CAN WE LEArN FroM ANIMAL ModELS oF dyStoNIA/dySKINESIAS IN VEtErINAry ANd HuMAN NEuroLogy?

Prof. Dr. Angelika Richter and Dr. Franziska Richter, Institute of Pharmacology, Pharmacy and Toxicology, VMF, University of Leipzig

More than 3 million people worldwide suffer from dystonia, the third most common movement disorder in humans characterized by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements, postures, or both. the term dyskinesia encompasses paroxysmal movement disorders which include dystonia, chorea and ballism in conscious individuals. Hence, dystonia/dyskinesias are diagnosed based on the clinical picture, but heterogeneity in symptoms and etiology result in a large percentage of misdiagnoses and incorrect or insufficient treatment. even in case of correct diagnosis, pharmacological treatment of the different clinical types of dystonia is insufficient or ineffective in most cases and largely based on empirical, rather than pathophysiological rationale. novel treatment options are urgently warranted, but will require more knowledge of the etiology and pathophysiology of dystonia. animal models are pivotal for studies of pathogenesis and treatment of disorders of the central nervous system which in its complexity cannot yet be modeled in vitro or using computer simulations. the choice of a specific model should be based on validity of the model for the approach: does the model reflect symptoms, pathogenesis and treatment response present in human patients? for dystonia, prior to the availability of genetically engineered mice, spontaneous mutants were chosen based on expression of dystonic features, including abnormal muscle contraction, movements and postures. interestingly, spontaneous occurrence of dystonia/dyskinesia is not only found in rodents. in fact, different hyperkinetic movement disorders, described in dogs, horses and cattle, show similarities to human types of these movement disorders. However, similar to the human condition there is a high rate of misdiagnosis due to lack of awareness that these movement disorders occur in animals. recently, a number of causative genes and gene products were discovered in dystonia in humans, and some forms of hyperkinetic movement disorders in animals are well characterized and the causing mutations are known. for rodents, this initiated the creation of novel genetically modified models based on gene mutations which now greatly enhance the knowledge of pathophysiology of dystonia and may be used for preclinical drug testing. Clearly, much could also be learned by exchanging experience between human and veterinary medicine on specific cases and treatment options in clinical practice. it is challenging to compare the human condition to how it may present in the animal, requiring experience and solid characterization especially if the condition in animals will be used to develop and test novel drug treatment to be applied for the human condition. Here we present a review of current models of dystonia, with a focus on genetic rodent models, which will likely be first choice in the future either for pathophysiological or for preclinical drug testing or both. We will first present models with episodic/paroxysmal dystonia/dyskinesias, followed by models which express persistent motor dysfunction. We conclude that current models do replicate features of dystonia/dyskinesias and are useful tools to develop urgently demanded treatment for these debilitating disorders. occurrence of hyperkinetic movement disorders in animals, including farm animals and pets, could provide a valuable resource to learn about etiology, pathophysiology and treatment. We therefore strongly encourage the ongoing exchange of experience between human and veterinary medicine on the clinical as well as scientific level.

affected dogs have episodes of dyskinesia or dystonia which last minutes to hours and may occur multiple times per day and a mutation in gene involved in anchoring proteins to the cell surface has been identified. some affected dogs have shown a dramatic response to acetazolamide therapy.19 other breeds with reports of dyskinesia are Bichon frise, Boxers, and springer spaniels.

CoNCLuSIoNthe increased availability of video capture with cell phones has meant that movement disorders are being increasingly recognized in veterinary medicine. in the case of hereditary diseases, current gene discovery techniques permits us to identify the mutations responsible and eliminate the disease from affected breeds. understanding the basis of these hereditary diseases can suggest new pathways to explore for effective therapies for acquired conditions. What we can learn from our patients can also shed light on the comparable human diseases.

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11. Kyostila K, Syrja P, Jagannathan V, et al. A Missense Change in the ATG4D Gene Links Aberrant Autophagy to a Neurodegenerative

Vacuolar Storage Disease. PLoS Genet 2015;11:e1005169.

12. Forman OP, De RL, Stewart J, et al. Genome-wide mRNA sequencing of a single canine cerebellar cortical degeneration case leads to the

identification of a disease associated SPTBN2 mutation. BMCGenet 2012;13:55.

13. O’Brien DP, Johnson GS, Schnabel RD, et al. Genetic mapping of canine multiple system degeneration and ectodermal dysplasia Loci.

Journal of Heredity 2005;96:727-734.

14. deLahunta A, Averill DR. Hereditary cerebellar cortical and extrapyramidal nuclear abiotrophy in Kerry blue terriers. Journal American

Veterinary Medical Association 1976;168:1119-1124.

15. Packer RA, Patterson EE, Taylor JF, et al. Characterization and mode of inheritance of a paroxysmal dyskinesia in Chinook dogs. Journal of

Veterinary Internal Medicine 2010;24:1305-1313.

16. Gill JL, Tsai KL, Krey C, et al. A canine BCAN microdeletion associated with episodic falling syndrome. NeurobiolDis 2012;45:130-136.

17. Urkasemsin G, Olby N. Canine paroxysmal movement disorders. Vet Clin North Am (Small Anim Pract) 2014;44:1091-1102.

18. Black V, Garosi L, Lowrie M, et al. Phenotypic characterisation of canine epileptoid cramping syndrome in the Border terrier.

The Journal of small animal practice 2014;55:102-107.

19. O’Brien DP. Proceedings of the ACVIM Forum, Indianapolis IN June 2015.


orals


anxiety, noise phobia, and gait abnormalities. Mri documented bilateral symmetrical changes predominately in the caudate nuclei. in one case these were shown to be progressive. Clinicopathological analysis of blood and Csf, infectious disease screening and urine metabolite screening were unremarkable. post-mortem examination of brain tissue identified malacia of the caudate nucleus as the most marked and consistent finding. genealogical analysis supports an autosomal recessive mode of inheritance.in conclusion a degenerative encephalopathy has been identified in young adult nsdtrs, with a world-wide distribution. Mri and histopathological lesions are characteristic. the prognosis is guarded due to progressive disease which is minimally responsive to empirical treatment.

EPILEPtogENIC ELECtroENCEPHALogrAPHIC FINdINgS IN CANINE EPISodIC HEAd trEMor SyNdroME

F.M.K. James1, S. Dugas2, M.A. Cortez3, S. Sanders4, L. Barnard1, G. Leblond1, T. Jokinen5, H. Lohi6 1Ontario Veterinary College, University of Guelph, Guelph, Ontario, Canada, 2Southern California Veterinary Specialty Hospital, Irvine, California, USA, 3Neurosciences & Mental Health Program, Peter Gilgan Centre for Research and Learning, SickKids Research Institute, Toronto, Ontario, Canada, 4Seattle Veterinary Specialists, Kirkland, Washington, USA, 5Department of Clinical Veterinary Sciences, University of Helsinki, Helsinki, Finland, 6Department of Medical Genetics, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland

Canine episodic head tremor syndrome (CeHts) is considered a benign paroxysmal movement disorder of unknown pathogenesis. CeHts is diagnosed based on signalment, history, and clinical description. electroencephalographic (eeg) investigation into this condition has only been reported in doberman pinschers and was unrewarding. However, eeg abnormalities were reported in focal juvenile canine epilepsies that presented with tremor. it was hypothesized that further eeg recording of CeHts would help to clarify nature of the pathogenesis. ten dogs clinically diagnosed with CeHts and video confirmation of tremor underwent video or routine eeg recording with client consent for our multicenter collaboration. there were 6 english Bulldogs and one each of labrador retriever, Boxer, lapponian Herder, and alaskan Klee Kai. four dogs demonstrated head tremor during video-eeg recording. in three cases (one each of Boxer, Bulldog, and lapponian Herder), there were ictal eeg abnormalities that consisted of right-sided predominant 6 Hz spike-and-wave discharges associated with the head tremor. in the remaining case (alaskan Klee Kai), a 12-14 Hz polyspike-and-wave pattern was recorded. of the six dogs that did not demonstrate tremor during recording, there were no ictal eeg abnormalities. these findings support the reclassification of CeHts as an epileptic syndrome of 6Hz spike-and-wave with focal onset seizures in some dogs. further investigation is required to determine whether there are breed-specific differences and whether the presence of ictal or interictal patterns correlate with the natural history of the syndrome or treatment outcomes. Video-eeg facilitates the proper diagnosis of epileptic-like syndromes for subsequent genetic analysis.

EPILEPtoId CrAMPINg SyNdroME IN tHE NorWICH tErrIEr: CLINICAL CHArACtErISAtIoN ANd PrEVALENCE IN tHE uK

L De Risio, J FreemanNeurology Unit, Animal Health Trust, Newmarket, UK

episodic muscular hypertonicity in norwich terriers (nt) was first reported in a brief letter in the Veterinary record in 1984. since then there have been anecdotal reports and the condition has remained poorly characterised. the aims of this study were to characterise clinically nt epileptoid cramping syndrome (eCs), and to estimate its prevalence in the uK. the owners of nt born since 1 January 2000 were invited by the uK Kennel club and nt breed club to complete a specifically designed questionnaire aimed at identifying affected and unaffected nt, and clarifying the clinical characteristics of nteCs.the questionnaire was returned for 198 nt. of these, 26 (13%) nt were classified as affected by nteCs following revision of the questionnaires, videos of the episodes, veterinary medical records and telephone interview with the owners. all nt were clinically normal between episodes. no significant abnormalities were detected on diagnostic investigations, including electroencephalography (which was performed in 2 nt). Mean age at the first episode of nteCs was 3 years. the episodes were characterised by sustained muscular hypertonicity, dystonia of the pelvic or all 4 limbs, and difficulty or inability standing up and walking. Consciousness was normal. episode frequency varied both between and within individuals. stress, anxiety, excitement, and variation in daily routine were recognised as episode triggers in 13 nt. episode duration was 2-5 minutes in the majority of nt (range <1-30 minutes). several affected nt were genetically related. genetic investigations to identify causal mutations are in progress.

Ethical permission was not required for this study

dEgENErAtIVE ENCEPHALoPAtHy oF NoVA SCotIA duCK toLLINg rEtrIEVErS

E. Barker1, D. O’Brien2, L. Dawson1, G. Johnson2, J. Rose1, S. Van Meervenne3, K. Sörensen4, C. Rohdin4, A. Leijon5, O. Frykman6, N. Granger1

1 University of Bristol, Bristol, UK; 2 University of Missouri, Columbia, MO, USA; 3 AniCura Läckeby Djursjukhus, Läckeby, Sweden; 4 National Veterinary Institute (SVA), Uppsala, Sweden; 5 Department of Biomedical Sciences and Veterinary Public Health, Section of Pathology, Swedish University of Agricultural Sciences, Uppsala, Sweden; 6 Herrgårdskliniken, Aneby, Sweden

Hereditary neurodegenerative diseases have been reported in both human and veterinary literature. Clinical signs are often progressive, but may be delayed in onset, and typically reflect the area of the central nervous system most affected most altered pathologically.eight young adult nova scotia duck-tolling retrievers (nsdtrs) from sweden, Canada and uK have been evaluated for neurological dysfunction in the last two years. the aim of this study was to characterize the clinical and histopathological features of this disease.Clinical history, Mri imaging and laboratory analysis were retrospectively reviewed. nervous tissue was collected prospectively from selected cases following owner decision to euthanase on welfare grounds.neurological dysfunction was reported from four months to five years of age, and was progressive in nature. Clinical signs were characterised by marked sleep disorder (paddling, vocalisation), increased



three scottish terriers (sts), 2 Cavalier King Charles spaniels (CKCss) suffering from scottie Cramp (sC) and episodic falling, respectively, then an english setter with a dyskinesia of unknown origin, displayed many daily episodes, triggered by exercise and/or excitement that definitely prevented them from living normally. all dogs received fluoxetine as a single treatment (2-4 mg/kg q24h). four dogs displayed early and complete remissions that persisted over long periods (1 year for 1 CKCs then 2, 6 and 7 years for the 3 sts). the remaining 2 cases showed a significant improvement with a decline to approximately one single episode every 2 months for both dogs. transient relapses occurred when treatment was interrupted or tapered in 3 dogs. no treatment resistance or side effect was observed.fluoxetine may be a good and safe option for the long-term management of Cpds, allowing dogs for resuming to normal activity and lifestyle. it can directly correct serotoninergic transmission imbalance suspected in sC. its activity remains unclear in other Cpds; direct serotoninergic action is likely but indirect effect through a reduction of behavioral reactivity to triggering factors like stress, excitation or environmental stimulations is also plausible.

INtErICtAL CArdIAC AutoNoMIC NErVouS SyStEM dISturBANCES IN dogS WItH IdIoPAtHIC EPILEPSy

D. Mocanu1, M. Musteata1, G.D. Stanciu1, M. Armasu1, A. Baisan1, G. Solcan1

1Dept. of Clinical Science – Internal Medicine, Faculty of Veterinary Medicine Iași, Romania.

up to 65% of dogs with idiopathic epilepsy (ie) have an abnormal eeg in the interictal phase, but no neurological deficits or other positive findings on imagistic and blood examination are observed at that moment. in humans, an impaired activity of autonomic nervous system (ans) is seen in the interictal phase of ie patients and appears to have an important role in long term prognosis of the cases. until now there are no reports in which ans is analyzed in dogs with ie.to asses ans we used time domain and spectral power analysis of heart rate variability (HrV) on 5 minutes eCg day time recordings in 26 newly diagnosed and chronic ie dogs with positive eeg epileptic discharges the control group was represented by 13 healthy dogs, age and weight matched. Cardiac depolarization time was assessed by measuring p wave dispersion (pWd) and corrected Qt interval in all dogs.there were no differences between ie and normal dogs in overall HrV (sdann and lf/Hf), but a significant increase in vagal tone (Hf and pnn50%), pWd and Qt interval was observed in the epileptic group. those are proved triggers for sever cardiac arrhythmias in dogs (atrial fibrillation and ventricular tachyarrhythmia) and are involved in the pathogenesis of sudden death epileptic syndrome in humans. in conclusion, dogs with subclinical brain epileptic activity have a permanent alteration in cardiac ans function. these changes may have a contribution in increasing the risk of premature death in dogs with ie.

MyoCLoNIC EPILEPSy WItH PHotoSENSItIVIty IN rHodESIAN rIdgEBACKS

F. Wielaender1, F. James2, M. A. Cortez3, G. Kluger4, M. Kornberg5, A. Bathen-Noethen6, T. Flegel7, S. Bhatti8, V. Hülsmeyer1, H. Lohi9, A. Fischer1

1Centre for Clinical Veterinary Medicine, LMU University of Munich, Munich, Germany, 2Department of Clinical Studies, Ontario Veterinary College, University of Guelph, Ontario, Canada, 3Neurosciences & Mental Health Program, Peter Gilgan Centre for Research and Learning, SickKids Research Institute, Ontario Canada, 4Department of Neuropediatrics, Epilepsy Center, Vogtareuth, Germany and Paracelsus Medical University, Salzburg, Austria, 5Veterinary Hospital Trier, Trier, Germany, 6Veterinary Practice Bathen-Noethen, Cologne, Germany, 7Department of Small Animal Medicine, University of Leipzig, Leipzig, Germany, 8Department of Small Animal Medicine and Clinical Biology, Ghent University, Belgium, 9Research Programs Unit, Molecular Neurology, University of Helsinki, Helsinki, Finland

a breed-specific syndrome characterized by frequent myoclonic jerks has been observed in rhodesian ridgebacks. the aim of the study was to provide a clinical and electroencephalographic description of this syndrome and to investigate its epileptic nature.seventeen dogs that shared a unique phenotype were identified. owners were asked to provide a videotape and to complete an online-questionnaire. extensive diagnostic work-up was offered and pedigrees were analyzed. awake ambulatory wireless video-electroencephalography (eeg) was performed in 11 affected rhodesian ridgebacks and five controls of the same breed. one dog underwent an additional video-eeg with photic stimulation in a neuropediatric epilepsy center. eeg was reviewed by a neurophysiologist, a neuropediatrician, and three veterinarians, with consensus results reported. Violent myoclonic jerks occurred in a recumbent and relaxed, drowsy or asleep state (n=17) and occasionally also while standing (n=10). in five dogs myoclonic seizures could be triggered by flashing lights. Median age of onset was 6 months (9w - 1.5y). over time seven dogs additionally developed other seizure types. Video-eeg confirmed the diagnosis of a myoclonic epilepsy in affected dogs. one dog showed photomyoclonic responses on video-eeg with photic stimulation. Control dogs displayed unremarkable eeg findings. none of the performed examinations (Mri, Csf, neurometabolic screening) demonstrated an underlying structural or metabolic cause. pedigree analyses pointed to an hereditary disorder. rhodesian ridgebacks suffer from an idiopathic (genetic) myoclonic epilepsy with photosensitivity. affected dogs show a characteristic eeg pattern. this is proposed as the definition of a peculiar electroclinical syndrome whose genetic base is currently under investigation.

LoNg-tErM trEAtMENt oF CANINE PAroxySMAL dySKINESIAS WItH FLuoxEtINE: 6 CASES

T.Bouzouraa1, C.Escriou2

1Internal Medicine, 2Neurology, VetAgro Sup, Lyon, France

it is only recently that both clinical features and genetic basis of canine paroxysmal dyskinesias (Cpds) have been documented. their management remains challenging though phenothiazine, benzodiazepines even anticonvulsants yielded unsatisfactory results. fluoxetine, a selective serotonin reuptake inhibitor, seems promising.



30% and 50%, and the remaining one third of patients experience little or no effect2. increased insight into the Moa may help to identify responders and increase clinical efficacy. also, from a veterinary point of view, research towards neurostimulatory treatments for refractory canine epilepsy is needed. only one study evaluated the efficacy and safety of Vns in dogs with idiopathic epilepsy and the results seemed promising3. We examined the Moa of Vns in healthy Beagle dogs and demonstrated changes in cerebral perfusion using µ-speCt and increases in Csf norepinephrine concentrations induced by Vns4.1. Ben-Menachem E. Vagus-nerve stimulation for the treatment of epilepsy. Lancet Neurol. 2002;1(8):477-82.

2. Boon P, Raedt R, de Herdt V, Wyckhuys T, Vonck K. Electrical stimulation for the treatment of epilepsy. Neurotherapeutics.

2009;6(2):218-27.

3. Muñana KR, Vitek SM, Tarver WB, Saito M, Skeen TM, Sharp NJ, Olby NJ, Haglund MM. Use of vagal nerve stimulation as a treat-

ment for refractory epilepsy in dogs. J Am Vet Med Assoc. 2002;221(7):977-83.

4. Martlé V, Boon P, Vonck K, Raedt R, Van Ham L, Bhatti S. Canine epilepsy: the role of functional brain imaging and vagus nerve

stimulation. PhD thesis, Ghent University, 2014.

tHE EFFECt oF IMEPItoIN, A rECENtLy dEVELoPEd ANtIEPILEPtIC drug, oN tHyroId FuNCtIoN tESt PArAMEtErS ANd FAt MEtABoLISM IN HEALtHy BEAgLE dogS

K. Bossens1, S. Daminet1, M. Rick2, L. Duchateau3, L. Van Ham1, S. Bhatti1

1Department of Small Animal Medicine and Clinical Biology, Ghent University, Belgium. 2Department of Pathobiology and Diagnostic Investigation, Michigan State University, United States. 3Department of Physiology and Biometrics, Faculty of Veterinary Medicine, Ghent University, Belgium.

since early 2013, imepitoin has been introduced in most european countries for the management of recurrent single generalized epileptic seizures in dogs with idiopathic epilepsy. it has been demonstrated that imepitoin is similarly effective as phenobarbital in controlling seizures in dogs with newly diagnosed idiopathic epilepsy. furthermore, a clinically significant superior safety profile was shown compared to phenobarbital administration. as the use of imepitoin gains popularity, its effect on serum thyroid function test parameters warrants further investigation. it is well known that long-term phenobarbital administration influences thyroid function test parameters in dogs. this alteration in serum thyroid hormone concentrations can lead to misinterpretation of results and incorrect diagnosis of thyroidal illness. a prospective study was conducted to compare the effect of phenobarbital and imepitoin on serum concentrations of total thyroxine (tt4), triiodothyronine, free thyroxine, thyroglobulin auto-antibodies, thyroid-stimulating hormone, cholesterol and triglycerides in healthy Beagle dogs. these parameters were determined prior to initiation of antiepileptic drug administration, and after 6, 12 and 18 weeks of antiepileptic drug administration. the oral starting dose of phenobarbital was 5 mg/kg po q12h and was monitored and adjusted to obtain optimal therapeutic serum concentrations (30-35 µg/ml). imepitoin was given at 30 mg/kg po q12h .the results of our study showed that, firstly, imepitoin administration did not affect mean serum tt4 concentrations over an 18 week period. in contrast, mean serum tt4 concentrations decreased significantly over time in dogs where phenobarbital was administered. secondly, mean serum cholesterol concentrations increased significantly over time in the dogs on imepition but not to the same extent as commonly seen in dogs with primary hypothyroidism.

