proceedings-movement-disorders-congres-2015

Transcription

Congres proceedings
European Veterinary congress ON Movement disorders
2015
28 ESVN-ECVN CONGRES
st
18–19 September
Amsterdam
Number 400 Date . September 2015 Editors . Mandigers P.J.J. & Granger N. Dear friends and colleagues,
Dear colleagues and friends,
Dear ESVN/ECVN family,
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.
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 Volk
ECVN President
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’.
Holger Volk
ECVN President
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.
Paul Mandigers
Chairman of the 28th ESVN-ECVN congress
Good to have you over. Please enjoy!
Paul Mandigers
Chairman of the 28th ESVN-ECVN congress
2
Proceedings 28st ESVN-ECVN Congress - Amsterdam 2015
3
Executive Committee ESVN-ECVN Congress 2015
Holger Volk
Veronika Stein
Thomas Flegel
Laurent Garosi
President
Secretary
Vice-president
Past President
Table of contents
Valentina Lorenzo
Lara Matiasek
Sam Long
Julien Guevar
Treasurer
Head of Examination Committee
Head of Education Committee
ESVN Representative
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 abstracts37
15. Poster abstracts55
Local
Organising
Committee
4
Paul Mandigers
Niklas Bergknut
Susanne Pauwels
Chairman
5
PLatinum sponsor OF THE ESVN-ECVN CONGRESS
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sponsors OF THE ESVN-ECVN CONGRESS
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De IDEXX Catalyst One™ biedt de veterinaire praktijk snelle en accurate in huis diagnostiek met de kwaliteit
van een referentielaboratorium. Met de ‘One’ doet u sneller en ef ciënter biochemisch onderzoek en kunt u uw
patiënten nog completere en hoogwaardigere veterinaire zorg bieden.
Meer informatie? Bel ons op telefoonnummer 00800 1234 3399 of ga naar www.idexxcatalystone.nl
Bekijk de video om te zien hoe gebruiksvriendelijk de Catalyst One™ is.
6
7
29th Annual Symposium of the ESVN-ECVN
S
E
OK OR AT
BO W F D R
R
NO BI
Y
RL
EA
JOIN US IN
EDINBURGH NEXT YEAR!
who is who?
useful information
ESVN-ECVN Board
Holger 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)
Venue
The congress will take place in:
The Royal Tropical Institute (KIT)
Mauritskade 63, 1092 AD Amsterdam
The Netherlands
T: +31 20 56 88 711, F: +31 20 66 84 579
www.kit.nl, communication@kit.nl
Examination committee
Lara Matiasek (chair)
Mike Targett
Christine Thomson
Sebastien Behr
Tom Harcourt-Brown (examination observer)
Tarja Joniken (examination observer)
Iris Van Soens (examination observer)
15 – 17 September 2016
Royal College of Surgeons, Edinburgh, UK
Education Committee
Sam Long (chair)
Elsa Beltran
Caroline Hahn
Nick Jeffery
Merav Shamir
Jean Laurent Thibaut
Andrea Tipold
Accessibility The Royal Tropical Institute
By 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
Parking
There 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.
Scientific committee
Nicolas Granger (chair)
Laurent Garosi
Peter Smith
Symposium committee
Paul Mandigers (chair)
Niklas Bergknut
Registration desk
The 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.
PCO Symposium
Susanne Pauwels
Certificate of attendance
All participants will receive a certificate of
attendance by email after the congress.
Register your attendance at: www.vetneuro2016.com
9
Congress badges
All 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.
Currency
The Dutch currency is EURO. Most hotels,
restaurants and shops accept international
credit cards.
Venue Welcome Reception:
Thursday 17 September 19.00 hrs.
Artis
Natura Artis Magistra
Plantage Kerklaan 38-40 Amsterdam
The Netherlands
Venue Dinner
NH Grand Hotel Krasnapolsky
Dam 9 Amsterdam
The Netherlands
nhkrasnapolsky@nh-hotels.com
Venue Dance
Olofskapel
Zeedijk 2 Amsterdam
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.
Toilets
Congress Secretariat
Pauwels Congress Organisers
Alexander Battalaan 7
6221 CA Maastricht
The Netherlands
Contact person: Susanne Pauwels
T +31 (0) 43 321 81 80
s.pauwels@pauwelspco.nl
Reception
Language
The official language of the congress is English.
Mobile Phone Manners
As 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.
Liability
Upon 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.
10
ESVN-ECVN 2015
Royal Tropical Institute,
Amsterdam, The Netherlands
11
Time table ESVN/ECVN congress
ThurSdAy 17-9-2015 residents and Practioneers day at uu-utrecht (from 10 to 16 hrs)
SATurdAy 19-9-2015
Welcome party - Artis Zoo with guided tours from 18.30 to ... hrs (registration is required!)