CANINE EPILEPtoId CrAMPINg SyNdroME: A gLutEN SENSItIVE PAroxySMAL MoVEMENt dISordEr – MorE tHAN A gut FEELINg

M Lowrie 1, O Garden2, M Hadjivassiliou3, R Harvey4, D Sanders5, R Powell6, L Garosi1

1Davies Veterinary Specialists, Higham Gobion, Hitchin, UK; 2Department of Clinical Sciences and Services, Royal Veterinary College, Hatfield, UK; 3Department of Neurology, Royal Hallamshire Hospital, Sheffield, UK; 4Department of Pharmacology, UCL School of Pharmacy, London, UK; 5Department of Gastroenterology, Royal Hallamshire Hospital, Sheffield, UK; 6Powell Torrance Diagnostic Services, Higham Gobion, Hitchin, UK Canine epileptoid cramping syndrome (CeCs) is a paroxysmal movement disorder of Border terriers (Bts). previous work has suggested these dogs may respond to a gluten-free diet. the objective of this study was to investigate the possibility of an immune response to a gluten and to study the effect of a gluten-free diet in Bts with CeCs. our hypothesis was that CeCs is a manifestation of gluten sensitivity.six Bts with clinically confirmed CeCs were tested for anti-transglutaminase 2 (tg2 iga) and anti-gliadin (aga igg) antibodies in the serum at presentation, and subsequently three, six and nine months after the introduction of a gluten-free diet. duodenal biopsies were performed in one patient. serum samples were also collected from five Bts having medical investigations for conditions unrelated to neurological or gastrointestinal disease to serve as healthy controls.serum tg2 iga titers were increased in 6/6 Bts and aga igg titers were increased in 5/6 Bts at presentation compared to controls. after nine months there was clinical and serological improvement in all Bts with CeCs strictly adherent to a gluten-free diet. one dog had persistently increased antibody titres, but was found to have scavenged horse manure. on the strict introduction of a gluten-free diet this dog also had an improved clinical and serological response. the diet-associated improvement was reversible in two dogs on completion of the study, both of which suffered a clinical relapse of CeCs on the re-introduction of gluten.CeCs is best described as a gluten sensitive movement disorder triggered and perpetuated by gluten and thus responsive to a gluten-free diet.

NEuroStIMuLAtIoN IN EPILEPSy – VAguS NErVE StIMuLAtIoN –

Sofie F. M. Bhatti, Ghent University, Faculty of Veterinary Medicine, Dept. of Small Animal Medicine and Clinical Biology, Neurology and neurosurgery unit neurostimulation is a treatment modality in which electrical pulses are administered to nerve tissue in order to manipulate a pathological substrate and to achieve a symptomatic or even curative therapeutic effect1. in human epilepsy, a substantial number of patients either lack good seizure control with pharmacological or surgical treatment, or they experience major adverse effects (or both)1. therefore, neurostimulation-based treatments have gained considerable interest the last 10-15 years.electrical stimulation of the tenth cranial nerve or vagus nerve stimulation (Vns) is an extracranial form of neurostimulation that was developed in the 1980s and is currently routinely and worldwide available for the management of human epilepsy1,2. Vns is indicated in patients with refractory epilepsy who are unsuitable candidates for epilepsy surgery or who have had insufficient benefit from such a treatment1,2. Vns influences crucial brainstem and intracranial structures; including the nucleus of the solitary tract, the locus coeruleus, the thalamus, and limbic structures1,2. the precise mechanism of action (Moa) by which Vns exerts its antiepileptic effect is still unknown2. the current consensus on efficacy is that one third of patients have a considerable improvement in seizure control with a reduction in seizure frequency of at least 50%, one third of patients experience a worthwhile reduction in seizure frequency between



a total of 120 dogs met the inclusion criteria. an abnormal Csf was only found in 5.8% (7/120) of dogs. the prevalence found for diagnosis other than ie was 1/120 dogs (0.8%). the site of Csf sampling, the interval between last seizure and Csf collection and the seizure type had no correlation with having an abnormal Csf. the number of red blood cells in the sample was significantly different between dogs with normal and abnormal Csf (P=.016). these results suggest that Csf analysis has a poor incremental diagnostic value for other than idiopathic epilepsy in patients with the same inclusion criteria of this study.

PHENotyPIC CHArACtErIZAtIoN oF SPINNINg ANd tAIL-CHASINg IN gErMAN SHEPErd ANd JACK ruSSEL tErrIEr

Catherine Escriou1, Julie Meynet1, Caroline Dufaure de Citres2, Anne Thomas2 1Neurology, VetAgro Sup, Lyon Veterinary Campus, France; 2Antagène, France

a predisposition to develop “spinning” (s) and “tail chasing” (tC) behavior has been observed in Bull terriers (Bt). these stereotypic behaviors are related to obsessive Compulsive disorder (oCd) and genetic basis have been demonstrated. signs of hallucination and psychotic like behavior (freezing, staring, unprovoked aggression, unexplained growling, fly catching) are commonly associated and a complex neurological and evolutive syndrome related to autism is suspected were oCd coexists with focal/partial seizures.

in order to determine if others breeds could be affected by this disease, we recruited other dogs than Bt affected by spinning or tail-chasing using a web questionnaire. We recruited 20 german shepherd (gs) and 14 Jack russell terrier (Jrt). a precise phenotypic characterization could have been done and compared to Bt’s one. as in Bt, we describe an association between spinning/tail chasing and psychotic like behavior with alteration of dog’s personality.trance like behavior were observed in a majority of dogs with disconnection from the environment during episodes. same stages of disorders reflecting the severity and evolutive nature of the disease were applied to gs or Jrt as for Bt. some minor breed specificities seems to exists as high spinning velocity in Jrt, spinning with tail in the mouth in Jrt and gs (but not in Bt) for example. spinning or tail chasing in gH and Jrt must be considered as the same complex neurobehavioral disease as in Bt although its prevalence in this breeds seems to be lower than in Bt.

VLdLr-ASSoCIAtEd CErEBELLAr HyPoPLASIA IN EurASIEr dogS

A. Fischer1, K. Rentmeister2, S. Lindsteding3, F. Bernardino1, E. Manz4

1Centre for Clinical Veterinary Medicine, LMU University of Munich, Munich, Germany; 2Tierärztliche Praxis für Neurologie, Dettelbach, Germany; 3Kynologische Zuchtgemeinschaft Eurasier e. V.¸ Germany; 4Generatio Sol. GmbH, Heidelberg, Germany the very low density lipoprotein receptor (Vldlr) is part of the reelin signaling pathway, which directs neuroblast migration. Vldlr-associated cerebellar hypoplasia in eurasier dogs is an autosomal recessive inherited cerebellar malformation due to a one base pair deletion in the very low density lipoprotein receptor (gerber et al., 2015). it is characterized by absence of the caudal portions of the cerebellar vermis and the

EFFICACy oF IMEPItoIN AS FIrSt CHoICE drug IN tHE trEAtMENt oF 53 NAÏVE dogS AFFECtEd By IdIoPAtHIC EPILEPSy

A. Gallucci1, T. Gagliardo1, M. Menchetti1, A. Ruffini1, E. Bianchi1,2, A. Milici3, P. Tosolini4, A. Cauduro5, G. Gandini1. 1Department of Veterinary Medical Sciences, University of Bologna, Ozzano Emilia, Italy. 2Department of Veterinary Medical Sciences, University of Parma, Parma, Italy 3Veterinary Clinic “Città di Saronno”, Saronno, Italy. 4Veterinary Clinic “Schiavi”, Udine, Italy, 5Veterinary Clinic “Ass. Prof. Neurovet”, Legnano, Italy.

the efficacy and safety of imepitoin, a novel antiepileptic drug, were rectrospectively evaluated in 53 naïve idiopathic epileptic dogs that met the inclusion criteria (diagnosis of idiopathic epilepsy and imepitoin monotherapy). follow-up information was obtained through a questionnaire sent to the owners: 53 (100%), 35 (66%) and 13 (25%) dogs had follow-up information at 3, 6 and 9 months, respectively.imepitoin starting dosage (expressed as mg/kg Bid) was 8-10 in 11 dogs (21%), 11-20 in 40 dogs (75%) and 21-30 in 2 dogs (4%). during time, dosage was increased in 20 dogs (34%), becoming 11-20mg/kg in 39 dogs (74%) and 21-30mg/kgin 10 dogs (19%). successful treatment, defined as >50% reduction in seizures was noted in 25 (47%), in 20 (57%) and 9 (69%) dogs at 3, 6 and 9-months follow-up, respectively. Complete remission was achieved in 15 (28%), 9 (26%) and 3 (23%) dogs at 3, 6 and 9-months follow-up. Cluster seizures (before treatment: n=16, 30%) turned to single seizures in 8 (15%), 4 (11%) and 1 (8%) at 3, 6 and 9 months follow-up.side effects were observed in 19 dogs (36%) and consisted in transient sedation/somnolence, hyperexcitability, aggressiveness, tremors, gastrointestinal problems. two dogs still showed mild aggressiveness in long term.lack of efficacy and consequent change/association of drug was the reason for 9 and 11 dogs that missed the follow-up at 6 and 9 months. in this study imepitoin showed its major efficacy at a dosage >15mg/kg Bid.side effects were mild and, mostly, transient.

VALuE oF CErEBroSPINAL FLuId ANALySIS IN EPILEPtIC dogS tHAt LACK INtErICtAL NEuroLogICAL ABNorMALItIES ANd HAVE uNrEMArKABLE MAgNEtIC rESoNANCE IMAgINg oF tHE BrAIN

A M Coelho, T Maddox, D Sanchez-Masian, R Gonçalves. Small Animal Teaching Hospital, University of Liverpool, Neston, CH64 7TE, UK.

to diagnose idiopathic epilepsy (ie), Csf analysis is essential to exclude other causes of seizures. dogs with interictal neurological deficits are likely to have a underlying brain disease but the value of performing Csf analysis in dogs that lack interictal changes and have normal advanced imaging of the brain has not yet been assessed.the database of the university of liverpool was searched for dogs presenting for recurrent seizures with no interictal abnormalities according to the owners. inclusion criteria for the study comprised an unremarkable neurological examination, exclusion of possible causes of reactive seizures (including a normal haematology and biochemistry profiles) and normal magnetic resonance (1-tesla) of the brain. results of the Csf analysis in these patients were evaluated and considerate abnormal if the protein concentration was >30mg/dl and/or the total nucleated cell count was >5cells/μl. dogs were excluded if the Csf rBC count was >5,000μl.



a finite element model was constructed, using geometry extracted from Mri scans of a Cavalier King Charles spaniel with syringomyelia, to explore possible mechanisms of syrinx formation. the model included the spinal cord, subarachnoid space (sas), dura mater, and the epidural space. it has been shown in patients with restricted Csf flow, that there is exaggerated movement of the spinal cord during the cardiac cycle. this motion was applied to the cranial end of the spinal cord of the model.the peak longitudinal and radial pressure differences in the sas oscillated between -22.3 to +90.0 pa, and -100 to +100 pa, respectively.low-amplitude cyclic shear stresses were present in the cervical spinal cord (C2 – C6), where the cavities typically originate.in conclusion it was proposed that the Csf pressure gradients are unlikely to cause fluid movement into the cord, sufficient to generate syrinxes. on the other hand, although the shear stress in the cord is low, its location and cyclic nature indicates the possibility that this may be the factor that generates the initial tissue damage, which eventually leads to the formation of syrinxes.

A PrELIMINAry Study oF tHE PENLIgHt-CoVEr tESt IN dIFFErENtIAtINg BEtWEEN PErIPHErAL ANd CENtrAL VEStIBuLAr dISEASE IN dogS ANd CAtS

G. E. Longson, C. Turner, A. E. Vanhaesebrouck, E. J. Ives, T. L. Williams and P. M. Freeman. Department of Veterinary Medicine, University of Cambridge, Cambridge, UK

differentiating between peripheral and central vestibular disease is important for clinical decision-making and prognostication. Current diagnostic methods used for differentiation are infrequently available in general practice, require general anaesthesia and carry a high cost. the penlight-cover test (pCt) may provide a simple, safe and cost-effective clinical test to overcome these limitations.Masking visual input using a bright penlight should reduce suppression of spontaneous nystagmus in cases of peripheral but not central vestibular disease.the utility of the pCt to differentiate between peripheral and central vestibular disease was evaluated by measuring changes in slow phase velocity (spV) and beat frequency (Bf) of nystagmus whilst masking visual input. data were collected from 5 peripheral and 8 central cases in a referral population of dogs and cats. spV increased when visual input was removed in 60% of peripheral cases but 0% of central cases (fisher’s exact test, p=0.035). Bf increased when visual input was removed in 80% of peripheral cases but 12.5% of central cases (fisher’s exact test, p=0.0319). the Bf increased by a median of 11 beats in 7 seconds in peripheral cases and 0 beats in 7 seconds in central cases (Mann-Whitney u test, p=0.0128). in conclusion, increased spV or Bf when visual input is removed may increase suspicion of peripheral vestibular disease, whereas unchanged spV, or unchanged or decreased Bf, may increase suspicion of central vestibular disease. further studies are required to calculate the sensitivity, specificity and predictive values of the pCt in a larger population of dogs and cats.

cerebellar hemispheres, large retrocerebellar fluid accumulations, enlarged fourth ventricle and variable caudal fossa size (Bernardino et al., 2015). non-progressive ataxia is the main neurologic sign. phenotypic variation in the severity of the ataxia may occur, ranging from severe cerebellar ataxia in puppies, to improved ataxia in adults, and an almost normal gait in one affected dog despite the presence of a severely hypoplastic cerebellum.therefore the aim of the present investigation was to estimate the prevalence of the Vldlr:c.1713delC mutation in a population of eurasier dogs. edta blood samples from 397 eurasier dogs were collected in association with the respective breed club and stored frozen at -20oC until further analysis. genetic testing for the Vldlr-mutation was done as described previously (gerber et al., 2015).results identified 46 heterozygous carriers of the mutation and indicated an estimated prevalence of 11.59% (Ci95% 8.44% –14.74%). in conclusion, the Vldlr:c.1713delC mutation has a high prevalence in this population. genetic testing is recommended prior to breeding in any eurasier dog to avoid breeding carriers to each other, and also as a simple diagnostic tool in any eurasier dog with non-progressive ataxia.

MrI ProtoCoL IN EPILEPSy, MoVEMENt dISordEr CASES ANd AN outLooK For tHE FuturE

Magnetic resonance imaging (Mri) is a pivotal diagnostic test for epilepsy and movement disorders (Md) however the sensitivity is limited because diagnosis of idiopathic epilepsy is one of exclusion. reliability is limited by available technology and variations in protocol which may not be optimized for detection of subtle epileptogenic lesions. there are 3 main aims: 1) rule out diseases which may be treatable with means other than anticonvulsant therapy (e.g. inflammatory or infectious brain disease) 2) identify lesions which are caused by seizures but not necessarily the source of seizures, for example hippocampal sclerosis 3) to provide data to further advance the field of research into the pathogenesis and/or treatment of epilepsy and Md. there is a need for a standardized veterinary epilepsy and Md Mri protocol which will: facilitate more detailed examination of areas susceptible to generating and perpetuating seizures / Md; complement pathological studies; is economical; simple to perform; and can be adapted for both low and high field scanners. standardisation of imaging will improve clinical communication and uniformity of case definition between research studies.the international Veterinary epilepsy task force proposes a 6-7 sequence epilepsy-specific Mri protocol including sequences orientated parallel and perpendicular to the hippocampus.

CoMPutEr SIMuLAtIoN oF tHE CANINE SPINE: tHE EFFECtS oF INCrEASEd SPINAL Cord MotIoN oN tHE dEVELoPEMNt oF SyrINgoMyELIA

R. Lloyd1, S. Cirovic1, J. Jovanovik2, H, Volk3, C. Rusbridge 2, 4. 1.Dept. of Mechanical Engineering Sciences, University of Surrey Guildford, Surrey, UK; 2Fitzpatrick Referrals, Halfway Lane, Eashing, Godalming, Surrey, UK; 3Royal Veterinary College, University of London, London, UK. 4School of Veterinary Medicine, University of Surrey, Guildford, Surrey, UK.

syringomyelia is a disorder characterised with the presence of fluid-filled cavities in the spinal cord. the condition occurs in both humans and animals. the mechanism(s) of cavity formation are not clear, leading to limited treatment. Current theories are based on the assumption that abnormities in the circulation of the cerebrospinal fluid (Csf) generates pressures that drive the fluid into the cord.



recent developments in human guillain-Barre research challenge the classification of iMpn according to axonal and demyelinating features even though unsupported by morphological investigations. to contribute to this discussion, this study screened for an association of inflammatory features and fibre pathologies amongst iMpn affected nerves from dogs and cats.archived nerves from dogs and cats exhibiting fibre-invasive inflammatory cells underwent duodichromatic teasing preparation (dtp) and were reevaluated for affection of functional fibre subunits. the features were correlated to clinical records and electrophysiological data.altogether 19 iMpn affected dogs and 15 cats were included. in each species, the mode of inflammation and fibre degeneration gave rise to four iMpn subtypes, with affection of schmidt-lanterman clefts (slC) (9/34), nodes-paranodes (npn) (10/34) or both (14/34). amongst dogs displaying npn (9/19) two different stages were distinguished suggesting humoral immune mechanisms to precede cellular infiltrates (4/19). feline biopsies mostly featured involvement of both subunits (12/15) at advanced stages. electrophysiology was rarely predictive of the primarily affected subunit in pure slC and npn types.evaluation of fibre subunits provide a better insight into the immunobiology of iMpn by unravelling the primary targets. like in humans, nodo-paranodopathies and internodopathies can be distinguished in animals. in a strict sense, the former relates to acute motor axonal neuropathy (aMan) while the latter corresponds to acute inflammatory demyelinating polyneuropathy (aidp) in people. Correct iMpn subtyping by dtp is recommended in order to achieve a correct diagnosis and to base prospective clinical studies on a scientific ground.