SPEAKEr
SubjECT
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
Andrea Fischer
Vldlr-associated cerebellar hypoplasia in eurasier dogs
the 28th European
10.15-10.45
ESVN-ECVN congress
Chair:
Caroline hahn
Movement disorders in large animals
KIT, Amsterdam
The Netherlands
www.ecvn.org
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
Gemma Elizabeth
Longson
A preliminary study of the penlight-cover test in differentiating between
peripheral and central vestibular disease in dogs and cats
Chair:
FrIdAy 18-9-2015
Chair:
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
9.45-10.00
18-19 September 2015
10.00-10.15
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
Lunchbreak
12.30-13.45
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
12.30-14.00
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
Coffeebreak
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
Florian Salger*
Immunohistochemical characterization of the anti-inflammatory effect of two
treatment protocols in dogs with granulomatous meningoencephalomyelitis
or necrotizing (meningo)-encephalitis
Invited Speakers:
15.15-15.30
Dr. Hans Stroink (md)
Canisius ZKh Nijmegen (nl)
Chair:
Dr. Ronal Corbee (dvm)
15.30-16.00
utrecht university (nl)
Clinical, imaging characteristics and long term outcome of dogs with intranasal
meningoencephalocele: a case series
Sarah hanemann*
Multiple thoracolumbar partial lateral corpectomies in 17 dogs
Cristoforo Francesco
ricco*
Comparison of conventional and high definition video telescope assisted ventral
slot decompression for cervical intervertebral disc herniation in 51 dogs
Antonella Gallucci*
Acquisition of involuntary spinal locomotion (spinal walking) in dogs with
irreversible thoraco-lumbar spinal cord lesion: a retrospective study on 81 dogs
dominik Faissler
Dr. Franziska Richter (dvm)
17.15-17.30
university of Leipzig (dui)
Role of therapy with growth factors in the management of pain perception
negative dogs caused by thoracolumbar disk extrusions
Patricia Montoliu
Identification of behavioral states in canine neonates and their influence on
neurological examination
17.30-17.45
)
Dr. Caroline Hahn (dvm
Edinburgh (uK)
Paul Mandigers &
Niklas bergknut
Mushroom, other drugs and smartshops in
Amsterdam and what kind of movements disorders can follow, closing remarks
16.30-16.45
Prof.dr. Dennis O’Brien
(dvm)
university of Missouri (usa)
Prof.dr. Angelika Richter (dvm)
university of Leipzig17.00-17.15
(dui)
17.10-18.00
Venu
Artis
Natu
Plan
Ams
Venu
Nh G
dam
The
nhkr
Venu
Olof
Zeed
Teabreak
Kali Tulle Lazzerini*
16.00-16.15
Prof.dr. Bas Bloem (md)
radboud university 16.15-16.30
(nl)
16.45-17.00
Chair:
12
Platinum sponsor of the
12.15-12.30
ESVN-ECVN Congress
for 2015-2017
Con
The
Mau
1092
The
+31
www
com
Con
Pauw
Alex
6221
The
Cont
Mrs.
31 (0
www
s.pa
Farewell
* young neurologist in training / resident
Thursday 17 September 2015: welcome party
Friday 18 September 2015: congre
st
From 19.00 to 21.00 hours in ArTIS, the famousProceedings
Amsterdam28
Zoo.
20.00
to 01.00 hours.
and after the s
ESVN-ECVNFrom
Congress
- Amsterdam
2015during 13
music. Without registration no admittance! Cost
The Welcome reception will take place in the ‘Koningszaal’.
There are a million reasons
why owners love their dogs
NONE OF THEM ARE
WORTH GIVING UP
invited speakers
Reason 16: Duets are always more fun.
Introducing PEXION® for canine epilepsy.
The first 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.
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 significant 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.
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.
14
PEXION® is a registered trademark of Boehringer Ingelheim Vetmedica GmbH.
© 2015 Boehringer Ingelheim Vetmedica GmbH.
15811
15
There are a million reasons
why owners love their dogs
Epilepsy in children, classification and diagnostics,
when is it epilepsy?
NONE OF THEM ARE
WORTH GIVING UP
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.
Introduction
Nutrition 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).
Reason 125: His nose gets into everything.
Introducing PEXION® for canine epilepsy.
Nutrition induced disorders regarding epilepsy and movement disorders
The first 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.
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 significant 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.
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.
16
PEXION® is a registered trademark of Boehringer Ingelheim Vetmedica GmbH.
© 2015 Boehringer Ingelheim Vetmedica GmbH.
15811
Nutrition 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 epilepsy
The 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,
17
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 disorders
Movement 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.
Brain diet: effects of nutrition on cognition
The 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).
References
1. 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
18
19
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.
Neurobiol 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
1
Department 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
Summary
Movement 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: akineticrigid syndromes, and for the various types of hyperkinetic disorders (myoclonus, chorea, tics, dystonia, and
tremor).
Background
Movement 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
20
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 syndromes
The 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
21
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 syndromes
This category includes myoclonus (together with excessive startle), chorea and tics. Jerky movements
may be seen in isolation or in combination with non-jerky movements.
Myoclonus
Myoclonic 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
22
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 stimulussensitive, 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
Chorea
Chorea 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.
23
Tics
Tics 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 syndromes
This 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.
Tremor
By 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
24
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).
25
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
Dystonia
One 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 epsilonsarcoglycan 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
26
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 disorders
A 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 levels
A 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
27
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 nonneurological 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.
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.
Conclusion
We 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.
Acknowledgement
This clinical approach was handed down to us by the late Prof. David Marsden.
Conflict of interest statement
This 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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2. Dogu,O. et al. Prevalence of essential tremor: door-to-door neurologic exams in Mersin Province, Turkey. Neurology 61,
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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”).
3. Moghal,S., Rajput,A.H., D’Arcy,C., & Rajput,R. Prevalence of movement disorders in elderly community residents.
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7. Litvan,I. et al. Movement Disorders Society Scientific Issues Committee report: SIC Task Force appraisal of clinical diagnostic
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
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28
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9. Caviness,J.N. & Brown,P. Myoclonus: current concepts and recent advances. Lancet Neurol. 3, 598-607 (2004).
10. Shibasaki,H. & Hallett,M. Electrophysiological studies of myoclonus. Muscle Nerve 31, 157-174 (2005).
11. Roze,E. et al. Propriospinal myoclonus revisited: Clinical, neurophysiologic, and neuroradiologic findings. Neurology 72,
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29
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).
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.
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.
Mov Disord. 13 Suppl 3, 2-23 (1998).
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).
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tremor? Arch. Neurol. 63, 1100-1104 (2006).
25. Brown,P. New clinical sign for orthostatic tremor. Lancet 346, 306-307 (1995).
26. Morris,J.G. et al. Athetosis II: the syndrome of mild athetoid cerebral palsy. Mov Disord. 17, 1281-1287 (2002).
27. Geyer,H.L. & Bressman,S.B. The diagnosis of dystonia. Lancet Neurol. 5, 780-790 (2006).
28. van de Warrenburg,B.P. et al. The syndrome of (predominantly cervical) dystonia and cerebellar ataxia: new cases indicate a
distinct but heterogeneous entity. J. Neurol. Neurosurg. Psychiatry 78, 774-775 (2007).
29. Schrag,A., Trimble,M., Quinn,N., & Bhatia,K. The syndrome of fixed dystonia: an evaluation of 103 patients. Brain 127,
2360-2372 (2004).
30. Nahab,F.B., Peckham,E., & Hallett,M. Essential tremor, deceptively simple... Pract. Neurol. 7, 222-233 (2007).
TREMORS
Tremor 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.
31. Stolze,H., Petersen,G., Raethjen,J., Wenzelburger,R., & Deuschl,G. The gait disorder of advanced essential tremor. Brain 124,
2278-2286 (2001).
32. Quinn,N. Multiple system atrophy--the nature of the beast. J. Neurol. Neurosurg. Psychiatry Suppl, 78-89 (1989).
33. Wenning,G.K., Colosimo,C., Geser,F., & Poewe,W. Multiple system atrophy. Lancet Neurol. 3, 93-103 (2004).
34. van Rootselaar,A.F., van Westrum,S.S., Velis,D.N., & Tijssen,M.A. The paroxysmal dyskinesias. Pract. Neurol. 9, 102-109 (2009).
35. Bhatia,K.P. Familial (idiopathic) paroxysmal dyskinesias: an update. Semin. Neurol. 21, 69-74 (2001).
36. Gerrits,M.C. et al. Phenotype-genotype correlation in Dutch patients with myoclonus-dystonia. Neurology 66, 759-761 (2006).
37. Schmitz-Hubsch,T. & Klockgether,T. An update on inherited ataxias. Curr. Neurol. Neurosci. Rep. 8, 310-319 (2008).
38. Cardoso,F., Seppi,K., Mair,K.J., Wenning,G.K., & Poewe,W. Seminar on choreas. Lancet Neurol. 5, 589-602 (2006).
39. Dimutru, Amato,A.A., & Zwarts,M.J. Electrodiagnostic medicine Philadelphia, 2002).
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
30
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 ataxia
Cerebellar 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
31
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.
Parkinsonism
Parkinson’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.
32
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 Dystonia
Parkinsonism 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.
33
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.
Conclusion
The 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.
References
1. Garosi LS, Rossmeisl JH, de LA, et al. Primary orthostatic tremor in Great Danes. Journal of Veterinary Internal Medicine 2005;19:606-609.
2. Guevar J, De Decker S, Van Ham LM, et al. Idiopathic head tremor in English bulldogs. Movement disorders : official journal of the
Movement Disorder Society 2014;29:191-194.
3. Wolf M, Bruehschwein A, Sauter-Louis C, et al. An inherited episodic head tremor syndrome in Doberman pinscher dogs. Movement
Disorders 2011;26:2381-2386.
4. Lohi H, Young EJ, Fitzmaurice SN, et al. Expanded repeat in canine epilepsy. Science 2005;307:81.
5. Awano T, Katz ML, O’Brien DP, et al. A frame shift mutation in canine TPP1 (the ortholog of human CLN2) in a juvenile Dachshund with
neuronal ceroid lipofuscinosis. Molecular Genetics & Metabolism 2006;89:254-260.
6. Gill JL, Capper D, Vanbellinghen JF, et al. Startle disease in Irish wolfhounds associated with a microdeletion in the glycine transporter
GlyT2 gene. NeurobiolDis 2011;43:184-189.
7. Zeng R, Farias FH, Johnson GS, et al. A truncated retrotransposon disrupts the GRM1 coding sequence in Coton de Tulear dogs with
Bandera’s neonatal ataxia. Journal of Veterinary Internal Medicine 2011;25:267-272.
8. Gerber M, Fischer A, Jagannathan V, et al. A Deletion in the VLDLR Gene in Eurasier Dogs with Cerebellar Hypoplasia Resembling
a Dandy-Walker-Like Malformation (DWLM). PLoS One 2015;10:e0108917.
9. Gilliam D, O’Brien DP, Coates JR, et al. A Homozygous KCNJ10 Mutation in Jack Russell Terriers and Related Breeds with Spinocerebellar
Ataxia with Myokymia, Seizures, or Both. Journal of veterinary internal medicine / American College of Veterinary Internal Medicine
2014;28:871-877.
10. Agler C, Nielsen DM, Urkasemsin G, et al. Canine hereditary ataxia in old english sheepdogs and gordon setters is associated with a defect
in the autophagy gene encoding RAB24. PLoS Genet 2014;10:e1003991.
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.
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.
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.
34
35
orals
36
37
EPILEPTOID CRAMPING SYNDROME IN THE NORWICH TERRIER:
clinical characterisATION AND Prevalence in the UK
L De Risio, J Freeman
Neurology 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
38
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 worldwide 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
1
Ontario 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.
39
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
1
Centre 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,
4
Department 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
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
1
Dept. 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.
T.Bouzouraa1, C.Escriou2
1
Internal 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.
40
41
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
1
Davies 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;
4
Department of Pharmacology, UCL School of Pharmacy, London, UK; 5Department of Gastroenterology, Royal
Hallamshire Hospital, Sheffield, UK; 6Powell Torrance Diagnostic Services, Higham Gobion, Hitchin, UK
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.
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
42
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 treatment 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
1
Department 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.
43
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.
Department 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.
1
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 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
1
Neurology, 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.
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.