IMMuNoHIStoCHEMICAL CHArACtErIZAtIoN oF tHE ANtI-INFLAMMAtory EFFECt oF tWo trEAtMENt ProtoCoLS IN dogS WItH grANuLoMAtouS MENINgoENCEPHALoMyELItIS or NECrotIZINg (MENINgo)-ENCEPHALItIS

F. Salger1,2, A. Oevermann1, L. Kreipe2, T. Flegel3, M. Vandevelde1,2, B. Vidondo Curras4, D. Henke1,2. 1Division of Neurological Sciences, 2Division of Clinical Neurology, 1,2Department of Clinical Veterinary Medicine, 3Department of Small Animal Medicine, Faculty of Veterinary Medicine, University of Leipzig, Germany, 4Department of Veterinary Public Health, Vetsuisse Faculty, University of Bern, Switzerland.

there is little objective evidence about the effect of immunosuppressive treatment of canine granulomatous meningoencephalomyelitis (gMe) and necrotizing encephalitides (nMe/nle summarized as ne). to assess the effect of two different treatment protocols for gMe and ne, the inflammatory reaction in these conditions was evaluated quantitatively and qualitatively in 18 untreated dogs (5 gMe, 13 ne), in 10 dogs treated with prednisolone (4 gMe, 6 ne), and in 7 dogs treated with prednisolone and lomustine (CCnu-p) (4 gMe, 3 ne) which were all euthanized because of their Cns disease or other reasons. randomly selected areas of representative lesions were examined for the total inflammatory cell count (tCC), and the number and relative distribution of t-lymphocytes (Cd3), B-lymphocytes (Cd20) and macrophages (Cd18) using immunohistochemistry. in all untreated dogs, macrophages were the most common cell population, followed by B-lymphocytes and much less t-lymphocytes. the tCC was decreased following both treatment protocols as compared to untreated dogs; however, only after CCnu-p this difference reached significance. in dogs treated with CCnu-p for gMe, all cell types, and in dogs with nMe/ne specifically macrophages and t-lymphocytes were significantly decreased. our results regarding the qualitative distribution of inflammatory cells were consistent with previous reports in dog with gMe; however, we did not find a predominance of t-lymphocytes in in dog with ne as reported before. the immunosuppressive effect of both treatment protocols was evident, but the CCnu-p

INtErLEuKIN-17 ANd Cd40 LIgANd IN CANINE StEroId-rESPoNSIVE MENINgItIS-ArtErItIS

J. Freundt Revilla1, R. Carlson1, A. Maiolini1, A. Tipold1.1Dept. of Small Animal Medicine and Surgery, University of Veterinary Medicine, Hannover, Germany.

steroid-responsive Meningitis-arteritis (srMa) is an immune mediated disorder characterized by a neutrophilic pleocytosis in the cerebrospinal fluid (Csf). previous studies of the disease have shown increased levels of il-6 and tgf-ß1 in Csf indicating the presence of th17 lymphocytes.il-17 induces and mediates inflammatory responses and plays an important role in recruitment of neutrophils. the hypothesis of a th17 skewed immune response in srMa should be confirmed by evaluating il-17 and Cd40l, inducing B-t cell interaction.enzyme-linked immunosorbent assays (elisa) were performed to measure il-17 and Cd40l in serum and Csf of patients suffering from srMa in the acute stage (srMa a),under treatment with glucocorticosteroids (srMa t), during recurrence of the disease (srMa r) and with other neurological disorders and in healthy dogs (animal experiment05-14a453).significant higher levels of il-17 were found in Csf of dogs with srMa a compared with srMa t, other neurological disorders and healthy dogs (p<0.0001). in addition, levels of Cd40l in Csf in dogs with srMa a and srMa r were significantly higher than in healthy controls (p<0.05). furthermore, Csf concentrations of il-17 and Cd40l showed a strong positive correlation among each other (rspear= 0.4215; p<0.0003) and with the degree of pleocytosis (rspear= 0.8924; p<0.0001 and rspear= 0.3817; p<0.0034).these results imply that th17 cells are inducing the autoimmune response in srMa and are involved in the development of the severe neutrophilic pleocytosis. the investigation of the role of il-17 and Cd40l in srMa adds to the knowledge of pathophysiological mechanisms in srMa and opens the discussion about new therapeutic strategies.

MorPHoLogICAL rECLASSIFICAtIoN oF IMMuNE-MEdIAtEd NEuroPAtHIES (IMPN) IN dogS ANd CAtS: BEyoNd tHE CoNCEPt oF AxoNAL ANd dEMyELINAtINg dISEASE

S. Gross1, M. Rosati1, L. Matiasek2, D. Corlazzoli3, R. Capello4, T. Harcourt-Brown5, A. Fischer6, V. Huelsmeyer6, H. Schenk7, G. Gandini8, K. Gnirs9, A. Jeandel10, M. Baroni11, S. Loderstedt12, T. Flegel13, K. Jurina2, G. Abbiati14, K. Matiasek1

1Section of Clinical & Comparative Neuropathology, Centre for Clinical Veterinary Medicine, Ludwig-Maximilians University, Munich, Germany; 2Neurology Referral Service, Tierklinik Haar, Haar, Germany; 3Clinica Veterinaria Roma Sud, Rome, Italy; 4North Downs Specialist Referrals, Bletchingley, Surrey, UK; 5Langford Veterinary Services, University of Bristol, Bristol, UK; 6Section of Neurology, Centre for Clinical Veterinary Medicine, Ludwig-Maximilians University, Munich, Germany; 7Neurology Service, Small Animal Clinic, Lueneburg, Germany; 8Department of Veterinary Medical Science, University of Bologna, Italy; 9Advetia Clinic for Small Animal Medicine, Paris, France; 10Ecole Nationale Vétérinaire d’Alfort, Maisons Alfort, France; 11Clinica Veterinaria Valdinievole, Monsummano, Italy; 12Neurology Service, Clinic of Small Animal Medicine, University of Berlin, Berlin, Germany; 13Section of Neurology, Clinic of Small Animal Medicine, University of Leipzig, Leipzig, Germany; 14Clinica Veterinaria Malpensa, Samarate, Italy



seventeen dogs were treated by multiple tplCs for ventral spinal cord compression caused by Hansen type i or ii iVdd. the presurgical spinal cord compression and postsurgical decompression, as well as slot dimensions were measured based on computed tomography- myelography images. the neurological outcome was assessed based on repetitive examinations and owner questionnaires. fourteen dogs had two tlplCs, two dogs had three tlplCs and one dog had four tlplCs performed. the mean slot depth, height and length were 63%, 29% and 25% of the vertebral body, respectively. the mean residual vertebral interslot length between two adjacent tlplCs was 65% of the vertebral body length. at re-evaluation four weeks after surgery, seven dogs (35.3%) had the same modified frankel score compared to the presurgical examination, whereas eleven dogs (64.7%) had neurologically improved. according to the owners, 78.6% of the dogs showed a normal gait within six months after surgery. in conclusion, multiple spinal cord compressions caused by iVdd can be eliminated by multiple tlplCs. the benefit of complete spinal cord decompression at all relevant disc locations seems to outweigh the risk of potential spinal instability.

CoMPArISoN oF CoNVENtIoNAL ANd HIgH dEFINItIoN VIdEo tELESCoPE ASSIStEd VENtrAL SLot dECoMPrESSIoN For CErVICAL INtErVErtEBrAL dISC HErNIAtIoN IN 51 dogS

D. Rossetti, C. Ricco, G. Ragetly, C. Poncet, Centre Hospitalier Vétérinaire Frégis, Arcueil France

the ventral slot surgery is the treatment of choice for cervical intervertebral disc disease (iVdd) in dogs. little is known about the use of magnification in veterinary neurosurgery. the objective of this prospective study was to compare the use of a Video telescope operating Monitor (VitoM) with the conventional approach.fifty-one dogs that presented with cervical intervertebral disc disease between June 2013 and september 2014. the dogs were assigned to a VitoM group (n= 30) or a conventional group (n=21). signalement, pre-operative neurological status, preoperative spinal cord dimension at the compression level obtained with Ct myelography, operative time, surgical complications, ventral slot size, postoperative spinal height and diameter at the compression level obtained with Ct myelography, hospitalization time and the post-operative outcome were compared between the two groups.no significant differences in the surgical time were noted (62.4 ± 14.2 min, p = 0.6). the VitoM group was associated with a greater post-operative spinal diameter (p = 0.01) and spinal height (p = 0.002) as well as a smaller ventral slot (p = 0.007) in comparison with the conventional group. the VitoM group was associated with a better post-operative outcome (p < 0.01) and a shorter post-operative hospitalization time (p = 0.006).the VitoM installation was not time consuming and the learning curve was considered to be fast. the results of this study support the view that the VitoM technique could be advantageous compared with conventional ventral slot surgery.

seems to be more effective. interestingly, the percentage of B-lymphocytes was much higher following treatment in dogs with ne compared to dogs with gMe. this finding may imply a role for antibody mediated mechanisms in the pathogenesis of ne.

CLINICAL, IMAgINg CHArACtErIStICS ANd LoNg tErM outCoME oF dogS WItH INtrANASAL MENINgoENCEPHALoCELE: A CASE SErIES

K. Lazzerini1, J.Guevar1, G. Hammond1, F. McConnell2, J. McMurrough3, R. Goncalves2, R. Gutierrez-Quintana1

1Small Animal Hospital, University of Glasgow, UK, 2Small Animal Teaching Hospital, University of Liverpool, UK, 3PetMedics, Worsley, Manchester, UK. a meningoencephalocele is a protrusion of cerebral tissue and meninges through a cranium defect. there are few case reports describing this uncommon condition in dogs. the aim of this retrospective case series is to describe the clinical presentation, magnetic resonance imaging (Mri) or necropsy features, treatment and outcome of dogs with meningoencephalocele. four young dogs (aged between 8 weeks and 10 months) were presented with a history of seizures. in one dog neurological exanination was unremarkable. in three dogs, neurological deficits indicated a forebrain neurolocalisation. intranasal meningoencephalocele was diagnosed with Mri in all four cases. Mri revealed signs of inflammation of herniated meninges and brain parenchyma. one dog was euthanased after Mri. necropsy confirmed the imaging diagnosis. the three other dogs were treated with phenobarbitone. in the three cases, seizures were well controlled under treatment four months to four years after diagnosis.in these four cases, intranasal meningoencephalocele was diagnosed with Mri in young dogs presenting with seizures. it has been hypothesized that a meningoencephalocele could be a possible seizure focus. in humans, surgical excision of the herniated brain tissue is the treatment of choice. in veterinary medicine, two cases (one dog and one cat) were described in which the neurological signs disappeared after surgical treatment. in three of the dogs presented here, adequate seizure control and good quality of life were achieved with medical treatment only. antiepileptic treatment is a valid non invasive treatment option when there is no cerebrospinal fluid leakage and the neurological deficits are mild.

MuLtIPLE tHorACoLuMBAr PArtIAL LAtErAL CorPECtoMIES IN 17 dogS

S. Hanemann1, M. Münch1, K. Held1, F. Salger2, L. Ziegler3, P. Böttcher1, T. Flegel1

1Department of Small Animal Medicine, University of Leipzig, Germany; 2Devision of Clinical Neurology, Vetsuisse Faculty, University of Bern, Switzerland; 3Clinic for Birds, Reptiles, Amphibians and Fish, Faculty of Veterinary Medicine, Justus Liebig University Giessen, Germany thoracolumbar partial lateral corpectomies (tlplC) facilitates access to the ventral spinal canal and allows spinal cord decompression by minimizing spinal cord manipulation. in veterinary literature multiple tlplCs have not been recommended because of potential spinal instability.the aim of this retrospective study was to report the feasibility of multiple thoracolumbar partial lateral corpectomies in dogs with intervertebral disc disease (iVdd) and to describe the clinical outcome.



the median age of the 32 dogs enrolled was 5 years. dachshunds were the most common breed.one dog developed myelomalacia 4 days post-surgery and was euthanized.three month post-surgery 24/31 (78%) dogs regained ambulatory function whereas 7/31 (22%) did not. there was no overall difference between groups, although dogs treated with epo had a trend towards improved overall outcome with a reduction in incontinence (Chi square, p=0.081).despite the good outcome in all the groups, the application of erythropoietin might be beneficial. future studies should be directed towards the application of epo in a larger group of dogs.

IdENtIFICAtIoN oF BEHAVIorAL StAtES IN CANINE NEoNAtES ANd tHEIr INFLuENCE oN NEuroLogICAL ExAMINAtIoN

C. Morales1, J. Fatjó2, P. Montoliu1. 1Neurocat Veterinaris, Barcelona, Spain, 2Chair Affinity Foundation Animals and Health, Department of Psychiatry and Forensic Medicine, School of Medicine, Universitat Autònoma de Barcelona, Bellaterra, Barcelona, Spain.

in human neonatology, behavioural state (Bs) is defined as a group of physiological, motor and behavioural characteristics occurring at the same time indicating the infant´s levels of arousal. it is an extremely important variable while assessing newborns, as the same stimulus can produce different responses depending on the Bs.our objectives were to investigate whether Bs are recognizable in canine neonates by a descriptive behaviour classification and if Bs can determine the responses to stimuli during neurological examination. this study obtained ethical approval.an adaptation of the Behavioural states scale for human infants was developed for its application in dogs. as part of a larger study with the objective to develop a standardized neonatal neurological examination procedure for dogs, serial neurologic examinations were performed in 53 beagles ranging from 0 to 13 days of age. pup’s responsiveness to seven selected stimuli (palpebral reflex, superficial skin sensation, hopping response, walking, righting reflex, withdrawal reflex and muscle tone evaluation) was assessed in each identified state.five distinct behavioural states could be easily identified in neonate dogs: asleep, drowsy, quiet alert, active alert, and crying. responses to stimuli during neurological examination were observed to be influenced by Bs. thus, the optimal Bs for each item were established. our results show that, in order to standardize neurological assessment in canine neonates, instructions need to be provided about in which Bs a given item should be tested. Changes in Bs during exam also suggest the need to be flexible in the sequence of neurological examination.

ACquISItIoN oF INVoLuNtAry SPINAL LoCoMotIoN (SPINAL WALKINg) IN dogS WItH IrrEVErSIBLE tHorACo-LuMBAr SPINAL Cord LESIoN: A rEtroSPECtIVE Study oN 81 dogS

A. Gallucci1, G. Gandini1, M. Menchetti1, T. Gagliardo1, M. Pietra1, M. Cardinali2, L. Dragone3.1 Department of Medical Sciences, University of Bologna, Ozzano Emilia, Italy. 2”Istituto Veterinario di Novara”, Novara, Italy. 3

Physiotherapy and Rehabilitation Center “Dog Fitness”, Reggio Emilio, Italy.

spinal walking (sW) is described as the acquisition of an involuntary motor function in paraplegic dogs and cats without deep pain perception (dpp) affected by a thoracolumbar (tl) lesion.aim of this retrospective study, was to evaluate the number of tl paraplegic dogs without dpp that developed an autonomous spinal walking after intensive physical rehabilitation, consisting in passive and active assisted exercises. Cornerstone of the treatment were the use of underwater treadmill, and cage restriction to avoidthe dogs to drag on their hind limbs. the medical records of 81 acute paraplegic tl dogs were selected according to the inclusion criteria (intensive rehabilitation treatment in paraplegic dogs with absence of dpp on admission and during the whole treatment). nonparametric and parametric statistics were used to analyze possible correlation between variables and acquisition of sW. autonomous sW was achieved in 48 dogs (59%). 34 had intervertebral disk disease, 14 had traumatic injury. out of these, 31 underwent surgery.age and weight were significantly lower (p=0,0064 and p=0,0269) in sW than in no-sW group.type and site of the lesion and hospitalization were not significantly correlated to development of sW. early start of physiotherapy and its duration, were positively associated with becoming sW (p=0,0426 and p<0,0001). time of physiotherapy had a median of 86 days in sW and 64 days in no-sW dogs.our data suggested that dogs with irreversible tl lesion had significant possibilities to develop sW after intensive physiotherapy treatment, especially when started soon and in lightweight dogs.

roLE oF tHErAPy WItH groWtH FACtorS IN tHE MANAgEMENt oF PAIN PErCEPtIoN NEgAtIVE dogS CAuSEd By tHorACoLuMBAr dISK ExtruSIoNS

D. Faissler, E. Rozanski, M. Kowaleski, Cummings School of Veterinary Medicine at Tufts University, North Grafton 01532, MA, USA

the purpose of this prospective pilot study was to examine the hypothesis that dogs with an acute onset of paraplegia and absent pain perception treated with either subdural platelet rich plasma injections or the intravenous application of erythropoietin at the time of decompressive surgery will have a higher likelihood of a functional recovery than dogs treated with surgery alone.inclusion criteria included chondrodystropic dogs presenting with acute thoracolumbar disk extrusion, paraplegia, and absent pain perception. all dogs underwent decompression within 24 hours after admission and were randomly assigned to:1) saline subdural, 2) autologous platelet rich plasma subdural or 3) erythropoietin (epo) iV. initial and follow-up examinations were performed at the time of admission, and 1,3,7,14,42 and 84 days post-surgery, with a focus on ambulation and fecal/urinary continence. statistical analysis was performed with spss for Windows 20 software. the level of significance was defined as p< 0.05.



posters


fractionated radiotherapy). time to first event, survival times and statistical differences across categories were calculated by the Kaplan-Meier product limit method and log-rank test.forty-seven dogs (median age 9 years, male:female ra-tio 1.76) were included, with labrador retrieveroverrep-resented (17%). roots lesions were the most frequent (46.8%), with C5-t1, V nerve and left side more involved (25.5%, 19.1% and 61.7%). presenting sings were lame-ness, paresis and pain. Mean duration of clinical signs was 90 days. Mri findings comprises increased diam-eter, hyper intense and contrast enhancing nerve roots (57.1%), plexus or peripheral nerve (42.9%), focal hypo-miotropy and muscle hyper intensity (73%). the time to first event was 30 days after surgery and 240 days after srt. overall mean survival was 97, 144 and 371 days with palliation, surgery and srt.a predilection for labrador retriever is observed. Com-paring our results with published data, srt seem to promise better results than palliation or surgery and warrant further evaluation.

SurgICAL StABILIZAtIoN oF CANINE LuMBoSACrAL SPINE WItH StoP-SCrEWS ANd ILIAC WINgS SCrEWSM. Dolera1, L. Malfassi1, S. Pavesi1, M. Sala1, G. Mazza1, S. Marcarini1, N. Carrara1, S. Finesso1. 1La Cittadina Fondazione Studi e Ricerche Veterinarie, Romanengo, Italy.

surgical stabilization of canine lumbosacral spine can be challenging. the aim of this research was to evaluate two surgical techniques to achieve lumbosacral stabilization in dogs either with normal or transitional vertebrae.lumbosacral instability and degenerative stenosis were evaluated by dynamic Computed tomography (Ct) and Magnetic resonance imaging (Mri). in dogs with normal vertebrae two 4.5 mm screws were bicortically inserted in s1 with the heads behind the caudal articular process of l7 to prevent the extension of the lumbosacral joint; if ventral listhesis of s1 was evident, the head of the screws were augmented by methyl methacrylate. in dogs with transitional vertebrae, two 4.5 mm screws were inserted in the iliac wings, two 3.5 mm screws were inserted in the spinous process of l6 and l7; the emerging screws were embedded in methyl methacrylate after flexion of the lombosacral spine. in cases of residual radicular com-pression, dorsal laminectomy and partial discectomy were accomplished. serial clinical and imaging follow up examinations were performed.twenty-two large breed dogs were enrolled. in 14 dogs stop-screws (in 4 augmented) and in 8 dogs iliac wings screws were inserted. two dogs required additional de-compression. during a mean follow up of 36 months, clinical examination and imaging reveals amelioration of presenting complaints and reduction of radicular com-pression, with no surgical complications. stop-screws and iliac wings technique are effective methods to obtain stabilization and indirect decom-pression of the lumbosacral joint. Comparing with other described surgical procedures, our obtained results are better but with lesser complications.

StErEotACtIC IrrAdIAtIoN oF StAgE IV CANINE NASAL tuMorSM. Dolera1, L. Malfassi1, S. Pavesi1, M. Sala1, G. Mazza1, S. Marcarini1, N. Carrara1, S. Finesso1. 1La Cittadina Fondazione Studi e Ricerche Veterinarie, Romanengo, Italy.

the prognosis for canine nasal tumors with intracranial extension is poor with an expected survival of 1 month with palliation and 6.7 months with irradiation. Howev-er, studies regarding stage iV nasal tumors treated with brain-sparing irradiation techniques are lacking. the aim of this prospective study was to evaluate feasibility and efficacy of definitive intent stereotactic radiothera-py in dogs with nasal tumors with massive intracranial extension.seven dogs with stage iV nasal tumors were treated with high-dose hypo-fractionated stereotactic radiotherapy with volumetric modulated arc therapy technique. dose prescriptions were 32-36 gy in four consecutive-day fractions to the gross tumor and 30 gy to limphatics. adjuvant treatment included carboplatin. serial clini-cal and Computed tomography/Magnetic resonance imaging examination were performed. disease control and toxicity effects were evaluated according to response evaluation criteria in solid tumors and veterinary ra-diation therapy oncology group criteria. Median survival time (Mst) was evaluated using Kaplan-Meier curves.six carcinoma and 1 sarcoma were treated. prescription goals were obtained in four cases with V95%>95% and V107%>2% whereas in 3 dogs V95%=86-90% was ac-cepted to limit maximum brain punctual dose<27 gy. two partial response and 5 complete responses were obtained. Mst was 9 months. one grade ii late brain radiotoxicity and two brain ascending infections were observed. relapse pathways involves diffuse meningeal and sphenoid invasion.the initial experiences with the radiation therapy regi-men adopted indicate a feasibility and effectiveness in modified stage iV nasal tumors. the relapse pathways observed suggest to evaluate alternative adjuvant treat-ment in dogs treated with stereotactic radiotherapy.