44
VLDLR-ASSOCIATED CEREBELLAR HYPOPLASIA IN EURASIER DOGS
A. Fischer1, K. Rentmeister2, S. Lindsteding3, F. Bernardino1, E. Manz4
1
Centre 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
45
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 epilepsyspecific 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
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 decisionmaking 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.
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.
46
47
INTERLEUKIN-17 AND CD40 LIGAND IN CANINE STEROID-RESPONSIVE MENINGITISARTERITIS
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.
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 duo
dichromatic 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.
Division 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.
1
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
1
Section of Clinical & Comparative Neuropathology, Centre for Clinical Veterinary Medicine, LudwigMaximilians 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
48
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
49
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
Small Animal Hospital, University of Glasgow, UK, 2Small Animal Teaching Hospital, University of Liverpool,
UK, 3PetMedics, Worsley, Manchester, UK.
1
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
1
Department 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.
50
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 reevaluation 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 postoperative 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.
51
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.
52
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.
53
posters
54
55
EVALUATION OF MAGNETIC RESONANCE
IMAGING GUIDELINES TO DIFFERENTIATE
BETWEEN THORACOLUMBAR NUCLEUS
PULPOSUS EXTRUSIONS AND ANULUS
FIBROSUS PROTRUSIONS IN LARGE
BREED DOGS
S. 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 thoracolumbar nucleus pulposus extrusion (NPE) or anulus
fibrosus protrusion (AFP). Midline intervertebral disk
(IVD) herniation, and partial IVD degeneration were associated with AFP, while presence of a single IVD herniation 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 thoracolumbar 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 experience 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 (κ = 0.27) to moderate (κ =
0.41) after using the proposed guidelines. Diagnostic accuracy 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 imaging 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 hypertonia (hypometria) of thoracic limbs and flexor hypertonia (hypermetria) of pelvic limbs. In some there was
variable nystagmus. After several metres of asymmetric
ataxic gait they would fall to one side, sometimes adopt56
ing a sitting position. Recovery usually occurred in one
to several minutes. As lambs aged, it became more difficult to elicit the episodes of dysfunction and by 6 months
of age they appeared normal.
The disorder was diagnosed as a dominant familial episodic cerebellovestibular ataxia inherited as a dominant
trait, with incomplete penetration of observed clinical signs and variable expressivity. A proportion of affected 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 expressivity, many of the lambs carrying this mutation will survive without showing clinical signs and may enter breeding 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 ENCEPHALITIS
C. 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 despite the presence of neurological clinical signs.
The purpose of the study was to describe MR-Spectroscopy
(MRS) findings of dogs diagnosed with TBE. Inclusion criteria 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 confirmation of TBE with necropsy. 5 dogs were included.
Three dogs did not have any changes in the MRI conventional images. Single voxel spectroscopy was performed
in the region of the thalamus or hippocampus and compared with data previously reported from healthy dogs
using the same MRS technique. All dogs affected with
TBE had abnormal metabolite concentration that included: mild to moderate decrease in N-acetyl aspartate
and creatine peaks, and mild increase in choline and glutamate/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.
STEREOTACTIC IRRADIATION OF STAGE IV
CANINE NASAL TUMORS
M. 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. However, 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 radiotherapy 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 clinical 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 radiation 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 accepted 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 regimen adopted indicate a feasibility and effectiveness in
modified stage IV nasal tumors. The relapse pathways
observed suggest to evaluate alternative adjuvant treatment in dogs treated with stereotactic radiotherapy.
CANINE PERIPHERAL NERVE SHEATH TUMORS:
MAGNETIC RESONANCE AND COMPARISON OF
PALLIATION, SURGERY AND STEREOTACTIC
RADIOTHERAPY
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
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 ratio 1.76) were included, with Labrador retrieveroverrepresented (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 lameness, paresis and pain. Mean duration of clinical signs
was 90 days. MRI findings comprises increased diameter, hyper intense and contrast enhancing nerve roots
(57.1%), plexus or peripheral nerve (42.9%), focal hypomiotropy 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. Comparing 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 SCREWS
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 compression, 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 decompression. During a mean follow up of 36 months,
clinical examination and imaging reveals amelioration of
presenting complaints and reduction of radicular compression, with no surgical complications.
Stop-screws and iliac wings technique are effective
methods to obtain stabilization and indirect decompression of the lumbosacral joint. Comparing with other
described surgical procedures, our obtained results are
better but with lesser complications.
57
COMPUTATIONAL DEVELOPMENT AND
EVALUATION OF A CERVICAL INTERVERTEBRAL
DISC PROSTHESIS IN DOGS BY MEANS OF THE
FINITE ELEMENT METHOD
P.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-associated 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® software after applying extension, lateral and ventral bending 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 ventral 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 between 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 vertebral body, which lowered stress on vertebral endplates.
CHANGES IN INTERICTAL VS. POSTICTAL
DIFFUSION AND PERFUSION MR PARAMETERS
IN FAMILIAL SPONTANEOUS EPILEPTIC CATS
D. 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 hippocampus, as determined by seizure semiology (spontaneous orofacial automatisms and stimulation-induced
generalized seizures), EEG features, and volumetric MRI.
58
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 susceptibility 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 significantly increased.
In conclusion, FSECs have higher diffusion and lower perfusion 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 SIGNS
C.C. Zani1, M.V.B. Arias1, P.V.T. Marinho2, G.A.C. Diamante1.
1
Dept. 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 compression in 30 dogs (24 nonchondrodystrophic, 6 chondrodystrophic) 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-neurological 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 order to perform macroscopic classification of IVD according to Thompson (1990) scheme (I-healthy to V-severe
degeneration).
We observed that 12/30 dogs (40%) presented disc protrusion, and from these, seven (58%) had more than one
(maximum 5) intervertebral disc protrusion. Five dogs
were chondrodystrophic (83%) and seven nonchondrodystrophic (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
(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, being 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 measurement of serum cardiac troponin-I (cTnI) and echocardiography, and to monitor these changes during SRMA
treatment.
SRMA was diagnosed based on typical clinical presentation, blood/urinalysis, cerebral spinal fluid analysis,
and in some cases infectious disease serology and MRI.
Echocardiography was performed in all dogs, where possible prior to starting any anaesthesia, opiate or glucocorticoid 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 detected in 12/14 dogs, including spontaneous echo-contrast (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 NONCOMPRESSIVE NUCLEUS PULPOSUS EXTRUSION
J. 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)
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 noncompressive nucleus pulposus extrusion (ANNPE).
Medical records and MRI studies were reviewed, yielding
93 suitable dogs with an antemortem presumptive diagnosis of IM or ANNPE. Patient signalment, clinical presentation 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 institution, English Staffordshire Bull Terriers were overrepresented 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 hyperaesthesia (47.6%) and a C1-C5 myelopathy (16.7%) compared 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 reduced faecal continence (40.7%), compared to those
with ANNPE (7.7%).
In conclusion, differences were found in clinical presentation 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 faecal 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 treatment (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, proprioceptive deficits, other cranial nerve deficits, and tetraparesis. 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-
59
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 frequently 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 neurological 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 DOGS
A.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 survival of dogs undergoing intracranial surgery. This study
aimed to describe survival and early postoperative outcome 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 glucocorticoids or anti-epileptic drugs and specific imaging,
surgical and anaesthetic variables were evaluated as potential risk factors for survival, occurrence of postoperative 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) survived to discharge and 48% (23/48) experienced a
postoperative complication. Non-neurological postoperative complications were seen in 19% (9/48) of
dogs, with aspiration pneumonia being the most common 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 postoperative complications. Development of non-neurological
complications (P=0.0004) and higher postoperative serum 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 appropriate cases can offer a good outcome for dogs but more
investigation is needed to ascertain long-term survival
times.
60
MAGNETIC RESONANCE FEATURES OF
SUSPECTED LEUKOARAIOSIS IN ELDERLY DOGS
E. 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 welldemarcated sulci have been already described in veterinary 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 welldefined 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 noncontrast-enhancing. Given their topographical distribution 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 narrowing of the vessels lumen, and ultimately reduced blood
flow, is suspected. The pattern of vascularization, which
makes the periventricular white matter an arterial border zone, has been considered responsible for the topographical distribution typical of these lesions.
PREVALENCE AND BREED PREDISPOSITION
OF THORACOLUMBAR INTERVERTEBRAL DISC
DISEASE IN CATS
S. 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 prevalence and possible breed predilections for thoracolumbar 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, duration and severity of clinical signs was also evaluated.
Of 12900 cats presented during the study period, 31
(0.24%) were diagnosed with IVDD, including 17 purebred and 14 non-purebred cats. Of all presented purebred cats, 2.84% were diagnosed with IVDD. More specifically, 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 shorter duration of clinical signs (P=0.0002) and demonstrated more severe neurological deficits (P=0.04) compared
to cats with AFP.
Although IVDD is an uncommon condition in cats, purebred cats, British Shorthairs, and Persians were overrepresented. 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 STUDY
M. 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 canal occupying ratio of the spinal cord (C3-C7) in giant,
large, and small breeds hoping to gain insights regarding 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) representing 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 available 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 discrepancy in prevalence of CSM in small and large breeds.
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 nonaccidental injury (NAI); shaken baby syndrome (SBS) or nonaccidenteal 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 involvement. All of them undergo MR (Esaote 0,25T) which was
revealed as one of the best diagnostic clue to detect animal abuse. MRI is more difficult to perform in acute setting 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 zygomatic arch fracture. The third one presented residual
encephalomalacic lesions and a frontoparietal bone defect. Multi-organ system trauma was also found; rib fractures, 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 human medicine. Making a correct diagnosis could be crucial to the health and welfare of the animals and the family members involved.
RETROSPECTIVE STUDY OF SPINAL
ARACHNOID DIVERTICULUM IN 15 DOGS
DIAGNOSED WITH 3D-CISS MRI
A. 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 number of diagnosed cases is recently growing due to the
increase use of MR imaging and predisposed breed
popularity. SAD are defined as intradural, extramedullary 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 diagnosis 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
61
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 identify 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 imaging using the 3D-CISS sequences confirming the presence of SAD. Male Pugs were over-represented, while
caudal thoracic SAD were outnumbered. Pugs appeared
to be predisposed to multiple SAD located dorsally at C2C3 and thoracic spine. 3D-CISS sequences were beneficial 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
TERRIERS
A. 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-2hydroxyglutarate 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 available for 27 dogs, all with neurological abnormalities.
The mean age of onset of CS was 12 months (range 2.560). 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 changes 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 meningoencephalomyelitis 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 within 12 months.
62
L-2-HGA is considered a progressive neurological disease, 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 DISEASE
V. 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 progressively worsening tetraparesis with a spastic swimming-puppy-like position of the thoracic limbs. One
month later mild vestibular signs and myoclonic jerks
were noticed. Complete blood work, electrophysiological examination and CSF were within normal limits. The
pup was euthanized at the age of 4.5 months and on histopathological examination Alexander’s disease was diagnosed by the detection of GFAP containing Rosenthal
fibers in astrocytes throughout the brain and spinal
cord. From frozen brain tissue, the complete GFAP coding 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 retriever with multifocal central nervous system signs and
characteristic histopathological features of Alexander’s
disease. This is an orthologous mutation to the heterozygous 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
Department 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.