CANINE PErIPHErAL NErVE SHEAtH tuMorS: MAgNEtIC rESoNANCE ANd CoMPArISoN oF PALLIAtIoN, SurgEry ANd StErEotACtIC rAdIotHErAPyM. Dolera1, L. Malfassi1, S. Pavesi1, M. Sala1, G. Mazza1, S. Marcarini1, N. Carrara1, S. Finesso1. 1La Cittadina Fondazione Studi e Ricerche Veterinarie, Romanengo, Italy.

no updates for canine peripheral nerve sheaths tumor (pnst) appeared in recent literature. the aim of this study was to evaluate the correlation between clinical aspects and Mri findings of tumors involving a major peripheral nerve, plexus or root and to determine the survival time in dogs treated with palliation, surgery or stereotactic radiotherapy (srt).records of dogs with pnst evaluated from 2000 to 2014 were reviewed to determine signalment, duration of clinical signs, neurological examination, Mri features, treatment option (palliation, surgery, stereotactic hypo

ing a sitting position. recovery usually occurred in one to several minutes. as lambs aged, it became more diffi-cult to elicit the episodes of dysfunction and by 6 months of age they appeared normal.the disorder was diagnosed as a dominant familial epi-sodic cerebellovestibular ataxia inherited as a dominant trait, with incomplete penetration of observed clini-cal signs and variable expressivity. a proportion of af-fected lambs are likely to die in the neonatal period so the specific nature of the disorder may go unrecognised. Because of incomplete penetrance and varying expres-sivity, many of the lambs carrying this mutation will sur-vive without showing clinical signs and may enter breed-ing flocks, where the disorder may be perpetuated and contribute to neonatal deaths. several genes involved with episodic ataxias in rodents and humans have been assessed in affected sheep and have been inconclusive to date.

*ethical approval received from Massey university animal ethical Committee.

MAgNEtIC rESoNANCE SPECtroSCoPy FINdINgS IN CLINICAL CASES oF dogS WItH tICK-BorNE ENCEPHALItISC. Sievert1, P. Kircher1, I. Carrera1. 1Clinic of Diagnostic Imaging, Vetsuisse Faculty, University of Zurich, Winter-thurerstrasse 258c, 8057, Switzerland.

tick-borne encephalitis (tBe) is an infection caused by a flavivirus transmitted by tick bites. Common clinical signs in dogs include fever, behavioral changes, cranial deficits and paresis. In vivo diagnosis is difficult due to high seroprevalence and rapid viral clearance limiting detection of antibodies in blood and Csf. Mri may be used to support the diagnosis. typical Mri changes are bilateral symmetrical lesions affecting the gray matter, predominantly the thalamus, hippocampus and ventral horn of the spinal cord. Mri studies can be negative de-spite the presence of neurological clinical signs. the purpose of the study was to describe Mr-spectro scopy (Mrs) findings of dogs diagnosed with tBe. inclusion cri-teria were dogs with neurological symptoms suggestive of tBe, previous endemic stay and tick-bite, Mri and Mrs of the brain, Csf changes indicative of viral infection and positive antibody titers (serum/liquor) or confirma-tion of tBe with necropsy. 5 dogs were included.three dogs did not have any changes in the Mri conven-tional images. single voxel spectroscopy was performed in the region of the thalamus or hippocampus and com-pared with data previously reported from healthy dogs using the same Mrs technique. all dogs affected with tBe had abnormal metabolite concentration that in-cluded: mild to moderate decrease in n-acetyl aspartate and creatine peaks, and mild increase in choline and glu-tamate/glutamine peaks. no lactate or lipid signal was detected in any dog. in conclusion Mrs shows the metabolic changes in tBe and this may be detected earlier than morphological changes depicted by conventional Mri.

EVALuAtIoN oF MAgNEtIC rESoNANCE IMAgINg guIdELINES to dIFFErENtIAtE BEtWEEN tHorACoLuMBAr NuCLEuS PuLPoSuS ExtruSIoNS ANd ANuLuS FIBroSuS ProtruSIoNS IN LArgE BrEEd dogSS. De Decker, S.A. Gomes, R.M.A. Packer, P.J. Kenny, E. Beltran, B. Parzefall, J. Fenn, D. Nair, G. Nye, H.A. Volk. The Royal Veterinary College, University of London, Hatfield, UK.

four Mri variables have recently been identified, which are independently associated with a diagnosis of thora-columbar nucleus pulposus extrusion (npe) or anulus fibrosus protrusion (afp). Midline intervertebral disk (iVd) herniation, and partial iVd degeneration were as-sociated with afp, while presence of a single iVd hernia-tion and disk material dispersed beyond the boundaries of the iVd space were associated with npe. the aim of this study was to evaluate if using these Mri variables improves differentiation between npe and afp. no ethical approval was required for this study. eighty large breed dogs with surgically confirmed thoracolum-bar npe or afp that underwent Mri were included. studies were randomized and presented on 2 occasions to 6 blinded observers, which were divided into 3 experi-ence categories. during the first assessment, observers made a presumptive diagnosis of thoracolumbar npe or afp without guidelines. during the second assessment they were asked to make a presumptive diagnosis with the aid of guidelines. additionally, they were asked to record the presence or absence of each Mri variable. agreement was evaluated by Kappa-statistics. diagnostic accuracy improved from 70.8% to 79.6% and inter-observer agreement for making a diagnosis of npe or afp improved from fair (μ = 0.27) to moderate (μ = 0.41) after using the proposed guidelines. diagnostic ac-curacy was influenced by degree of observer experience. intra-observer agreement for the assessed variables was variable, while inter-observer agreement ranged from fair to moderate. the results of this study suggest that the proposed imag-ing guidelines can aid in differentiating thoracolumbar npe from afp.

FAMILIAL oVINE EPISodIC AtAxIA*Mayhew IG Joe, Jolly RD, Burnham D, Ridler AI, Poff GJ, Blair HT. IVABS, Massey University, Palmerston North, New Zealand.

a similar episodic neurological disorder occurred in crossbred lambs on 2 properties and in a proportion of lambs born to a sire from each property. some lambs were abnormal at birth, tended to adopt a head and neck extended posture and were slow to get to their feet and suckle when they then became apparently normal. When forced to move, they and other more robust lambs elicited an asymmetric gait, base-wide extensor hyper-tonia (hypometria) of thoracic limbs and flexor hyper-tonia (hypermetria) of pelvic limbs. in some there was variable nystagmus. after several metres of asymmetric ataxic gait they would fall to one side, sometimes adopt-


the objective of this study was to compare the clinical presentation and outcome of dogs with a presumptive diagnosis of ischaemic myelopathy (iM) and acute non-compressive nucleus pulposus extrusion (annpe). Medical records and Mri studies were reviewed, yielding 93 suitable dogs with an antemortem presumptive diag-nosis of iM or annpe. patient signalment, clinical pres-entation and short-term outcome were retrospectively retrieved from clinical records. long-term follow-up was achieved by telephone questionnaire with veterinarians and owners. Compared to the hospital population of the study insti-tution, english staffordshire Bull terriers were overrep-resented with iM, and Border Collies with annpe. dogs with annpe were significantly older (mean 7.0y ±2.2) than those with iM (mean 5.9y ±2.8). dogs diagnosed with annpe were significantly more likely to present with a history of onset vocalisation (50%), spinal hyper-aesthesia (47.6%) and a C1-C5 myelopathy (16.7%) com-pared to those with iM. dogs with iM were more likely to present with an l4-s3 myelopathy (11.8%), compared to dogs with annpe (0%). dogs with annpe were more likely to be ambulatory at discharge (69.0%) than those with iM (43.1%). although long-term follow-up did not reveal a difference in quality of life or outcome success, dogs with iM were significantly more likely to have re-duced faecal continence (40.7%), compared to those with annpe (7.7%). in conclusion, differences were found in clinical pres-entation that may aid differentiation between iM and annpe. annpe may lead to a faster recovery of function, and dogs with iM may be at higher risk of permanent fae-cal incontinence.

IS tHE NEuroLogICAL ExAMINAtIoN A VALId MEtHod to CorrECtLy IdENtIFy tHE LESIoN LoCALIZAtIoN oF VEStIBuLAr dySFuNCtIoN IN dogS?U. Bongartz1,2, J. Neßler1, A. Maiolini1, VM. Stein1, A. Tipold1, A. Bathen-Nöthen2. 1Department of Small Animal Medicine and Surgery, University of Veterinary Medicine Hannover, Germany. 2Veterinary Practice A. Bathen-Nöthen, Cologne, Germany.

the aim of this study was to prove the reliability of the neurological examination in localizing a vestibular syndrome in dogs with magnetic resonance imaging (Mri) as gold standard of correct lesion localization. neurological examination results and Mri findings of 91 dogs with vestibular signs were reviewed retrospectively encompassing central vestibular syndrome (CVs) and peripheral vestibular syndrome not responding to treat-ment (pVs). the majority of dogs (78/91; 85.7%) showed a head tilt as cardinal sign indicating vestibular disease. additional signs comprised ataxia, strabismus, nystagmus, proprio-ceptive deficits, other cranial nerve deficits, and tetrapa-resis. Based on the neurological examination, 31 dogs had pVs, 57 had CVs and 3 remained unclear. after Mri examination 20 dogs had pVs, 70 dogs had CVs, and the diagnosis remained unclear in one dog. the neuroana-

(14 discs), followed by grade iV, V (4 discs) and ii (3 discs). nonchondrodystrophic and chondrodystrophic old dogs may have disk asymptomatic protrusion and spinal cord compression representing a normal aging process, be-ing important to take this in consideration when dealing with old dogs with neurological signs.

tHE oCCurrENCE oF CArdIAC ABNorMALItES IN CANINE StEroId rESPoNSIVE MENINgIo-ArtErItIS (SrMA)G.McLauchlan1, J.Penderis2, L.Dickson1, K. Holmes1, J.Prieto-Ramos1, L.Cosgrove1, R. Gutierrez-Quintana1, J.Guevar1, I.Sanz-Gonzalez1 and A. French1. 1Small Animal Hospital, School of Veterinary Medicine, University of Glasgow, United Kingdom, 2Vet Extra Neurology, Stirling, United Kingdom.

Concurrent cardiac disorders, such as arrhythmias and myocarditis, are well-documented in human patients with central nervous system (Cns) diseases, including bacterial meningitis. similarly, single case reports in dogs with steroid responsive meningio-arteritis (srMa) have suggested concurrent cardiac abnormalities. this prospective study aimed to document the prevalence of cardiac changes in dogs with srMa based on measure-ment of serum cardiac troponin-i (ctni) and echocar-diography, and to monitor these changes during srMa treatment.srMa was diagnosed based on typical clinical presen-tation, blood/urinalysis, cerebral spinal fluid analysis, and in some cases infectious disease serology and Mri. echocardiography was performed in all dogs, where pos-sible prior to starting any anaesthesia, opiate or gluco-corticoid therapy. repeated neurological examination, C-reactive protein (Crp), ctni and echocardiography were performed after 14 days.fourteen dogs were prospectively enrolled (3fe, 1fn, 5Me, 5Mn) with a mean age of 12.5 months (range 6 months – 30 months). increased ctni was identified in 5/14 dogs (mean 4.16ng/l; range 0.59-14.5; reference range < 0.15) and echocardiographic abnormalities de-tected in 12/14 dogs, including spontaneous echo-con-trast (seC) in 12/14 and mild pericardial effusion in 5/14.treatment with glucocorticoids was associated with clinical improvement and Crp normalisation in all dogs. ctni normalised in 4/5 dogs and significantly reduced in 1/5 dogs. seC resolved in 9/12 dogs and reduced in 3/12 dogs. pericardial effusion resolved in all dogs. these results show that cardiac changes are common in dogs with srMa, and resolve with therapy in most dogs. longer term follow-up of dogs with persistent cardiac changes is warranted.

CoMPArISoN oF CLINICAL PrESENtAtIoN ANd outCoME IN dogS WItH PrESuMPtIVE ISCHAEMIC MyELoPAtHy ANd ACutE NoN-CoMPrESSIVE NuCLEuS PuLPoSuS ExtruSIoNJ. Fenn, R. Drees, H.A. Volk, S. De Decker. Department of Clinical Science and Services, Royal Veterinary College, Hawkshead Lane, North Mymms, Hertfordshire, AL9 7TA (UK)

to confirm and analyze their epileptogenic zone, we performed diffusion and perfusion Mri. this study was approved by the animal Care and use Committee of the university. using a 3.0t Mri system, diffusion-weighted imaging, diffusion tensor imaging, and dynamic sus-ceptibility contrast perfusion weighted imaging were performed, and the apparent diffusion coefficient (adC), fractional anisotropy, relative cerebral blood flow (rCBV), relative cerebral flow (rCBf), and mean transit time were calculated. six healthy control cats and 6 fseCs at the interictal state were compared. Compared with controls, adCs in the hippocampus of fseCs were significantly higher and rCBV and rCBf in the hippocampus of fseCs were significantly lower than in the controls. using the same 6 fseCs, diffusion and perfusion parameters were compared between the interictal and postictal states. images of the postictal state were obtained immediately after vestibular stimulation-induced seizures (<15 min). at the postictal state compared with the interictal state, adCs in the hippocampus were significantly decreased and rCBV and rCBf in the amygdala and cortex were sig-nificantly increased.in conclusion, fseCs have higher diffusion and lower per-fusion in the amygdala or hippocampus at the interictal state; in turn, these are reversed at the postictal state, as observed in pet/speCt studies of human epilepsy.

PoSt MortEM ASSESSMENt oF INtErVErtEBrAL dISK ProtruSIoN IN dogS WItHout NEuroLogICAL SIgNSC.C. Zani1, M.V.B. Arias1, P.V.T. Marinho2, G.A.C. Diamante1. 1Dept. of Veterinary Clinics, Londrina State University, Brazil; 2Dept. of Surgery, University of Sao Paulo, Faculty of Veterinary Medicine and Animal Science, Brazil.

Hansen type ii intervertebral disc degeneration (iVd) is a process that increases with age, but link between disc degeneration, protrusion with spinal cord compression and clinical signs remain unclear. our objective was to determine the presence of type ii disk degeneration with extradural spinal cord com-pression in 30 dogs (24 nonchondrodystrophic, 6 chon-drodystrophic) without neurological signs, aged more than 7 years old (median 10), weighing from 6 to 36 kg (median 12.9 kg). dogs were euthanized for non-neu-rological reasons and owners gave permission to the study. immediately after euthanasia, myelography was performed in order to identify sites of disc protrusion. all spines were opened by dorsal laminectomy to identify all sites of protrusion, identified or not by myelography. protruded disc was opened in a midsagittal plane in or-der to perform macroscopic classification of iVd accord-ing to thompson (1990) scheme (i-healthy to V-severe degeneration).We observed that 12/30 dogs (40%) presented disc pro-trusion, and from these, seven (58%) had more than one (maximum 5) intervertebral disc protrusion. five dogs were chondrodystrophic (83%) and seven nonchondro-dystrophic (29%). the most affected site was l4-l5 (6 discs), followed by l6-l7 region (3 discs), C6-C7 (3 discs), and t2-t3 (1 disc). grade iii iVd was the most common

CoMPutAtIoNAL dEVELoPMENt ANd EVALuAtIoN oF A CErVICAL INtErVErtEBrAL dISC ProStHESIS IN dogS By MEANS oF tHE FINItE ELEMENt MEtHodP.V.T. Marinho1, A.P. Macedo2, C.P. Sampaio3, A.C. Shimano4, C.C. Zani5, M.V.B. Arias5. 1Dept. of Surgery, University of São Paulo, Faculty of Veterinary Medicine and Animal Science, Brazil; 2Dept. of Dental Materials and Prosthodontics. Ribeirão Preto Dental School, University of São Paulo, São Paulo, Brazil; 3Dept. of Design, State University of Londrina, Brazil; 4Dept. of Biomechanics, Medicine and Locomotive Apparatus Rehabilitation, Ribeirão Preto Medical School, University of São Paulo, São Paulo, Brazil; 5Dept. of Veterinary Medicine, State University of Londrina, Brazil.

Currently the most effective treatment of disk-associat-ed cervical spondylomyelopathy is distraction-merger, however, this technique can lead to biomechanical changes in the adjacent segments increasing the risk of “domino” type injury.the objective of this study was to develop a cervical intervertebral disc prosthesis and evaluate main stress points in the prosthesis system - vertebral body using the finite element Method (feM). the prosthesis sizing was based on width, height and length measuring of the vertebral body of C5-C6 of the sixteen cervical spine of mature canine cadavers weighing between 25-35 Kg. the prosthesis was developed on rhinoceros® software and 3d prototyping to refine its design. the analysis was done using the feM using the ansys Workbench® soft-ware after applying extension, lateral and ventral bend-ing forces, assessing the average equivalent von-Mises stress on the prosthesis-vertebral body system. the vertebral body received much lower stress than the prosthesis for all applied forces. the average stresses on the vertebral body were superior on the lateral and ven-tral surfaces when compared to the cranial surface of C5 and the caudal of C6. finally, the average stress on the prostheses was intensely more focused on the bearing contact surface and less intensely on the interface be-tween the prosthesis and screw. for screws, the bigger stress happened on the cranial surface.the developed prosthesis had an adequate design and good fit on the intervertebral space between C5 and C6, allowing a homogeneous distribution of stresses on ver-tebral body, which lowered stress on vertebral endplates.

CHANgES IN INtErICtAL VS. PoStICtAL dIFFuSIoN ANd PErFuSIoN Mr PArAMEtErS IN FAMILIAL SPoNtANEouS EPILEPtIC CAtSD. Hasegawa1, S. Mizoguchi1, Y. Hamamoto1, T. Kuwabara1, Y. Yu1, A. Fujiwara1, M. Fujita1. 1Dept. Clinical Veterinary Medicine, Nippon Veterinary and Life Science University, Tokyo, Japan.

familial spontaneous epileptic cats (fseCs) are the only genetic model of epilepsy in cats. the epileptogenic zone of fseCs is thought to exist in the amygdala and/or hip-pocampus, as determined by seizure semiology (sponta-neous orofacial automatisms and stimulation-induced generalized seizures), eeg features, and volumetric Mri.


NoN ACCIdENtAL trAuMA (INFLICtEd BrAIN INJury)C.Centellas1, X.Raurell1, G.Feliz1, A.Zamora2. 1Hospital Veterinari Molins, 08620 Barcelona, Spain. 2Imagovet, 08970 Barcelona, Spain.

non accidental trauma (nat) synonyms like nonacciden-tal injury (nai); shaken baby syndrome (sBs) or nonac-cidenteal head injury (naHi) are often used in human medicine to describe inflicted brain injury (iBi).three cases with clear evidence of iBi were detected at our Hospital in a two month period. their histories and subsequent outcomes demonstrated human involve-ment. all of them undergo Mr (esaote 0,25t) which was revealed as one of the best diagnostic clue to detect ani-mal abuse. Mri is more difficult to perform in acute set-ting than computed tomography (Ct). However, overall increased sensitivity for most injuries except fractures and acute hemorrhages outweight difficulties. it may be also helpful as an adjunct for the evaluation of axonal shear injuries and for more precise dating of intracranial hemorrhage. diffusion-weighted imaging (dWi) could also detect early ischemic injury and is frequently used in trauma to help determine prognosis.in the first case, Mr findings were compatible with the sBs (medical terminology); subdural hemorrhage (sdH) over cerebral convexities and interhemispheric fissure which is the most common manifestation in nat. the second patient showed also subdural collections at the temporoparietal convexities, occipital contusion and zy-gomatic arch fracture. the third one presented residual encephalomalacic lesions and a frontoparietal bone de-fect. Multi-organ system trauma was also found; rib frac-tures, vitreous hemorrhage, a foreign body in the uterus and perineal burns.We have not found many veterinary bibliographies on this subject whereas there are extensive studies in hu-man medicine. Making a correct diagnosis could be cru-cial to the health and welfare of the animals and the fam-ily members involved.

rEtroSPECtIVE Study oF SPINAL ArACHNoId dIVErtICuLuM IN 15 dogS dIAgNoSEd WItH 3d-CISS MrIA. Tauro1, J. Jovanovik1, C. Driver1, C. Rusbridge1,2. 1Fitzpatrick referrals, Eashing, UK; 2University of Surrey, Guildford, UK.

spinal arachnoid diverticula (sad) are considered rare conditions in veterinary medicine, although the num-ber of diagnosed cases is recently growing due to the increase use of Mr imaging and predisposed breed popularity. sad are defined as intradural, extramedul-lary cavitations filled with Csf; the aetiology is not well understood and disorders that cause alterations of the arachnoid trabeculae and interference with the Csf flow are implicated. a better outcome is based on an early di-agnosis and intervention, and the interpretation of the advanced images can be challenging often leading to misdiagnosis and treatment delay.the purpose of this retrospective study was to describe a three-dimensional (3d) constructive interference in

of 12900 cats presented during the study period, 31 (0.24%) were diagnosed with iVdd, including 17 pure-bred and 14 non-purebred cats. of all presented pure-bred cats, 2.84% were diagnosed with iVdd. More spe-cifically, 1.29% of all British shorthairs and 1.83% of persians were diagnosed with iVdd. Compared to the general hospital population, purebred cats (P<0.0001), British shorthairs (P<0.0001) and persians (P=0.0006) were significantly overrepresented with thoracolumbar iVdd. of 31 cats with iVdd, 19 were diagnosed with npe and 12 with afp. Cats with npe had a significantly short-er duration of clinical signs (P=0.0002) and demonstrat-ed more severe neurological deficits (P=0.04) compared to cats with afp.although iVdd is an uncommon condition in cats, pure-bred cats, British shorthairs, and persians were overrep-resented. it is currently unclear if this represents a true breed predisposition or a higher likelihood of owners of purebred cats to seek referral for advanced diagnostic imaging procedures.

CoMPArISoN oF CErVICAL CANAL oCCuPANCy IN gIANt, LArgE, ANd SMALL BrEEd dogS: AN MrI MorPHoMEtrIC StudyM. Bonelli1,2, R. da Costa2. 1Federal Rural University of Pernambuco, Recife-PE, Brazil, 2The Ohio State University, Columbus-OH, USA.

the pathophysiology of cervical spondylomyelopathy (CsM) appears to involve a major static component, namely relative and absolute stenosis of the vertebral canal, which would facilitate or cause compression of the spinal cord. our objective was to compare the cervical vertebral ca-nal occupying ratio of the spinal cord (C3-C7) in giant, large, and small breeds hoping to gain insights regard-ing the prevalence of CsM in larger breed dogs compared to small breeds. Magnetic resonance images for 90 dogs were used: 30 small-breed dogs; 30 doberman pinschers (15 clinically normal and 15 CsM-affected) represent-ing large-breed dogs; and 30 great danes (15 clinically normal and 15 CsM-affected) representing giant-breed dogs. area and height of the spinal cord and vertebral canal/foramina between C3 and C7 were measured on transverse and sagittal images, respectively, at both the cranial and caudal edge of the vertebrae. Calculations were made to determine the vertebral canal occupying ratio of the spinal cord (cord:canal ratio) for each group. overall, small-breed dogs had higher cord:canal area and height ratios, suggesting they have less space avail-able for the spinal cord. great danes had the lower cord:canal area ratios, indicating they have less area of the canal occupied by the spinal cord. doberman pinschers generally had similar values of cord:canal area ratios to the small-breed dogs. our results suggest that the vertebral canal occupying ratio of the spinal cord cannot, by itself, explain the dis-crepancy in prevalence of CsM in small and large breeds.

MAgNEtIC rESoNANCE FEAturES oF SuSPECtEd LEuKoArAIoSIS IN ELdErLy dogSE. Scarpante, G.B. Cherubini, A. de Stefani, O. Taeymans. Dick White Referrals, Six Mile Bottom, United Kingdom. age-related changes have been identified on brain Mri (magnetic resonance imaging) of dogs over 9 years of age. Brain atrophy, ventricular enlargement, and well-demarcated sulci have been already described in veteri-nary medicine. this case series describes the Mri features of suspected leukoaraiosis in 7 elderly dogs.the clinical database between october 2009 and May 2015 was reviewed. dogs with bilaterally symmetrical periventricular areas of t2 and flair hyperintensity compatible with leukoaraiosis and older than 9 years were included. seven dogs met the inclusion criteria, two neutered females and five neutered males, mean age was 13 years 5 months. Breeds included two Jack russell terrier, two cross breed, and one of each of the following breeds: labrador retriever, lhasa apso and Cavalier King Charles spaniel. all dogs underwent Mri of the brain for a suspected intracranial disease based on physical and neurological examinations.the t2 and flair hyperintensities appeared as well-defined bilaterally symmetrical periventricular areas of increased signal intensity, located dorso-laterally and dorso-caudally to the lateral ventricles, isointense to normal white matter on t1-weighted images and non-contrast-enhancing. given their topographical distribu-tion these lesions were considered most compatible with an age-related white matter change.pathophysiology of leukoaraiosis remains incompletely understood, but an ischaemic origin of these lesions has been favoured. endothelial damage, leading to narrow-ing of the vessels lumen, and ultimately reduced blood flow, is suspected. the pattern of vascularization, which makes the periventricular white matter an arterial bor-der zone, has been considered responsible for the topo-graphical distribution typical of these lesions.

PrEVALENCE ANd BrEEd PrEdISPoSItIoN oF tHorACoLuMBAr INtErVErtEBrAL dISC dISEASE IN CAtSS. De Decker, A-S. Warner, H.A. Volk. The Royal Veterinary College, University of London, Hatfield, United Kingdom.

although several studies have evaluated the prevalence and breed predisposition of intervertebral disk disease (iVdd) in dogs, such information is not yet available for cats. the aims of this study were to evaluate the preva-lence and possible breed predilections for thoracolum-bar iVdd in cats. Medical records and imaging studies of cats diagnosed with iVdd were retrospectively reviewed and compared to the general hospital population between January 2008 and august 2014. the association between type of iVdd [i.e. nucleus pulposus extrusion (npe) or anulus fibrosus protrusion (afp)] and breed, age, gender, dura-tion and severity of clinical signs was also evaluated.

tomical localization after neurological examination was in accordance with Mri results in 80.6% (54/67) for CVs and 85% (17/20) for pVs. after Mri and cerebrospinal fluid analysis clinical diagnoses of inflammation (21/70; 30%), neoplasia (16/70; 22.9%) and infarcts (10/70; 14.3%) were assessed as causes for CVs and idiopathic (12/20; 60%) and otitis media/interna (6/20; 30%) for pVs. in contrast to other studies, CVs occurred more frequent-ly than pVs in the current study referring to the fact that only dogs with severe pVs not responding to the first treatment attempt underwent a complete diagnostic workup including Mri. despite this bias the neurologi-cal examination is still a valid method for identifying the correct localization in dogs with vestibular dysfunction.

EVALuAtIoN oF PoStoPErAtIVE SurVIVAL ANd CoMPLICAtIoNS AFtEr INtrACrANIAL SurgEry IN dogSA.K. Forward, H.A. Volk, S. De Decker. Royal Veterinary College, University of London, Hatfield, United Kingdom.

although intracranial surgery is increasingly performed in veterinary medicine, little is known about the nature and prevalence of post-operative complications and sur-vival of dogs undergoing intracranial surgery. this study aimed to describe survival and early postoperative out-come following intracranial surgery in dogs. records were searched and analysed for dogs that had intracranial surgery performed between 2005-2015. signalment, clinical presentation, neurological deficits, concurrent medical conditions, perioperative laboratory data, diagnosis, administration of perioperative gluco-corticoids or anti-epileptic drugs and specific imaging, surgical and anaesthetic variables were evaluated as po-tential risk factors for survival, occurrence of postopera-tive complications and hospitalisation times. univariate linear and logistic regression followed by multivariable regression models were performed. fifty dogs were included. 96% (48/50) of dogs survived the immediate postoperative period, 92% (46/50) sur-vived to discharge and 48% (23/48) experienced a postoperative complication. non-neurological post-operative complications were seen in 19% (9/48) of dogs, with aspiration pneumonia being the most com-mon one [12% (5/48)]. early postoperative neurological deterioration was seen in 46% (22/48) of dogs, with this group more likely to develop non-neurological postop-erative complications. development of non-neurological complications (p=0.0004) and higher postoperative se-rum glucose concentrations (p=0.002) were associated with longer hospitalisation times. Higher postoperative lactate concentrations (p=0.009) were associated with longer hospitalisation times in the iCu.dogs undergoing intracranial surgery had a high rate of survival with a relative low number of postoperative complications. as a result, intracranial surgery for appro-priate cases can offer a good outcome for dogs but more investigation is needed to ascertain long-term survival times.


in all 10 dogs. the observed difference in the ratio of naa/Cr between patients may have been due to various epileptic stages of the dogs during the study.these preliminary results suggest the possible applica-tion of Mrs to determine the lateralization of seizure foci in canine epileptic patients. naa may be used as an indi-cator of neuronal dysfunction during seizures.

rELAPSES IN dogS WItH StEroId-rESPoNSIVE MENINgItIS-ArtErItISE. Biedermann1, A. Tipold2, T. Flegel1. 1Dept. of Small Animal Medicine, University of Leipzig, Leipzig, Germany, 2Dept. of Small Animal Medicine and Surgery, University of Veterinary Medicine Hannover, Hannover, Germany.

the purpose of this study was to describe relapse rates in dogs with steroid-responsive meningitis-arteritis (srMa) and, in addition, to identify factors influencing the occurrence of relapses. dogs with srMa were retrospectively identified from the hospital data base and were assigned to one of three groups: dogs without relapse, with at least one relapse and unknown relapse-status. the groups without and with at least one relapse were compared regarding the following parameters: sex, age, body weight, nucleated cell count, total protein concentration, and percentage of neutrophils on initial cerebrospinal fluid (Csf) analy-sis, iga in serum and Csf initially, nucleated cell count on Csf analysis at 3-month-re-evaluation, C-reactive protein (Crp) in serum and Csf initially and at 3-month-re-evaluation, frequency of breeds.Between one and four relapses were seen in 32.4% of dogs whereas 55.4% were relapse free. the relapse sta-tus was unknown in 12.2% of dogs. none of the factors tested were different between dogs with and without relapse, except for the following three: 1. nucleated cell count in Csf at 3-month-re-evaluation was higher in dogs with relapses. 2. Beagles are more frequently af-fected by relapses. 3. there was a tendency for higher Crp levels in serum in dogs with relapse at 3-month-re-evaluation. We conclude that relapses are frequent but there is cur-rently no reliable indicator predicting relapses. elevated Crp in serum on re-evaluation, however, warrants con-tinuing therapy.

A MutAtIoN IN MFSd8 CAuSES NEuroNAL CEroId LIPoFuSCINoSES IN CHIHuAHuA dogSK. M. E. Faller1, J. Bras2, S. Sharpe1, L. Darwent2, C. Kun- Rodrigues2, J. Alroy3, J. Penderis4, S. E. Mole5, R. Gutierrez-Quintana1*, R. J. Guerreiro2*. * Joint senior authorship. 1School of Veterinary Medicine, College of Medical, Veterinary and Life Sciences, University of Glasgow, Bearsden Road, Glasgow, G61 1QH, UK. 2Department of Molecular Neuroscience, Institute of Neurology, University College London, Queen Square, London, WC1N 3BG, UK. 3Department of Pathology, Tufts University School of Medicine and Tufts-New England Medical Center, Boston, Massachusetts 02111, USA. 4VetExtra Neurology, Craig Leith Road, Broadleys, Stirling, FK7 7LE,

altered consciousness. Hereditary canine pd have been described in Chinooks, soft Coated Wheaten terriers, scottish terriers and Cavalier King Charles spaniels. this study provides the phenotypical description of a possible pd observed in 5 adult Maltese dogs. the epi-sodes always started at the age of 5 to 6 years and dogs appeared normal in between. in four dogs, the episodes were witnessed by video analysis and in one dog an epi-sode occurred during consultation. episodes seemed to be triggered by exercise, stress or excitement and were typically characterized by generalized stiffness of the limbs and alternating involuntary flexion of 1 or multiple limbs. often a kyphotic back posture was also noticed. all dogs remained fully conscious during the episodes, but seemed uncomfortable. the frequency and duration of the dyskinesia episodes varied between dogs. the clinical and neurological examination (3 dogs) and fur-ther diagnostic work-up (complete blood work (3 dogs), Mri brain and Csf analysis (2 dogs), electrophysiologi-cal exam (1 dog), urinalysis (1 dog) were unremarkable. three dogs were clear of the pign missense mutation recently discovered in soft Coated Wheaten terriers with pd. therapy with acetazolamide (2 dogs) provided an obvious improvement in 1 dog. a possible paroxysmal dyskinesia with an adult onset is suspected in the Maltese dog, although additional cases and expanding pedigree and genetic analysis is necessary.

APPLICAtIoN oF MAgNEtIC rESoNANCE SPECtroSCoPy IN CANINE EPILEPSy oF uNKNoWN orIgIN – tHE PrELIMINAry rESuLtSAgnieszka Olszewska1, Marta Płonek1, Józef Nicpoń2, Marcin Wrzosek1. 1Department of Internal Medicine and Clinic of Diseases of Horses, Dogs and Cats, 2Center of Experimental Diagnostics and Innovative Biomedical Technology, The Faculty of Veterinary Medicine, Wrocław University of Environmental and Life Sciences.

Canine epilepsy posts a diagnostic challenge for vet-erinary professionals. Magnetic resonance spectroscopy (Mrs) is a noninvasive method that determines the chemical composition of brain tissue and is displayed as a spectrum of peaks fit along the x-axis, labeled in parts per million (ppm). the three major peaks observed in the Mrs spectra are those of n-acetyl-aspartate (naa), cre-atine (Cr), choline (Cho). Mrs may be used to lateralize an epileptic focus.the study was carried out on 10 dogs of different breeds with a diagnosis of canine epilepsy of unknown origin, who underwent an Mri examination utilizing a 1.5t ingenia philips scanner under general anaesthesia. Mrs was performed using single-voxel 1 cm × 1 cm × 1 cm ac-quisitions. the voxel was located bi-hemispherically at the border of the piriform lobe and hippocampus. three main metabolites (naa, Cho, Cr) were determined in the analysis and compared between hemispheres.there was an interhemispheric difference in the naa to Cr ratios in 6 of the 10 dogs. four dogs presented a nor-mal naa/Cr ratio. the proportions of Cho/Cr were stable

l-2-Hga is considered a progressive neurological dis-ease, however symptoms can be successfully managed to allow dogs a good quality of life long term.

IdENtIFICAtIoN oF tHE CAuSAL gFAP MutAtIoN IN A LABrAdor rEtrIEVEr WItH ALExANdEr’S dISEASEV. Martlé1, M. Van Poucke2, L. Van Brantegem3, L. Van Ham1, S. Bhatti1, R. Ducatelle3, L. Peelman2. 1Department of Small Animal Medicine and Clinical Biology, 2Department of Nutrition, Genetics and Ethology and 3Department of Pathology, Bacteriology and Avian Diseases, Faculty of Veterinary Medicine, Ghent University, Belgium.

alexander’s disease is a neurodegenerative disorder of astrocyte dysfunction in humans, for which already a number of causal mutations have been described, mostly de novo dominant missense mutations in the glial fibrillary acidic protein (gfap). a similar frequently lethal disorder was already phenotypically described in 12 dogs and 4 sheep, but until now no causal mutations have been identified.a 3-month-old labrador retriever pup developed pro-gressively worsening tetraparesis with a spastic swim-ming-puppy-like position of the thoracic limbs. one month later mild vestibular signs and myoclonic jerks were noticed. Complete blood work, electrophysiologi-cal examination and Csf were within normal limits. the pup was euthanized at the age of 4.5 months and on his-topathological examination alexander’s disease was di-agnosed by the detection of gfap containing rosenthal fibers in astrocytes throughout the brain and spinal cord. from frozen brain tissue, the complete gfap cod-ing sequence was amplified by (rt)-pCr, sequenced and compared to the canine reference sequence. genetic examination of the gfap gene identified a heterozygous g→a nucleotide substitution resulting in an arginine to histidine amino acid substitution at position 240. We detected a causal point mutation in a labrador re-triever with multifocal central nervous system signs and characteristic histopathological features of alexander’s disease. this is an orthologous mutation to the het-erozygous de novo dominant r239H hotspot mutation in humans. to the best of our knowledge, this is the first report of a gfap mutation in an animal with alexander’s disease.

PAroxySMAL dySKINESIA IN AduLt MALtESE dogS?V. Martlé1, S. Bhatti1, D. O’Brien2, I. Gielen3, L. Van Ham1

1Department of Small Animal Medicine and Clinical Biology, Ghent University, Merelbeke, Belgium, 2College of Veterinary Medicine, University of Missouri-Columbia, Columbia, MO, USA, 3Department of veterinary Medical Imaging and Small Animal Orthopaedics, Ghent University, Merelbeke, Belgium.

paroxysmal dyskinesias (pd) are central nervous system disorders characterized by episodes of abnormal invol-untary hyperkinetic movement or muscle tone without

steady state (Ciss), which has a combination of high signal levels and extremely high spatial resolution and offers excellent contrast between Csf and pathological structures in providing anatomical information to iden-tify sad with minimal signal loss due to Csf pulsations.Medical records of 15 dogs between 2013 and 2015 were reviewed retrospectively. inclusion criteria were the presence of compatible clinical signs and advance im-aging using the 3d-Ciss sequences confirming the pres-ence of sad. Male pugs were over-represented, while caudal thoracic sad were outnumbered. pugs appeared to be predisposed to multiple sad located dorsally at C2-C3 and thoracic spine. 3d-Ciss sequences were benefi-cial in detecting sad secondary to scarring and adhesion following surgical intervention.findings from this study support the superiority of 3-d Ciss imaging in all cases particularly when spinal cord oedema, gliosis and/or syringomyelia may obscure the true spinal cord lesion.

CLINICAL FEAturES ANd dISEASE ProgrESSIoN oF L-2-HydroxygLutArIC ACIdurIA IN 27 StAFFordSHIrE BuLL tErrIErSA. Shea1, L. De Risio1, H. Carruthers2, E. Beltran3. 1Centre for Small Animal Studies, The Animal Health Trust, Newmarket, United Kingdom; 2Tay Valley Veterinary Centre, Perth, Scotland; 3Queen Mother Hospital for Animals, Royal Veterinary College, Potter’s Bar, United Kingdom.

l-2-hydroxyglutaric aciduria (l2Hga) results from autosomal recessive mutations within the l-2-hydroxyglutarate dehydrogenase (l2HgdH) gene. accumulation of l-2-hydroxyglutaric acid in brain tissue causes oxidative stress and interferes with cerebellar creatine kinase activity. there is no published data on clinical outcomes or prognostic factors. our aim was to describe the onset, pattern and nature of clinical signs (Cs) in a cohort of l-2-Hga-affected staffordshire Bull terriers (sBts). owners of 119 sBts positive for the l2HgdH genetic mutation were requested to complete a questionnaire regarding their pet’s symptoms. information was avail-able for 27 dogs, all with neurological abnormalities. the mean age of onset of Cs was 12 months (range 2.5-60). gait dysfunction was reported in all 26 dogs with available data, with stiffness of all four limbs the most common (24/26) and earliest recognised abnormality. Kyphosis (19/26), body and/or head tremors (19/26) and hypermetria (15/26) were frequent. Behavioural chang-es were present in 24/27 dogs; most commonly staring into space (21/27), signs of dementia (15/27) and loss of training (15/27). fifteen dogs demonstrated paroxysmal seizure-like or dyskinetic episodes. nineteen (70%) dogs were alive at a mean of 76.6 months (12-170) after onset of Cs; eight were ≥99 months from onset. l2Hga was the cause of euthanasia in six dogs with meningoencephalo-myelitis and suspected stroke resulting in euthanasia of two dogs. euthanasia occurred at a mean of 44 months (8.5-93) after onset of Cs, with 2/8 dogs euthanased with-in 12 months.