1
Paroxysmal dyskinesias (PD) are central nervous system
disorders characterized by episodes of abnormal involuntary hyperkinetic movement or muscle tone without
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 episodes 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 episode 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 further diagnostic work-up (complete blood work (3 dogs),
MRI brain and CSF analysis (2 dogs), electrophysiological 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
RESULTS
Agnieszka 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 veterinary 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), creatine (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 acquisitions. 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 normal NAA/Cr ratio. The proportions of Cho/Cr were stable
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 application of MRS to determine the lateralization of seizure foci
in canine epileptic patients. NAA may be used as an indicator of neuronal dysfunction during seizures.
RELAPSES IN DOGS WITH STEROIDRESPONSIVE MENINGITIS-ARTERITIS
E. Biedermann1, A. Tipold2, T. Flegel1. 1Dept. of Small
Animal Medicine, University of Leipzig, Leipzig, Germany,
2
Dept. 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) analysis, 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-monthre-evaluation, frequency of breeds.
Between one and four relapses were seen in 32.4% of
dogs whereas 55.4% were relapse free. The relapse status 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 affected by relapses. 3. There was a tendency for higher
CRP levels in serum in dogs with relapse at 3-month-reevaluation.
We conclude that relapses are frequent but there is currently no reliable indicator predicting relapses. Elevated
CRP in serum on re-evaluation, however, warrants continuing therapy.
A MUTATION IN MFSD8 CAUSES NEURONAL
CEROID LIPOFUSCINOSES IN CHIHUAHUA
DOGS
K. M. E. Faller1, J. Bras2, S. Sharpe1, L. Darwent2, C. KunRodrigues2, J. Alroy3, J. Penderis4, S. E. Mole5, R. GutierrezQuintana1*, 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,
63
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 neurodegenerative 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 intracytoplasmic 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 coding or splicing regions of four genes previously identified
as causing NCL (ARSG, CLN2=TPP1, CLN6, CLN7=MFSD8).
Segregation analysis by Sanger sequencing characterised 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 mutation 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 relationship between both breeds. Considering the strong similarity of the clinical presentation and histological changes 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 Beagle
I. 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,
3
Program 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 epilepsy, 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 mutation in the wire-haired dachshunds but a genetic mutation 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 beagle with progressive myoclonic episodes was presented
for neurological examination. We observed mild myo64
clonic movements of the head exacerbated by sudden
sounds. A routine haematology, biochemistry and urinalysis were unremarkable. Magnetic resonance of the
brain and cerebrospinal fluid examination were unremarkable. 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 mutation causing progressive myoclonic epilepsy in a beagle
dog breed. This case report suggests that the similar mutations 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 currently is in neurology training under Dr. Viktor Palus, DVM,
Dipl. ECVN, MRCVS.
EXPRESSION OF Epidermal growth factor
receptor and Ki-67 in canine gliomas
A. Fraser1, B Bacci2, M le Chevoir1, S Long1. 1Translational
Research and Animal Clinical Trial Studies Group.
2
Department of Anatomic Pathology, Faculty of Veterinary
and Agricultural Sciences, The University of Melbourne,
Werribee, Victoria, Australia.
The histologic classification of gliomas can be challenging. In people accurate diagnosis is essential as the treatment 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 therapies 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 immunopositivity was evaluated using a semi-quantitative score
and the Ki-67 LI was calculated.
Thirty-one canine gliomas were evaluated. EGFR expression 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 expression 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 between 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.
IDENTIFICATION OF MOTOR PATTERNS AND
ASSESSMENT OF PRIMITIVE REFLEXES IN
CANINE NEONATES
C. 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,
3
Departament 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 behaviour 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 neurological examination. This is part of a larger study with
the objective to develop a neurological examination
procedure for neonatal dogs. This study obtained ethical 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 primitive reflexes and responses described in previous studies, 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 behavioural states for each item were identified. This work
establishes a basis for standardization of canine neonates 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 aetiology (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.
Medical records were reviewed for dogs diagnosed with
MUA between 2004 and 2015. Previously described inclusion criteria were used, and for all dogs 7-day survival
data needed to be available. A poor outcome was defined 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 seizures were significantly associated with a poor outcome.
Total nucleated cell count in cerebrospinal fluid and lactate levels on venous blood analysis at time of diagnosis
were significantly associated with poor outcome. Age,
sex, neuroanatomical localisation(s), total protein concentration 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 prognostic factors. Presence of seizures and presence of cluster seizures at time of presentation, increased venous
lactate concentrations and a higher total nucleated cell
count in the cerebrospinal fluid are significantly associated 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 anti-epileptic drug in dogs. In human medicine, a clinical
syndrome called “anticonvulsant hypersensitivity syndrome (AHSS) can occur within 1-8 weeks after initiation
of phenobarbital treatment, consisting of a triad of fever,
internal organ involvement (lymphadenopathy, hepatomegaly, 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 necropsy 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 periacinar 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.
65
This is the first case report of suspected AHSS after phenobarbital treatment in a dog and the first description of
the pathological findings. Clinicians should be aware of
this serious and possibly fatal complication. With aggressive 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 medicine, it has been described only twice in veterinary literature.
A 6-year-old crossbreed presented with acute, progressive 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 anaesthesia were uneventful. One day after surgery, the dog
demonstrated slight deterioration, being non-ambulatory 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 associated with marked spinal cord compression. A hyperdense lesion possibly surrounding the gas bubble was
concurrently identified, so the dog was presumptively
diagnosed with an extradural gas bubble and hematoma, causing marked spinal cord compression. Revision
surgery confirmed the presence of a hematoma, which
was removed. The dog gradually improved and was neurologically 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 decompressive spinal surgery. Surgical revision might result
in a good outcome. This is the first case report of postoperative pneumorrhachis after thoracolumbar hemilaminectomy in a dog.