Medical records were reviewed for dogs diagnosed with Mua between 2004 and 2015. previously described inclu-sion criteria were used, and for all dogs 7-day survival data needed to be available. a poor outcome was de-fined as death. one hundred and sixteen dogs met the inclusion criteria. thirty-two (38%) dogs died within 7 days after making a presumptive diagnosis of Mua. dogs were typically treated with steroids and/or cytosine arabinoside. Both the presence of seizures and the presence of cluster sei-zures were significantly associated with a poor outcome. total nucleated cell count in cerebrospinal fluid and lac-tate levels on venous blood analysis at time of diagnosis were significantly associated with poor outcome. age, sex, neuroanatomical localisation(s), total protein con-centration in cerebrospinal fluid, and white blood cell count were not associated with 7-day survival. every third dog died within one week after diagnosis, emphasising the need for evaluation of short-term prog-nostic factors. presence of seizures and presence of clus-ter seizures at time of presentation, increased venous lactate concentrations and a higher total nucleated cell count in the cerebrospinal fluid are significantly associ-ated with 7-day survival.

ANtICoNVuLSANt HyPErSENSItIVIty SyNdroME IN A dog AFtEr PHENoBArBItAL AdMINIStrAtIoN L. Bosseler1, I. Cornelis2,3, P. Defauw2, S. Bhatti2, R. Ducatelle1. 1Dept. of Pathology, Bacteriology and Avian Medicine and 2Dept. of Medicine and Clinical Biology of Small Animals, Faculty of Veterinary Medicine, Ghent University, Belgium. 3Clinical Science and Services, The Royal Veterinary College, Hatfield, United Kingdom.

phenobarbital is the most commonly used first-line an-ti-epileptic drug in dogs. in human medicine, a clinical syndrome called “anticonvulsant hypersensitivity syn-drome (aHss) can occur within 1-8 weeks after initiation of phenobarbital treatment, consisting of a triad of fever, internal organ involvement (lymphadenopathy, hepato-megaly, splenomegaly) and a skin rash. Here we report the clinical and histopathological findings in a dog with suspected aHss. a 6-year-old, male neutered Beagle was presented with acute onset of lethargy, icterus, fever and coagulopathy 7 weeks after initiation of phenobarbital treatment. the dog developed acute liver failure and despite cessation of phenobarbital and institution of supportive treatment his clinical condition deteriorated quickly and he died 3 days after the onset of clinical signs. a complete nec-ropsy revealed multiple hemorrhagic foci, generalized icterus, splenomegaly, markedly enlarged abdominal lymph nodes, and an enlarged, pale and fragile liver. no skin abnormalities were seen. pCr testing for Leptospira spp returned negative. Histopathology revealed per-iacinar liver damage, in favor of a toxic event. Based on these findings, the dog was diagnosed with a toxic hepatopathy, most likely caused by phenobarbital, and the combination with the lymphadenopathy raised the suspicion of aHss.

IdENtIFICAtIoN oF Motor PAttErNS ANd ASSESSMENt oF PrIMItIVE rEFLExES IN CANINE NEoNAtESC. Morales1, J. Fatjó2, V. Aige3, P. Montoliu1. 1Neurocat Veterinaris, Barcelona, Spain, 2Chair Affinity Foundation Animals and Health, Department of Psychiatry and Forensic Medicine, School of Medicine, Universitat Autònoma de Barcelona, Bellaterra, Barcelona, Spain, 3Departament de Sanitat i Anatomia Animals, Universitat Autònoma de Barcelona, Bellaterra, Barcelona, Spain.

primitive reflexes are brainstem-mediated, complex, automatic and stereotyped movement patterns that appear during development. they are usually present at birth and become more difficult to elicit with central nervous system maturation or are replaced by more complex postural responses. the early motor behav-iour of the newborn is related to primitive reflexes. descriptions of primitive reflexes in dogs are sparse, and their influence on neurological examination is poorly documented. the purpose of this study was to describe in detail the main primitive reflexes that can be assessed in canine neonates and how these motor patterns influence neu-rological examination. this is part of a larger study with the objective to develop a neurological examination procedure for neonatal dogs. this study obtained ethi-cal approval.serial neurologic examinations were performed in 110 pups ranging from 0 to 13 days of age and of different breeds, mainly beagles. assessed items included primi-tive reflexes and responses described in previous stud-ies, human primitive reflexes adapted for evaluation in dogs and observation of characteristic motor patterns. a total of 13 primitive reflexes were evaluated. it was possible to elicit righting, withdrawal and crossed extensor reflexes, walking reflex, hopping, and pelvic limb straightening-supporting reflex from birth in most dogs, and uniform and reproducible responses were observed. for all these reflexes, detailed descriptions of initial posture, stimulus, supporting manoeuvres, and a gradation of normal responses were established. influences of instinctive motor patterns and optimal be-havioural states for each item were identified. this work establishes a basis for standardization of canine neo-nates neurological assessment.

ProgNoStIC FACtorS For oNE WEEK SurVIVAL IN dogS dIAgNoSEd WItH MENINgoENCEPHALItIS oF uNKNoWN AEtIoLogy I. Cornelis, H.A. Volk, S. De Decker. Clinical Science and Services, The Royal Veterinary College, Hatfield, United Kingdom.

although several studies have evaluated the long-term outcome of meningoencephalitis of unknown aetiol-ogy (Mua), little is known about short-term survival and initial response to therapy. the aims of this study were therefore to evaluate possible prognostic factors for 7-day survival after diagnosis of Mua.

clonic movements of the head exacerbated by sudden sounds. a routine haematology, biochemistry and uri-nalysis were unremarkable. Magnetic resonance of the brain and cerebrospinal fluid examination were unre-markable. southern blot analysis of genomic dna from the patient´s blood collected in edta tube detected a sequence repeat for an EPM2B gene.in conclusion, this is the first report of an EPM2B muta-tion causing progressive myoclonic epilepsy in a beagle dog breed. this case report suggests that the similar mu-tations can be present also in other breeds suffering of progressive myoclonic epilepsy.

Preferred format: Poster presentation. Submitting author has finished his postgraduate study in neurology and cur-rently is in neurology training under Dr. Viktor Palus, DVM, Dipl. ECVN, MRCVS.

ExPrESSIoN oF EPIdErMAL groWtH FACtor rECEPtor ANd KI-67 IN CANINE gLIoMASA. Fraser1, B Bacci2, M le Chevoir1, S Long1. 1Translational Research and Animal Clinical Trial Studies Group. 2Department of Anatomic Pathology, Faculty of Veterinary and Agricultural Sciences, The University of Melbourne, Werribee, Victoria, Australia.

the histologic classification of gliomas can be challeng-ing. in people accurate diagnosis is essential as the treat-ment and prognosis varies between tumour type and grade. numerous biomarkers have been investigated in human gliomas to aid in their diagnosis and to act as potential therapeutic targets. to utilise these thera-pies in veterinary medicine investigation of biomarkers in canine gliomas is required. epidermal growth factor receptor (egfr) is associated with glioma grade and is a therapeutic target in human glioma trials. the Ki-67 labelling index (li) is a marker of proliferation which is a prognostic indicator in human gliomas. the objectives of the current study were to evaluate egfr and Ki-67 expression immunohistochemically in canine gliomas and to determine if immunopositivity is associated with histologic tumour type and grade.formalin-fixed paraffin-embedded canine gliomas were assessed for egfr and Ki-67 expression. egfr immuno-positivity was evaluated using a semi-quantitative score and the Ki-67 li was calculated.thirty-one canine gliomas were evaluated. egfr expres-sion was identified in 16/31 (51.6%) tumours; expression was significantly greater in high grade tumours when compared to low grade tumours (p=0.041). egfr expres-sion was also significant in gliomatosis cerebri. Ki-67 was expressed in 28/31 (90.3%) gliomas and the Ki-67 li was significantly greater in the high grade tumours (p=0.024). a significant moderate correlation was identified be-tween egfr immunopositivity and Ki-67 li (r=0.472, p=0.007). While egfr is expressed in approximately 50% of canine gliomas, investigation in to other therapeutic targets is required. egfr may be a suitable therapeutic target for gliomatosis cerebri.

UK. 5MRC laboratory for Molecular Cell Biology, University College London, Gower Street, London, WC1E 6BT, UK.

two littermates Chihuahua dogs (one male, one female) were investigated for progressive blindness, ataxia and cognitive impairment with an onset from around one year of age. Magnetic resonance imaging revealed marked generalized brain atrophy suggestive of a neurodegen-erative disorder. due to worsening of the signs, both dogs were euthanized before the age of two years. Brain histopathological examination demonstrated abundant neuronal accumulation of autofluorescent intracytoplas-mic storage material characteristic of neuronal Ceroid lipofuscinosis (nCl), with a lamellar ultrastructure. following ethical approval, dna was collected from both affected dogs and five related dogs including the sire and dam. Whole genome sequencing was performed on one of the affected dogs. sequence alignment and variant calling was done against the canine reference genome. Homozygous variants were found in the cod-ing or splicing regions of four genes previously identified as causing nCl (ARSG, CLN2=TPP1, CLN6, CLN7=MFSD8). segregation analysis by sanger sequencing character-ised Mfsd8:c.843delt - predicted to cause a truncated protein - as the causal mutation. although nCl has been previously reported in Chihuahuas on three different occasions, the causal mu-tation had remained unknown. in a recent report, the identical mutation uncovered in this study was strongly suspected to be the cause of disease in a single case in the Chinese Crested dog, suggesting a genetic relation-ship between both breeds. Considering the strong simi-larity of the clinical presentation and histological chang-es between humans with Cln7 disease and the two dogs presented here, Chihuahua could potentially be used as a large animal model of the human disease.

LAForA dISEASE IN A BEAgLEI. Hajek1, V. Simerdova2, P. Wang3, S.F.M. Bhatti4, B.A. Minassian5, V. Palus1. 1Centre of Veterinary Medicine Sibra, Bratislava, Slovakia, 2Small Animal Clinic, Faculty of Veterinary Medicine, University of Veterinary and Pharmaceutical Sciences Brno, Brno, Czech Republic, 3Program in Genetics and Genome Biology, Hospital for Sick Children and University of Toronto, Toronto, Ontario, Canada, 4Department of Small Animal Medicine and Clinical Biology, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium, 5Department of Paediatrics, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.

lafora disease, also called progressive myoclonic epilep-sy, is a fatal inherited neurodegenerative disease caused by deposits of inclusion bodies within the cells of several organs including the brain. there is a known genetic mu-tation in the wire-haired dachshunds but a genetic mu-tation has not yet been identified in different dog breeds. this case report describes the mutation in a clinically affected beagle. an eight year old neutered male bea-gle with progressive myoclonic episodes was presented for neurological examination. We observed mild myo-


dIStAL PoLyNEuroPAtHy IN A BIrMAN CAt WItH toxoPLASMoSIS L. Mari1, G.D. Shelton2, L. De Risio1. 1 Animal Health Trust, Newmarket, UK.2 Department of Pathology, School of Medicine, University of California, San Diego, USA

a 6-year-old female spayed Birman cat presented with a history of weight loss and stiff and short-strided gait in the pelvic limbs progressing to non-ambulatory tetrapa-resis over six weeks. at presentation, poor body condition, dehydration and generalized muscles wastage were evident. neurological examination revealed mildly depressed metal status, non-ambulatory flaccid tetraparesis and severely de-creased proprioception and spinal reflexes in all four limbs. no hyperalgesia was elicited on spinal or muscles palpation. the neuroanatomic localisation was to the peripheral nervous system.Haematology, fiV/felV serology, serum biochemistry in-cluding CK and t4, thoracic radiographs and abdominal ultrasound did not reveal significant abnormalities.electromyography revealed fibrillation potentials and positive sharp waves in axial and appendicular muscles. Motor nerve conduction velocity was decreased and am-plitude was severely reduced in ulnar and sciatic-tibial nerves. on muscle biopsies, several intramuscular nerve branches were variably depleted of myelinated fibers and contained myelin ovoids. some of the depleted nerve branches showed an excessive mononuclear cel-lularity. the biopsy of the common peroneal nerve was normal. igg and igM Toxoplasma Gondii serology titres were 1:200 and 1:160 respectively. fluid therapy and oral clindamycin 15mg/kg every 12 hours were initiated. the cat started improving within 24 hours and was ambulatory within 4 days. serology titres and neurological examination were normal 11 and 16 weeks post initiation of the treatment respectively. Clindamycin was discontinued after 16 weeks. no re-lapse was reported during the following 6 months.to our knowledge, this is the first report of distal poly-neuropathy associated with toxoplasmosis in a cat.

dIAgNoStIC VALuE oF MyoCytIC MHC-II ExPrESSIoN IN tHE dIAgNoSIS oF CANINE IMMuNE-MEdIAtEd MyoSItIS (CIMM) M. Rosati, M. Leipig, K. Matiasek. Section of Clinical & Comparative Neuropathology, Ludwig-Maximilians University, Munich, Germany.

lymphocytic invasion of predegenerate myofibres re-sembles the hallmark of CiMM. However, patchy lesion distribution and preceding treatment may preclude detection of specific infiltrates on microscopy. thus im-munohistochemical markers have been used to increase sensitivity and specificity of biopsy studies. amongst those MHC-ii was evaluated in immune cells. since my-ocytes also may act as antigen-presenting cells, their MHC-ii expression was evaluated with regards to aiding CiMM diagnosis. 34 CiMM dogs, 10 dogs with non-inflammatory myopa-thy and 10 dogs with neurogenic muscle atrophy were

paraplegic dogs had significantly (p<0.05) higher tau protein and Mip3b levels than the control group of which lumbar concentrations were also significantly higher compared to cisternal Csf samples. gfap only showed significantly higher values in cisternal Csf in dogs with grade V compared to the control group. Csf concentra-tions of tau protein, Mip3b and gfap could not discrimi-nate between grade iV and V. Cisternal tau protein values were significantly lower in dogs showing neurological improvement at least one grade within four weeks.in conclusion tau protein, Mip3b, and gfap values were significantly increased in dogs with iVdH and only cisternal tau protein concentrations seem to be correlated with the outcome of paraplegic dogs. the measurement of multiple biomarkers did not enhance outcome prediction.

BoNE rEModELINg AFtEr CoNSErVAtIVE MANAgEMENt oF HyPoVItAMINoSIS A IN AN AFrICAN LIoNJ. Siedenburg1, S. Wicha1, V. Molnár2, P. Dziallas1, M. Shamir3, V.M. Stein1 , A. Tipold1, 1Department of Small Animal Medicine and Surgery, University of Veterinary Medicine Hannover, Hannover, Germany, 2Zoo Hannover, Hannover, Germany, 3Koret School of Veterinary Medicine, Hebrew University of Jerusalem, Jerusalem, Israel.

a four-month-old, intact, captive male african lion (Panthera leo) was presented with a history of mild ves-tibular signs. serum Vitamin a levels were decreased. to confirm the diagnosis of suspected hypovitaminosis a associated occipital bone malformation, computed tomography (Ct) and magnetic resonance imaging (Mri) of the skull were performed. to obtain compa-rable ratios, Ct and Mri based measurements were normalized with skull width and diameter of vitreous humor. tentorium cerebelli and occipital bone were thickened and cerebellar herniation was evident on Mri t2w midsagittal planes. the tentorium cerebelli/skull width ratio (tCr) was 0.0839, basisphenoid/skull width ratio (BBr) 0.067, occipital bone/vitreous humor ratio (oBr) 0.5. a cervical intramedullary t2w hyperintensity extending for at least two cervical vertebrae was visible. Conservative treatment consisted of intramuscular vitamin a supplementation (2000 iu/kg/week for four weeks, 2000 iu/kg/14 days for five months, than 1000 iu/kg/14 days) and feeding of whole carcasses.after three months the neurological status improved and only a very slight ataxia was visible. in control Mri examinations the tCr declined to 0.0538, the BBr to 0.0462, and the oBr to 0.46. though the tentorium cerebelli osseum and the occipital bone were still thick-ened and the cerebellum remained mildly herniated, cervical hyperintensities were no longer visible. another five months later Mri ratios and pathologies in Ct scans changed again (tCr 0.0463, BBr 0.0429, oBr 0.51). a subtle cerebellar herniation was still evident. in conclu-sion, vitamin a supplementation seems to ameliorate clinical signs and positively influence bone remodeling in young lions with hypovitaminosis a.

Health, Institute of Animal Pathology, Vetsuisse Faculty, University of Bern, Switzerland.

the pathophysiology of ascending / descending my-elomalacia (adMM) following canine intervertebral disc (iVd) extrusion remains poorly understood. Vasoactive molecules may contribute to this lesion.the aim of the study was to investigate the expression of endothelin-1 (et-1) in the uninjured and injured canine spinal cord and its potential association with intramed-ullary haemorrhage and extension of myelomalacia.spinal cord tissue of 11 normal control dogs and 34 dogs with iVd extrusion was examined histologically at the level of the extrusion (epicenter) and in segments remote from the epicenter. endothelin-1 expression was examined immunohistochemically and by in situ hybridisation. using statistical analysis, we searched for associations between the expression of et-1 and the se-verity of intramedullary haemorrhage or the extension of myelomalacia.endothelin-1 was mainly expressed by astrocytes, mac-rophages and neurons and only rarely by endothelial cells in both control and affected dogs. in astrocytes at the epicenter, et-1 expression was significantly higher in affected dogs than in control dogs irrespective of the grade of haemorrhage or myelomalacia (P< 0.001, P= 0.001, respectively). et-1 expression in neurons at the epicenter was lower than in control dogs (P= 0.004, P= 0.008, respectively). in both astrocytes and neurons, there was a higher et-1 expression in spinal cord regions remote from the epicenter than in the epicenter itself.our observation of enhanced et-1 expression over mul-tiple spinal cord segments could help to explain the pathogenesis of adMM. However, more effective quanti-tative techniques and larger case numbers are required to investigate this further.

EVALuAtIoN oF CErEBroSPINAL FLuId BIoMArKErS IN PArAPLEgIC dogS WItH INtErVErtEBrAL dISC HErNIAtIoNS.I. Wicha; R. Carlson; A. Tipold; V.M. Stein; Dept. of Small Animal Medicine and Surgery, University of Veterinary Medicine Hannover, Hannover, Germany.

the definition of a reliable prognosis is challenging in paraplegic dogs with intervertebral disc herniation (iVdH). tau protein, macrophage inflammatory protein 3 beta (Mip3b) and glial fibrillary acidic protein (gfap) are potential markers of spinal cord injury. in the cur-rent prospective study the value of these substances as biomarkers in cerebrospinal fluid (Csf) for establishing prognosis in paraplegic dogs should be assessed.Concentrations of tau protein, Mip3b and gfap were measured in cisternal and lumbar Csf samples using elisa assays in 42 dogs. the dogs were classified as grade iV or grade V according to the presence (n = 19) or absence (n = 17) of deep pain sensation. six healthy dogs served as controls. outcome of dogs was monitored by neurological control exams over at least four weeks after surgery.

this is the first case report of suspected aHss after phe-nobarbital treatment in a dog and the first description of the pathological findings. Clinicians should be aware of this serious and possibly fatal complication. With aggres-sive and early treatment, chances of survival are good in human patients.