ENDOTHELIN-1 EXPRESSION IN A CANINE
MODEL OF SPINAL CORD INJURY
D. Mayer1,2, A. Oevermann1,3, T. Seuberlich1,3, M. Vandevelde1,2,
A. Casanova-Nakayama4, S. Selimovic-Hamza1,3,D. Henke1,2.
1
Division of Neurological Sciences, 2Department of Clinical
Veterinary Medicine, 3Department of Clinical Research
and Veterinary Public Health, 4Centre for Fish and Wildlife
66
Health, Institute of Animal Pathology, Vetsuisse Faculty,
University of Bern, Switzerland.
The pathophysiology of ascending / descending myelomalacia (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 intramedullary 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 severity of intramedullary haemorrhage or the extension
of myelomalacia.
Endothelin-1 was mainly expressed by astrocytes, macrophages 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 multiple spinal cord segments could help to explain the
pathogenesis of ADMM. However, more effective quantitative techniques and larger case numbers are required
to investigate this further.
EVALUATION OF CEREBROSPINAL FLUID
BIOMARKERS IN PARAPLEGIC DOGS WITH
INTERVERTEBRAL DISC HERNIATION
S.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 current 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.
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 concentrations of tau protein, MIP3b and GFAP could not discriminate 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 LION
J. 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 vestibular 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 comparable 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 thickened 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 conclusion, vitamin A supplementation seems to ameliorate
clinical signs and positively influence bone remodeling
in young lions with hypovitaminosis A.
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 tetraparesis 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 decreased 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 including 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 amplitude 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 cellularity. 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 relapse was reported during the following 6 months.
To our knowledge, this is the first report of distal polyneuropathy 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 resembles the hallmark of CIMM. However, patchy lesion
distribution and preceding treatment may preclude
detection of specific infiltrates on microscopy. Thus immunohistochemical markers have been used to increase
sensitivity and specificity of biopsy studies. Amongst
those MHC-II was evaluated in immune cells. Since myocytes 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 myopathy and 10 dogs with neurogenic muscle atrophy were
67
evaluated immunohistologically for expression of CD3,
CD8, CD20, IBA-1 and MHC-II in immune cells and myocytes, respectively. The expression was scored (all markers) 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% sensitivity 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 DOGS
M. 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 performed 13 days after admission. T2w, FLAIR and diffusion
weighted sequences revealed bilateral symmetrical diffuse and homogneous hyperintensity of the caudate nuclei. ADC mapping showed a hyperintensity of the caudate 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 surrounding 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, hippocampus and cerebellum in T2w and FLAIR images
with restricted diffusion were major findings in the acute
phase. In the chronic phase changes involve predominantly the white matter. Lesions were observed as bilateral, diffuse hyperintense signal changes in T2w and
FLAIR sequences with a restricted diffusion. Cerebellar involvement was observed in the acute and chronic phase.
68
residual disc volumes in chondrodystrophic versus non-chondrodysrophic
dogs with intervertebral disc disease
treated by Assisted mini-hemilaminectomy
F. 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 advocated decompression technique for surgical therapy
of intervertebral disc disease (IVDD) in chondrodystrophic (CDD) and non-chondrodystrophic dogs (NCDD).
However mini-hemilaminectomy (MH) very early has
been shown to preserve better the stability of the vertebral 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 thoracolumbar 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 material 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 decompression 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 STUDY
J. 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 intervertebral disc herniation (IVDH) has been subject to
extensive investigations. Magnetic resonance imaging
(MRI) morphometric measurements such as L2 normalized ratios of compression length (CLR) and T2 weighted
hyperintensities (T2WLR) correlate with severity of clinical signs but do not provide information about func-
tional integrity of the spinal cord. Transcranial magnetic
stimulation (TMS) induces magnetic motor evoked potentials (MMEPs) reflecting spinal cord functional impairment 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 before 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 noted 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 peakto-peak amplitudes whereas onset latency significantly
decreased. CLR and T2WLR were not significantly correlated 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 significance 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 population After limb amputation
M. Menchetti1,2, A. Gallucci2, G. della Rocca3, L. Matiasek4,
K. Matiasek1, F.Gentilini2, G. Gandini2, M. Rosati1. 1Section
of Clinical & Comparative Neuropathology, LudwigMaximilians University, Munich, Germany; 2Department of
Veterinary Medical Science, University of Bologna, Italy;
3
Department 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 prevalence, risk factors and owner´s perception of their pets´
quality of life (QoL).
The 75 questions survey evaluated reasons of amputation, 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 reasons for amputation were cancer (59%) and trauma
(35%). According to the owners´ perception, pain appeared similar before (81%) and after (86%) amputation (p=0.44). Over time, 66% of dogs experienced pain
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 affecting 86% of patients and requiring appropriate treatment. 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 compression
M. 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;
7
North 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 morphological changes of entrapped blood vessels and increase
neuronal VEGF expression in entrapped dorsal root ganglia (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 expression 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-/breedmatched non-compressed DRG.
All entrapped DRG showed significant neuronal positivity for NGB (p<0.0001), CA-IX (p<0.0001), MCT-1 (p<0.0001)
and MCT-4 (p<0.0001). Substantial increase of endothelial 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 immunoreactivity 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 adaptative survival mechanism to hypoxic conditions
through increased neuronal oxygen binding capacity.
A shift towards glycolytic metabolism had been identified through increased expression of CA-IX and of MCTs
meant to prevent intracellular acidosis. The involvement
69
of satellite cells further indicates activation of scavanging 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 EPILEPSY
T. 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;
2
Genefast, 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;
8
Portoni 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; 2536m; >36m) and seizure type (cluster/single and generalized/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 experienced 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 seizure 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 different from BC.
Besides identifying clinical risk factors, the study demonstrates that other polymorphisms may be responsible
for RIE in dogs.