PoSt-oPErAtIVE SyMPtoMAtIC PNEuMorrHACHIS IN A dog WItH A tHorACoLuMBAr INtErVErtEBrAL dISC ExtruSIoN I. Cornelis1, P. Monticelli1, S. De Decker1. Clinical Science and Services, The Royal Veterinary College, Hatfield, United Kingdom.

although pneumorrhachis, the presence of air in the vertebral canal, is extensively described in human medi-cine, it has been described only twice in veterinary lit-erature.a 6-year-old crossbreed presented with acute, progres-sive ambulatory paraparesis localized to the t3-l3 spinal cord segments. Mri revealed an l1-l2 intervertebral disc extrusion, which was removed by a right-sided t13-l2 hemilaminectomy. surgery and recovery from anaes-thesia were uneventful. one day after surgery, the dog demonstrated slight deterioration, being non-ambula-tory paraparetic. the dog however became paraplegic with intact nociception and marked thoracolumbar hyperesthesia 48 hours after surgery. a Ct scan of the thoracolumbar vertebral column revealed the presence of a spherical, gas filled structure at the level of t13. the structure had a maximum diameter of 4.8mm, filling up approximately 50% of the vertebral canal and was as-sociated with marked spinal cord compression. a hyper-dense lesion possibly surrounding the gas bubble was concurrently identified, so the dog was presumptively diagnosed with an extradural gas bubble and hemato-ma, causing marked spinal cord compression. revision surgery confirmed the presence of a hematoma, which was removed. the dog gradually improved and was neu-rologically normal 6 weeks after surgery. in agreement with reports in human medicine, pneumorrhachis in this dog was possibly caused by ongoing intervertebral disc disease (vacuum phenomenon) or by entrapment of air in the vertebral canal during surgery. although pneumorrhachis is a rare condition, it should be considered a possible cause for early post-operative neurological deterioration in dogs undergoing decom-pressive spinal surgery. surgical revision might result in a good outcome. this is the first case report of post-operative pneumorrhachis after thoracolumbar hemi-laminectomy in a dog.

ENdotHELIN-1 ExPrESSIoN IN A CANINE ModEL oF SPINAL Cord INJuryD. Mayer1,2, A. Oevermann1,3, T. Seuberlich1,3, M. Vandevelde1,2, A. Casanova-Nakayama4, S. Selimovic-Hamza1,3,D. Henke1,2. 1Division of Neurological Sciences, 2Department of Clinical Veterinary Medicine, 3Department of Clinical Research and Veterinary Public Health, 4Centre for Fish and Wildlife


between 24 hours to 1 week, 20% between the second and fourth week, 9% between one and three months and 5% between three and six months after amputation. duration of preamputation pain correlated positively to the frequency of painful episodes after amputation (p=0.001). despite 22% of owners were not satisfied with pain control, 86% of them did not regret the decision of amputation.post-amputation pain is a common problem in dogs af-fecting 86% of patients and requiring appropriate treat-ment. Besides pain reported within the first week after amputation, 20% of dogs showed pain at a later moment resembling plp. duration of preamputation pain is a risk factor associated with occurrence of plp.

VASCuLAr ANd MEtABoLIC CoMProMISE oF L7 dorSAL root gANgLIA IN dogS WItH PAINFuL NErVE root CoMPrESSIoNM. Menchetti1,2, U. Foitzik1, M. Rosati1, T. Gödde3, A. Blutke1, F. Steffen4, H. Volk5, T. Flegel6, R. Cappello7, M. Lowry8, G. Gandini2, K. Matiasek2. 1Section of Clinical & Comparative Neuropathology, Ludwig-Maximilians University, Munich, Germany; 2Department of Veterinary Medical Science, University of Bologna, Italy; 3Neurology Referral Service, Tierarztpraxis Stauffeneck, Piding, Germany; 4Neurology Unit, Tierspital, Vetsuisse Faculty, University of Zurich, Switzerland; 5Clinical Science & Services, Royal Veterinary College, UK; 6Section of Neurology, Department of Small Animal Medicine, University of Leipzig, Leipzig, Germany; 7North Downs Specialist Referrals, Bletchingley, UK;8 Davies Veterinary Specialists, Higham Gobion, Herts, UK.

neuroforaminal stenosis (nfs) and consequent nerve root compression has been shown to cause morpho-logical changes of entrapped blood vessels and increase neuronal Vegf expression in entrapped dorsal root gan-glia (drg). these findings indicate adaptive changes to hypoxia and circulatory impairment. reduced oxygen supply could furthermore stimulate a shift in neuronal metabolsim and ultimately influence neuronal function. to challenge this hypothesis we evaluated the expres-sion of neuroglobin (ngB), carbonic anhydrase iX (Ca-iX), monocarboxylate transporter-1 (MCt-1) and -4 (MCt-4) in compressed canine drg via immunohistochemistry.altogether, 15 l7-drg were evaluated from nine dogs by lumbosacral nfs. results were compared to age-/breed-matched non-compressed drg.all entrapped drg showed significant neuronal positivi-ty for ngB (p<0.0001), Ca-iX (p<0.0001), MCt-1 (p<0.0001) and MCt-4 (p<0.0001). substantial increase of endothe-lial MCt-1 (p=0.005) and MCt-4 (p=0.02) expression throghout the endoneurium was seen. furthermore, in all entrapped drg satellite cells showed significant im-munoreactivity for ngB (p=0.02), Ca-iX (p=0.001), MCt-1 (p=0.02) and MCt-4 (p=0.03) expression.local increase of neuronal ngB is indicative of ad-aptative survival mechanism to hypoxic conditions through increased neuronal oxygen binding capacity. a shift towards glycolytic metabolism had been identi-fied through increased expression of Ca-iX and of MCts meant to prevent intracellular acidosis. the involvement

tional integrity of the spinal cord. transcranial magnetic stimulation (tMs) induces magnetic motor evoked po-tentials (MMeps) reflecting spinal cord functional impair-ment due to spinal cord diseases.this prospective study aimed to correlate morphometric Mri findings and MMeps with the course of neurological signs of 20 paraplegic dogs due to thoracolumbar iVdH and neurological improvement within one month after surgical decompression. MMeps were assessed in thoracic and pelvic limbs be-fore decompressive surgery, at improvement within one month and 3 months after surgery and Mri was conducted before and 3 months after surgery. Before decompressive surgery no MMeps could be measured in the plegic limbs. in 9/20 dogs MMeps could be elicited in the pelvic limbs when motor improvement was not-ed within one month and in 18/20 dogs 3 months after surgery. statistical analysis of post-surgically recorded pelvic limb MMeps showed a significant increase in peak-to-peak amplitudes whereas onset latency significantly decreased. Clr and t2Wlr were not significantly cor-related with the MMeps metrics. the comparison of Mri morphometric ratios pre surgery and three months post surgery revealed a significant decrease of Clr (p<0.004) whereas decrease of t2Wlr did not reach the signifi-cance level. in conclusion, MMeps reflect spinal cord recovery after severe functional impairment. However, correlation of MMeps with Mri morphometrics could not be confirmed.

ASSESSMENt oF PrESENCE, PrEVALENCE ANd rISK FACtorS ASSoCIAtEd to PHANtoM LIMB PAIN IN A CLIENt-oWNEd dog PoPuLA-tIoN AFtEr LIMB AMPutAtIoNM. Menchetti1,2, A. Gallucci2, G. della Rocca3, L. Matiasek4, K. Matiasek1, F.Gentilini2, G. Gandini2, M. Rosati1. 1Section of Clinical & Comparative Neuropathology, Ludwig-Maximilians University, Munich, Germany; 2Department of Veterinary Medical Science, University of Bologna, Italy; 3Department of Veterinary Medicine, University of Perugia, Italy, 4Neurology Referral Service, Tierklinik Haar, Haar, Germany.

phantom limb pain (plp) refers to pain perceived in the area of an amputated limb. despite the comparatively high rate of limb amputation in dogs, occurrence of plp has not been systematically studied. Hence, we screened a client-owned population of dogs with limb amputation through an online survey aimed to document plp preva-lence, risk factors and owner´s perception of their pets´ quality of life (Qol).the 75 questions survey evaluated reasons of amputa-tion, pain before and after amputation, pain frequency (expressed as daily, weekly, monthly or yearly episodes) and Qol after amputation. data were analysed with a Chi-squared test.156 dog owners completed the survey. the main rea-sons for amputation were cancer (59%) and trauma (35%). according to the owners´ perception, pain ap-peared similar before (81%) and after (86%) amputa-tion (p=0.44). over time, 66% of dogs experienced pain

rESIduAL dISC VoLuMES IN CHoNdrodyS-troPHIC VErSuS NoN-CHoNdrodySroPHIC dogS WItH INtErVErtEBrAL dISC dISEASE trEAtEd By ASSIStEd MINI-HEMILAMINECtoMyF. Innerkofler1, K. Matiasek2, S. Medl1. 1Neurology Referral Service, Tierklinik Babenhausen, Germany, 2Clinical & Comparative Neuropathology, Centre for Clinical Veterinary Medicine, Ludwig-Maximilians University of Munich, Germany.

for years, hemilaminectomy (Hl) has been the most ad-vocated decompression technique for surgical therapy of intervertebral disc disease (iVdd) in chondrodys-trophic (Cdd) and non-chondrodystrophic dogs (nCdd). However mini-hemilaminectomy (MH) very early has been shown to preserve better the stability of the ver-tebral column and to yield considerably more promising results than Hl in terms of both postoperative status and recovery time. this monocentre trial evaluated the efficacy of volume reduction by MH in combination with power-fenestation or small corpectomy in Cdd and nCdd suffering from thoracolumbar iVdd. Medical charts of dogs with thora-columbar iVdd from 2010-2015 were reviewed. inclusion criteria were (1) iVdd documented by native-phase Ct images pre and post surgery and (2) treatment via MHl plus small corpectomy or power fenestration. on serial images, the area of the spinal canal occupied by disc ma-terial was assessed via image analysis. thereby, filling percentage (fp), Maximum filling percentage (Mfp) pre surgery, residual filling percentage (rfp) and Maximum residual filling percentage (Mrfp) post surgery, as well as residual disc percentage (rdp) were calculated.a total of 74 patients were included (Cdd: 59, nCdd:15). the mean fp was 27.9±13,2%, mean rfp 10,3%±5,1%, mean Mfp 48,5%±19,8%, mean Mrfp 18,9%±9,1% and mean rdp was 31,2%±18,5% (Cdd: 31,0%±17,5%, nCdd: 31,8%±22,7%). assisted MHl comprises a tissue sparing decompres-sion technique that proved successful in both CCd and nCdd, likewise. Volume reduction as assessed by rdp appears superior to previously published

CorrELAtIoN oF trANSCrANIAL MAgNEtIC Motor EVoKEd PotENtIALS ANd MrI MorPHoMEtry IN dogS WItH FuNCtIoNAL Motor rECoVEry AFtEr INtErVErtEBrAL dISC HErNIAtIoN: A FoLLoW-uP StudyJ. Siedenburg1, H.-L. Amendt1, P. Dziallas1, K. Rohn2, A. Tipold1, V.M. Stein1, 1Dept. of Small Animal Medicine and Surgery, 2Dept. of Biometry, Epidemiology and Information Processing, University of Veterinary Medicine Hannover, Hannover, Germany.

the definition of a reliable prognosis in dogs with in-tervertebral disc herniation (iVdH) has been subject to extensive investigations. Magnetic resonance imaging (Mri) morphometric measurements such as l2 normal-ized ratios of compression length (Clr) and t2 weighted hyperintensities (t2Wlr) correlate with severity of clini-cal signs but do not provide information about func-

evaluated immunohistologically for expression of Cd3, Cd8, Cd20, iBa-1 and MHC-ii in immune cells and myo-cytes, respectively. the expression was scored (all mark-ers) and sorted for subcellular distribution (MHC-ii) after which group specific data were obtained according to standard algorithms. Myocytic MHC-ii expression was significantly increased in CiMM if compared to the other diseases (p≤0.02), which only stained weakly positive in 35% of cases. there was a moderate correlation (0.52; p=0.01) between Cd3 and MHC-ii for CiMM cases. With a cut off between scores 1 and 2, MHC-ii reached 100% specificity and 75% sensitiv-ity with 23/34 CiMM (67.6%) staining positive. the overall calculated accuracy was 83%. MHC-ii expression is a valid diagnostic marker for CiMM that extends beyond inflammatory foci. subthreshold MHC-ii expression requires further investigation since animals treated with corticosteroids might have not reached cut-off threshold.

MrI FINdINgS IN A CArBoN MoNoxIdE INtoxICAtIoN IN 2 dogSM. Kolecka1, S. Schulze1, D. Farke1, Ch. Söffler1, M. Kramer1, K. von Pückler1, M. Schmidt1. 1Small Animal Clinic Dept. Of Small Animal Surgery, JL University, Giessen, Germany.

a six years old female intact Jack russel terrier was found in a burning house without consciousness. after emergency treatment the dog showed ataxia, circling and vocalisation. Magnetic resonance imaging was per-formed 13 days after admission. t2w, flair and diffusion weighted sequences revealed bilateral symmetrical dif-fuse and homogneous hyperintensity of the caudate nu-clei. adC mapping showed a hyperintensity of the cau-date nuclei. four weeks after admission the dog showed no neurological deficits and was discharged. a second dog (4 years old neutered male crossbreed) was presented 2 weeks after smoke exposure. initially the dog showed no abnormalities. at the presentation the dog was obtunded and disorientated, showing signs of cerebellar ataxia and proprioceptive deficits. t2w and flair images revealed a heterogenous hyperintensity of both caudate nuclei. their signal was hypointense in t1. generalised hyperintensity of the grey matter surround-ing the cerebellar foliae was visible in t2w and flair sequences. due to progressive deterioration of clinical signs the dog was euthanized 5 months later. the Mri findings presented in this report are partially compatible with acute and chronic findings reported in human patients after carbon monoxide intoxication. Hyperintense signal changes of the basal nuclei, hip-pocampus and cerebellum in t2w and flair images with restricted diffusion were major findings in the acute phase. in the chronic phase changes involve predomi-nantly the white matter. lesions were observed as bi-lateral, diffuse hyperintense signal changes in t2w and flair sequences with a restricted diffusion. Cerebellar in-volvement was observed in the acute and chronic phase.


the relationship between Mri-assessed iVd degeneration and recurrence of clinical signs in surgically treated dogs. Medical records and Mri-studies of dogs undergoing hemi-laminectomy without fenestration for thoracolumbar iVde at two centres (2010-2014) were reviewed. recurrence was assessed by telephone follow-up to either referring vets or owners. recurrence was recorded if thoracolumbar pain or neurological deficits occurred after a period of at least 6 months during which recovery was seen. fifty-four dogs were included and Mri studies from t11 to l3 were as-sessed for number of degenerated discs in addition to the affected one in mid-sagittal t2W-images. in common with previous studies, most animals were dachshunds (43%) and mean age was 5.75yrs (2.6-11). 96% of extruded discs were between t11 and l2. recurrence of clinical signs was seen in 13/54 (24%) of cases, and 100% of these cases had at least one other degenerate iVd seen on initial Mri. in the non recurrence group 23/41 (56%) showed no other degenerate discs. there was a significant correlation between number (p=0.022) of degenerate discs and recurrence. these results might be of value in predicting recurrence in dogs, assisting surgical decision making with regard to prophylactic fenestration.

outCoME ANd CoMPLICAtIoN rAtE IN CANINE CErVICAL dISK ExtruSIoNS trEAtEd EItHEr WItH A VENtrAL SLot or A CErVICAL HEMILAMINECtoMy ProCEdurE D. Faissler, S. Samuels. Cummings School of Veterinary Medicine at Tufts University, Grafton, MA 01532, USA.

Cervical disk extrusions accounts for 15-25% of canine iVdd. the purpose of this study was to assess post-surgi-cal complications, short and long-term outcome canine cervical iVdd treated with either a ventral slot (Vsl) or cervical hemilaminectomy (CHl) procedure. our hypothesis is that dogs undergoing Vsl or CHl have a similar incidence of post-surgical complications and out-come, but a significantly higher incidence of recurrence at an adjacent disk space after a Vls procedure. inclusion criteria were complete medical history, advanced diag-nostic imaging and postsurgical follow-up of > 2 years.eighty-seven dogs were included; 61 dogs underwent a Vsl surgery and 26 dogs had a CHl procedure. there was no difference in breed, weight, age, sex, onset, and clini-cal presentation, affected disk space and degree of spinal cord compression between the two groups. dogs under-going CHl had a lateral or formaninal extrusion more fre-quently. surgery time, days on a fentanyl Cri and hospi-talization time were significantly shorter in the Vsl group. the rate of adverse events assessed with saVes grades was similar in both groups (8.4% versus 7.7%). Both pro-cedures had good return to normal function (80% versus 88%). dogs in the Vsl group had a higher recurrence rate than in the CHl group (21.7% versus 7.7%) with the adja-cent disk space affected frequently (13.3% versus 3.8%).the Vsl procedure is faster, requires less post-operative pain medication, and has a shorter hospitalization time. However, with the Vsl procedure patients are at a higher risk of recurrence, especially at the adjacent disk.

ALtErEd ExPrESSIoN oF AN ExCItAtory tACHyKININ NEuroPEPtIdE IN SEIZurE-AS-SoCIAtEd FELINE HIPPoCAMPAL SCLEroSISM. Rosati¹, E. Wagner¹, A. Fischer², L. Matiasek3, T. Flegel4, K. Matiasek¹. 1Section of Clinical & Comparative Neuropathology, Ludwig-Maximilians University, Munich, Germany; 2 Section of Clinical & Comparative Neurology, Ludwig Maximilians University, Munich, Germany; 3Neurology Referral Service, Tierklinik Haar, Haar, Germany; 4Section of Neurology, Department of Small Animal Medicine, University of Leipzig, Leipzig, Germany.

substance p (sp) has pro-epileptic effects due to its neu-rokinin-1 receptor activation evoking neuronal depolari-sation and enhancing excitation. during status epilepti-cus hippocampal expression of sp increases the electri-cal activity of the region, which becomes more prone to seize. Considering sp a candidate for neuromodulation we investigated its expression in feline hippocampi with (Hs) and without (nHs) seizure-associated hippocampal sclerosis.immunohistochemical distribution of sp at the tempo-ro-ventral body of the hippocampus was assessed in 26 epileptic cats and compared to non-neurologic controls. algorithms for analysis comprised semiquantitative scoring of sp expression throughout hippocampal sub-regions and its subcellular distribution. all hippocampi showed sp synaptic immunoreactivity in the external and internal stratum moleculare of dentate gyrus, pyramidal layer, stratum radiatum, stratum oriens and more diffusely within parahippocampal gyrus (pHg). sp expression was reduced in epileptic cats reaching sta-tistical significance (p<0.02) in all segments but dentate gyrus. sp was significantly decreased in Hs compared to controls in Ca3, Ca2, Ca1 and pHg. nHs differed from con-trols only in Ca1. a significant reduction of sp expression was seen after se in Ca3 (p=0.052) and pHg (p=0.004).decrease of sp expression in the hippocampus of epi-leptic cats in course of Hs could be attributed to loss of synapses in course of Hs. se and prolonged excitatory electrical activity might as well decrease sp expression through its synaptic depletion. assessment of candidate neuropeptides for neuromodulation is a preliminary step towards development of adjuvant therapies to as-sist conventional antiepileptic treatments.

ASSoCIAtIoN BEtWEEN MrI ASSESSEd dISC dEgENErAtIoN ANd rECurrENCE oF CLINICAL SIgNS FoLLoWINg SurgICAL trEAtMENt oF tHorACoLuMBAr INtErVErtEBrAL dISC dISEASE IN dogSS. Longo1, D. Burnand1, S.A. Gomes1, P. Freeman1. 1The Queen’s Veterinary School Hospital, Department of Clinical Veterinary Medicine, University of Cambridge, UK.

an association between the number of calcified interver-tebral discs (iVds) on survey radiographs and recurrence of clinical signs following surgery for thoracolumbar in-tervertebral disc extrusion (iVde) in dogs has been pre-viously described. Mri is now the imaging modality of choice in canine iVde. the aim of this study is to examine

syringomyelia (sM) is a well-recognised spinal cord mal-formation that often affects the cervical segment and can manifest clinically by pain, phantom scratching, and proprioceptive deficits. this disease has been well described in the Cavalier King Charles spaniel (CKCs) and more recently in the griffon Bruxellois (gB). the aim of this study was to assess the prevalence of sM in the french Bulldog (fB) and to describe the common clinical manifestations, outcome and prognosis. of the 850 fBs that presented within 3,5 years at our institution, 9,5% (12 cases) of fBs with clinical signs referring to a lesion along the cervical spinal cord tract, presented sM. unlike the clinical signs in the CKCs and gB, the typical neck pain and scratching behaviour were rare features; propriocep-tive deficits were a common finding. it is hypothesised that this prevalence may be higher considering the possi-ble silent sM and the lack of magnetic resonance imaging in all dogs with cervical involvement. We emphasize that sM should be considered a differential diagnosis for fB with a primary complaint referring to the cervical region.

SEIZurES do Not MASK tHE PAttErN oF PErVASIVE CHANgES IN CAtS WItH HyPEr-tENSIVE ENCEPHALoPAtHyS. Bertram1,2, L. Matiasek3, M. Rosati1, E. Wagner1, H.A. Volk4, A. Fischer2, K. Matiasek1. Sections of 1Clinical & Comparative Neuropathology and 2Neurology, Centre for Clinical Veterinary Medicine, Ludwig-Maximilians University, Munich, Germany; 3Neurology Referraf Service, Tierklinik Haar, Haar, Germany; 4Clinical Science & Services, Royal Veterinary College, Hatfield, UK.

systemic arterial hypertension impacts on the brain by malperfusive and pervasive effects that show a charac-teristic topography and therefore may allow for an im-aging diagnosis of feline hypertensive encephalopathy (fHe). neurological complications of fHe, on the other hand, include seizures in up to 30% of affected animals. it was the aim of this study to evaluate the impact of sei-zures on the spatial pattern of pervasive changes in or-der to differentiate target areas of hypertensive damage from those prone to seizure-related blood brain barrier breakdown (B4).the study enrolled brains of 31 cats, including 9 epi-leptics, with fHe identified through blood pressure increase, compatible primary lesions and target organ damage of brain vessels. Brain tissue was screened for actual and post-resorption stages of oedema, perivascu-lar microgliosis, parenchymal and vascular lesions.apart from a subsignificantly increased involvement of hippocampus, caudate nucleus and marginal gyrus by actual oedema and aquaporin-4 expression, there were no differences in between lesion maps or damage scores of epileptic and non-epileptic fHe cases (p≥0.05). Brain oedema and perivascular gliosis in fHe resemble blood pressure-induced vascular dysfunction rather than consequences of local excitotoxicity. the lesion pattern persists throughout epileptic and non-epileptic fHe courses and therefore allows for an accurate imag-ing diagnosis of systemic hypertension.

of satellite cells further indicates activation of scavang-ing mechanisms. these findings highlight significant neuronal distress, that is likely to contribute to aberrant electrical activity, neuronal drop out and persistence of neuropathic pain.

EVALuAtIoN oF tHE rISK FACtorS ANd ABCB1 gENotyPE IN dogS AFFECtEd By rEFrACtory IdIoPAtHIC EPILEPSyT. Gagliardo1, F. Gentilini1, A. Gallucci1, M. Menchetti1, M. Turba2, E. Bianchi3, A. Cauduro4, D. Corlazzoli5, S. Gianni6, M. Baroni7, M. Bernardini8, G. Gandini1. 1Department of Veterinary Medical Sciences, University of Bologna, Italy; 2Genefast, Bologna, Italy; 3Department of Veterinary Medical Sciences, University of Parma, Italy; 4Neurovet Professional Association, Milan, Italy; 5Roma Sud Veterinary Clinic, Rome, Italy; 6Gran Sasso Veterinary Clinic, Milan, Italy; 7Valdinievole Veterinary Hospital, Pistoia, Italy; 8Portoni Rossi Veterinary Hospital, Bologna, Italy.

the aims of this study were to evaluate the risk factors in a population of dogs affected by refractory idiopathic epilepsy (rie) and assess the frequency of the aBCB1 gene mutation (c.-6- 180t>g), previously associated to phenobarbital-resistant idiopathic epilepsy in Border Collies (BCs).the multicentric study had a cross-sectional design. among a population of idiopathic epileptic dogs, 52 dogs affected by rie (defined as a condition in which two anti-epileptic drugs at adequate serum concentration did not achieve a decrease in seizure frequency ≥50%) were found. Breed, gender, body weight (divided as > or < 20 kg), age at the onset of seizures (<12m; 12-24m; 25-36m; >36m) and seizure type (cluster/single and general-ized/focal) were analyzed.the most represented breeds were mongrel (40%) and BC (7%). the median weight was 19,5 kg. the median age at onset of seizures was 21 months. Cluster seizures were present in 55% of dogs, including 33%, which ex-perienced status epilepticus. the most common seizure type was generalized tonic-clonic (88%). BCs were significantly (p<0,001) at higher risk to develop rie. parameters significantly associated to rie were: weight >20kg (relative risk (rr):1,9), age at onset sei-zure between 12-24 month (rr: 2,7), and cluster seizure (rr: 4,8) .the aBCB1 mutation was present in the 56% of the dogs, 50% in a homozygous and 50% in a heterozygous state. the aBCB1 mutation was also identified in breeds differ-ent from BC.Besides identifying clinical risk factors, the study dem-onstrates that other polymorphisms may be responsible for rie in dogs.

SyNrINgoMyELIA IN tHE FrENCH BuLLdogC. Ricco, F. Samarani, E. Gomes, L. Cauzinille. Centre Hospi-talier Vétérinaire Frégis, Arcueil France. AHT Landwades Park Kentford Newmarket Suffolk CB8 7UU, United Kingdom.


evaluate the diagnostic yield and diagnostic accuracy of the Mri-guided BrainsighttM frameless stereotactic sys-tem in a series of dogs and cats with intracranial lesions. forty-five dogs and six cats with intracranial disease, which was confirmed on Mri, underwent Mri-guided sBB. routine histopathological examination was per-formed on the obtained brain biopsy specimen. Brain necropsy was available for comparison of histopatho-logical diagnoses in thirty-eight animals. Brain tissue was obtained in all biopsy procedures. the overall diagnostic yield was 80.4% (41/51). the histological diagnosis of sBB was confirmed (com-plete agreement) in twenty-six (86.7%) and slightly differed (minor disagreement) in four (13.3%) of the thirty diagnostic cases, which were also available for necropsy. for the thirty-one patients in the complete and major agreement groups of this study, the accu-racy of the histological diagnosis was 100% (31/31). in conclusion, Mri-guided sBB using the BrainsighttM frameless stereotactic system is an effective method to collect brain tissue samples resulting in a correct histo-pathological diagnosis in the majority of patients.

MorPHoLogy oF tHE CAudAL FoSSA IN MESAtICEPHALIC ANd BrACHyCEPHALIC CAtSK. Marioni-Henry1, T. Schwarz1, D. Gunn-Moore1. 1Hospital for Small Animals, Royal (Dick) School of Veterinary Studies, Roslin, United Kingdom.

Morphological abnormalities of the caudal fossa are in-creasingly recognized as a cause of morbidity in many brachycephalic dogs with round broad heads and short-ened facial bones such as Cavalier King Charles spaniels. the study objective was to investigate presence of simi-lar morphological abnormalities of the caudal fossa of mesaticephalic and brachycephalic cats. the records of the diagnostic imaging service at the r(d)sVs were searched for Mri studies of brain of cats from January 2014 to June 2015. twenty-six cases were identified, four Mri were eliminated due to struc-tural intracranial abnormalities. t2W sagittal images of the remaining 22 Mri studies were blindly analyzed by KMH. subjective assessments included coning of the cerebellar vermis, indentation of the cerebellum by the supraoccipital bone, iso- to hyper-intense material in the middle ear and, when concurrent Mri studies of the spine were available, presence of syringohydromyelia. Measurements of foramen magnum and cerebellar her-niation, area of the cerebellum, length of the forebrain and cerebellum were also acquired. after the Mri studies were reviewed they were unblind-ed and the data were divided in 2 groups based on the classification of the cat breeds among mesaticephalic (16 cats: 14 domestic shorthaired cats, 1 ragdoll and 1 Maine Coon) or brachycephalic (6 cats: 2 Burmese cats, 1 British shorthaired, 1 Burmilla, 1 Chinchilla, 1 tiffany). Cerebellar coning and cerebellar indentation by the fo-ramen magnum was reported in 5/6 cats (83%) of the brachycephalic group versus 8/16 cats (50% for cerebel-lar coning) and 3/16 (19% indentation) of the mesatice-phalic group.

epilepsy patients are warranted. the studies described here were approved by the relevant authorities for pro-tection of animals.

uSE oF gABAPENtIN For NEuroPAtHIC PAIN trEAtMENt IN dogS: A ProSPECtIVE CLINICAL trIALA. Seisdedos1, A. Galán Rodríguez1, J. Morgaz Rodríguez1, B. Blanco Navas1, E. Martín-Suárez1. 1Department of Internal Medicine, University of Córdoba, Spain.

neuropathic pain (np) is a chronic pain with many forms of presentation and multiple etiologies. Most clinical signs related to np are difficult to recognize in dogs. up to the date, there are few studies about the most ef-fective treatment (grubb 2010, Wolfe and poma 2010, Maden et al. 2014, plessas et al. 2015).the objective of this prospective clinical trial was to assess the effective-ness of gabapentin in the treatment of np in dogs.eleven patients followed a 6-week period treatment with gabapentin at dosage of 15mg/kg/12h during the 1st and 6th weeks and 15mg/kg/8h from the 2nd to the 5th weeks. they were examined at the first visit (t0) and 3th (t1) and 6th (t2) weeks, obtaining heart rate, respiratory rate, arte-rial pressure, blood count, blood levels of cortisol and fruc-tosamine. two questionnaires (Q1 and Q2) for the assess-ment of pain were performed. Q1 assessed dog’s behavior at home and Q2 assessed the patient’s pain at the visit. at the end of the treatment, although without significant differences, all dogs showed a notable decrease in the punctuation in Q2. Cortisol levels decreased progres-sively during the treatment and significant differences were observed between the t0 and t2. in conclusion, reductions in cortisol levels and decrease of clinical signs related to np at consultation make us consider gabapentin 15mg/kg/8h as useful for the np treatment in dogs.

dIAgNoStIC yIELd ANd dIAgNoStIC ACCurACy oF MAgNEtIC rESoNANCE IMAgINg-guIdEd FrAMELESS StErEotACtIC BrAIN BIoPSy IN dogS ANd CAtS WItH INtrACrANIAL dISEASEA. Staudacher1, A. Oevermann2, F. Forterre3, D. Henke4, D. Gorgas1. From the Department of Clinical Veterinary Medicine, 1Division of Clinical Radiology, 3Division of Small Animal Surgery and 4Division of Clinical Neurology and from the Department of Clinical Research and Veterinary Public Health, 2Division of Neurological Sciences, Vetsuisse-Faculty Bern, Switzerland.

stereotactic brain biopsy (sBB) is currently the least invasive method to obtain a specific histopathological diagnosis of intracranial disease, which is essential to establish a well-founded prognosis and a rational ther-apy plan. frameless magnetic resonance imaging (Mri)-guided sBB is becoming the standard of care for image-guided brain biopsy in human medicine, but its diagnos-tic success has never been investigated in veterinary pa-tients. therefore, the aim of this prospective study was to

patients were enrolled from the population referred to the neurology and neurosurgery service at the Queen Mother Hospital for animals, royal Veterinary College, between 2005 and 2014. inclusion was based upon pre-viously published criteria. Cytosine arabinoside adminis-tration was typically by subcutaneous injection at 50mg/m2 every 12 hours over a 48 hour period, initially, at three weekly intervals. prednisolone was started at 1mg/kg every 12 hours and tapered based on clinical response. outcome data were collected by regular re-examination visits at our dedicated cytosine arabinoside clinic and a standardised telephone questionnaire.135 dogs were included in this study. survival times ranged from 0 to 3030 days (mean 710 days, median 377.5 days, lower quartile 85 days, upper quartile, 1104 days). none of the evaluated variables were significantly associated with prognosis. 9% of dogs demonstrated side effects associated with cytosine arabinoside, which included vomiting or diarrhoea (5.2%), calcinosis cutis (1.5%), myelosupression (2.2%), and injection site infec-tion (0.7%). Clients reported 78% of dogs showed one or more side effects associated with glucocorticoid use, these were reduced or alleviated through dose reduction in 98% of cases.Cytosine arabinoside can be safely used for the long-term management of Mua, and it has the potential to significantly reduce the side effects associated with con-comitant glucocorticoid use through dose reduction.

IMEPItoIN IS WELL toLErAtEd By HEALtHy CAtS O. Engel1, J. Mueller1, F. de Vries1. 1 Boehringer Ingelheim Vetmedica GmbH, Ingelheim am Rhein, Germany.

epilepsy in the cat is a serious medical condition as in all species. to date there are no licensed treatments for feline epilepsy and no well-controlled clinical studies on the efficacy or safety of antiepileptic drugs in cats.the new antiepileptic drug imepitoin has demonstrated clinical efficacy and safety in dogs to reduce the frequen-cy of generalised seizures due to idiopathic epilepsy.the aim of this randomised, controlled, blinded glp study was to investigate the tolerance of imepitoin in clinically healthy male and female cats after repeated oral administration in a laboratory setting. in two stud-ies, 30 cats received twice daily doses of 0, 30, 40 or 80 mg/kg bodyweight for 30 days.no serious adverse events were observed in any of the dose groups. in the imepitoin treated groups, emesis was observed in some animals temporarily and inter-mittently mainly in the second and third weeks of treat-ment. at the highest doses (40 and 80 mg/kg), a slight reduction in food consumption was observed especially at the beginning of the study, with subsequently slightly lower body weights compared to controls. Haematology and clinical chemistry results revealed no relevant changes. the pharmacokinetic profile appeared to be similar to dogs with a tmax of 1.5 hours. in summary, in this laboratory study imepitoin was well tolerated in cats, even at very high doses. for definitive evidence on safety and efficacy, clinical trials in feline

INHErItANCE oF CHIArI-LIKE MALForMAtIoN: CAN A MIxEd BrEEd rEduCE tHE rISK oF SyrINgoMyELIA? S Knowler1, H v/d Berg2, A McFadyen3, E Noorman4, R La Ragione1, C Rusbridge1,2. 1School of Veterinary Medicine, Faculty of Health & Medical Sciences, University of Surrey, Guildford, Surrey, UK. 2Fitzpatrick Referrals, Halfway Lane, Eashing, Godalming, Surrey, UK 3akm-stats, Glasgow, Scot-land, UK 4Dierenkliniek den Heuvel, Oirschotesweg 113a 5684 NH Best, NL.

Chiari-like malformation (CM) and syringomyelia (sM) are complex multifactorial disorders. Quantitative analysis in a family group was used to investigate the inheritance and feasibility of crossbreeding a mesatice-phalic normal australian terrier and brachycephalic CM affected griffon Bruxellois (gB) and then backcrossing to produce individuals free of CMsM and regain breed type. the 27 dog family had 5 foundation dogs which had been members of a 155 gB dog cohort investigated in a previous study and which were identified for eight traits significant for CM and sM affectedness. Moreover, a Quantitative trait locus analysis had shown six of these to be associated with 5 Canis familiaris autosomes. t1-weighted sagittal diCoM images of the brain and cervico-cervical junction were analysed for five significant traits (2 angles, 2 lines and a “best fit” occipital lobe circle di-ameter) which were useful to distinguish the phenotype. the mean measurements for mixed and pure-breed groups were compared. the traits exhibited segregation that may be additive towards the severity of CM. further-more, the external phenotypes showed that by outcross-ing breed types and careful selection of appropriate conformation characteristics in the first generation, it is possible to regain the gB breed standard and reduce the degree of CM. the four dogs affected with sM in the study all exhibited reduced caudal skull development compared to their relatives. these traits may be useful to quantify CM and risk of sM to assist breeders with mate selection. such a system requires validation to ensure appropriateness for all breeds at risk.

A rEtroSPECtIVE rEVIEW oF 135 CASES oF MENINgIoENCEPHALoMyELItIS oF uNKNoWN AEtIoLogy trEAtEd WItH CytoSINE ArABINoSIdE ANd gLuCoCortICoIdSM.F.E. Hill1, R.M.A. Packer2, P.J. Kenny2, S. De Decker2, H.A. Volk2. 1Department of Clinical Neurosciences, University of Cambridge, Cambridge, United Kingdom, 2Department of Clinical Science and Services, Royal Veterinary College, University of London, Hatfield, United Kingdom.

Meningoencephalomyelitis of unknown aetiology (Mua) is a commonly diagnosed neurological condition in dogs that can be treated by a variety of immunomodulating drugs including cytosine arabinoside. the aims of this study were to review the outcomes (including death and response to treatment) and adverse effects associated with treatment with cytosine arabinoside and glucocor-ticoids in patients diagnosed with Mua.


was euthanized and a pathological examination was performed. Macroscopic examination revealed a pres-sure induced atrophy of the brainstem. Histological find-ings included satelitiosis, mild mononuclear cell infiltra-tion within the meninges and a mild vacuolization of the white matter adjacent to the mass. the mass itself was organized in nests of round to polygonal cells with eosin-ophilic cytoplasm. few mitoses were visible and within the stroma areas of necrosis and calcification were vis-ible around one big central necrosis. imunohistochem-istry showed that tumour cells strongly expressed epi-thelial marker, and ß-catenin (nse) and showed a low mitotic activity (MiB-1) <5%. the histology is consistent with a low grade tumor of epithelial differentiation and in combination with the radiological findings a crani-opharyngioma of papillary type was diagnosed.immunohistological stains were positive for vimentin, cytoceratine, nse within the stroma and the mass and synaptophysine. they were negative for gfap,s100 and nf. so the histopathological examination considered a pituitary gland neoplasia most likely.

gENEtIC EPILEPSy IN CANE CorSo ANd doguE dE BordEAuxCatherine Escriou1, Pascale Quignon2, Emilie Menzer1, Solenne Correard2, Catherine André2. 1Neurology, VetAgro Sup, Lyon Veterinary Campus, France. 2CNRS, UMR 6290, Genetic and development institute, Rennes, France.

genetic factors are increasingly being identified as the underlying mechanism of breed specific type of epilep-sy in dogs. prevalence and phenotypic characteristics of epilepsy are well described in popular breeds like Belgian shepherd, australian shepherd, Border Collie or labrador. to date, no descriptions have been reported in molossoid breeds like Cane Corso and dogue de Bordeaux. in order to determine breed specific epilepsy presenta-tion we asked breeders or owners to complete a ques-tionnaire about epilepsy.We collected 25 epileptic Cane Corso and 5 epileptic dogue de Bordeaux. Cane Corso displayed severe epilepsy with very homog-enous presentation appearing during teenage (median 17,5 months) with no sex predisposition. all dogs pre-sented generalized seizures and 91% have systematic clusters. 30% of dogs are euthanized or deceased from status epilepticus before 3 years. in 54% of dogs, sei-zure frequency didn’t decreased with anticonvulsants. epilepsy in dogue de Bordeaux was similar (generalized seizures and clusters for all dogs) but a juvenile form is observed in 4 dogs (first seizure before 4 months). in Cane Corso, 17 dogs were related and pedigree analy-sis is in favor of recessive autosomal transmission.Whether this severe epilepsy is linked to the size of the dogs as previously described or to the specific underly-ing genetic factors remains questionable.

SEIZurES IN A CoAtI (NASuA NASuA) WItH CrANIoPHAryNgIoMA-A CASE rEPortD.Farke1, M.Kolecka1, S. Kirsten2, L. Rydewski2, A.Schänzer3, H.Dohmen-Scheuffler3, C.Herden2, M.J.Schmidt1. 1Clinic for Small Animals-Surgery, Justus Liebig University, Giessen Germany. 2Institute of Veterinary Pathology, Justus Liebig University, Giessen, Germany. 3Institute of Neuropathol-ogy, Justus Liebig University, Giessen, Germany.

a ten years old coati was presented with a 3 week history of generalized seizures, altered consciousness, circling and blindness. abdominal and chest radiographs, com-plete blood cell count and biochemistry panel from the referring veterinarian revealed no abnormalities. neuro-logical examination showed a reduced menace response on both eyes. Magnetic- resonance-imaging showed an extra-axial, well demarcated mass lying in the middle cranial fossa, which had a mass effect on the brainstem, cerebellum, thalamus and corpus callosum. the mass was heterogenous with a central hyperintensity in t2, t2ffe and flair. in t1- weighted images a central hy-pointensity and a moderate contrast enhancement was visible. differential diagnosis included makroadenoma/ carcinoma of the pituitary gland, germinoma meningi-oma, lymphoma and craniopharyngioma. the animal

european Veterinary Congress on MoVeMent disorders 2015 · 2 stProceedings 28 ESVN-ECVN Congress -...

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