SYNRINGOMYELIA IN THE FRENCH BULLDOG
C. Ricco, F. Samarani, E. Gomes, L. Cauzinille. Centre Hospitalier Vétérinaire Frégis, Arcueil France. AHT Landwades Park
Kentford Newmarket Suffolk CB8 7UU, United Kingdom.
70
Syringomyelia (SM) is a well-recognised spinal cord malformation 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; proprioceptive deficits were a common finding. It is hypothesised
that this prevalence may be higher considering the possible 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 hypertensive encephalopathy
S. 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 characteristic topography and therefore may allow for an imaging 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 seizures on the spatial pattern of pervasive changes in order 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 epileptics, 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, perivascular 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 imaging diagnosis of systemic hypertension.
Altered Expression of an excitatory
tachykinin Neuropeptide in seizure-associated feline hippocampal sclerosis
M. 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;
3
Neurology 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 neurokinin-1 receptor activation evoking neuronal depolarisation and enhancing excitation. During status epilepticus hippocampal expression of SP increases the electrical 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 temporo-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 subregions 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 statistical 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 controls 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 epileptic 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 assist conventional antiepileptic treatments.
ASSOCIATION BETWEEN MRI ASSESSED
DISC DEGENERATION AND RECURRENCE
OF CLINICAL SIGNS FOLLOWING SURGICAL
TREATMENT OF THORACOLUMBAR
INTERVERTEBRAL DISC DISEASE IN DOGS
S. 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 intervertebral discs (IVDs) on survey radiographs and recurrence
of clinical signs following surgery for thoracolumbar intervertebral disc extrusion (IVDE) in dogs has been previously described. MRI is now the imaging modality of
choice in canine IVDE. The aim of this study is to examine
the relationship between MRI-assessed IVD degeneration
and recurrence of clinical signs in surgically treated dogs.
Medical records and MRI-studies of dogs undergoing hemilaminectomy 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 assessed 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 (2.611). 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-surgical 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 outcome, but a significantly higher incidence of recurrence
at an adjacent disk space after a VLS procedure. Inclusion
criteria were complete medical history, advanced diagnostic 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 clinical presentation, affected disk space and degree of spinal
cord compression between the two groups. Dogs undergoing CHL had a lateral or formaninal extrusion more frequently. Surgery time, days on a fentanyl CRI and hospitalization 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 procedures 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 adjacent 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.
71
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, Scotland, 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 mesaticephalic 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. T1weighted sagittal DICOM images of the brain and cervicocervical junction were analysed for five significant traits
(2 angles, 2 lines and a “best fit” occipital lobe circle diameter) 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. Furthermore, the external phenotypes showed that by outcrossing 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 GLUCOCORTICOIDS
M.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 glucocorticoids in patients diagnosed with MUA.
72
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 previously published criteria. Cytosine arabinoside administration 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 infection (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 longterm management of MUA, and it has the potential to
significantly reduce the side effects associated with concomitant 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 frequency 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 studies, 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 intermittently mainly in the second and third weeks of treatment. 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
epilepsy patients are warranted. The studies described
here were approved by the relevant authorities for protection of animals.
USE OF GABAPENTIN FOR NEUROPATHIC
PAIN TREATMENT IN DOGS: A prospective
clinical trial
A. 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 effective 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 effectiveness 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, arterial pressure, blood count, blood levels of cortisol and fructosamine. Two questionnaires (Q1 and Q2) for the assessment 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 progressively 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 DISEASE
A. 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 therapy plan. Frameless magnetic resonance imaging (MRI)guided SBB is becoming the standard of care for imageguided brain biopsy in human medicine, but its diagnostic success has never been investigated in veterinary patients. Therefore, the aim of this prospective study was to
evaluate the diagnostic yield and diagnostic accuracy of
the MRI-guided BrainsightTM frameless stereotactic system 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 performed on the obtained brain biopsy specimen. Brain
necropsy was available for comparison of histopathological 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 (complete 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 accuracy 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 histopathological diagnosis in the majority of patients.
MORPHOLOGY OF THE CAUDAL FOSSA IN
MESATICEPHALIC AND BRACHYCEPHALIC CATS
K. 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 increasingly recognized as a cause of morbidity in many
brachycephalic dogs with round broad heads and shortened facial bones such as Cavalier King Charles Spaniels.
The study objective was to investigate presence of similar 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 structural 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 herniation, area of the cerebellum, length of the forebrain
and cerebellum were also acquired.
After the MRI studies were reviewed they were unblinded 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 foramen magnum was reported in 5/6 cats (83%) of the
brachycephalic group versus 8/16 cats (50% for cerebellar coning) and 3/16 (19% indentation) of the mesaticephalic group.
73
GENETIC EPILEPSY IN CANE CORSO AND
DOGUE DE BORDEAUX
Catherine 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 epilepsy 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 presentation we asked breeders or owners to complete a questionnaire about epilepsy.
We collected 25 epileptic Cane Corso and 5 epileptic
Dogue de Bordeaux.
Cane Corso displayed severe epilepsy with very homogenous presentation appearing during teenage (median
17,5 months) with no sex predisposition. All dogs presented generalized seizures and 91% have systematic
clusters. 30% of dogs are euthanized or deceased from
status epilepticus before 3 years. In 54% of dogs, seizure 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 analysis 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 underlying genetic factors remains questionable.
was euthanized and a pathological examination was
performed. Macroscopic examination revealed a pressure induced atrophy of the brainstem. Histological findings included satelitiosis, mild mononuclear cell infiltration 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 eosinophilic cytoplasm. Few mitoses were visible and within
the stroma areas of necrosis and calcification were visible around one big central necrosis. Imunohistochemistry showed that tumour cells strongly expressed epithelial 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 craniopharyngioma 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.
SEIZURES IN A COATI (NASUA NASUA) WITH
CRANIOPHARYNGIOMA-A CASE REPORT
D.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 Neuropathology, 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, complete blood cell count and biochemistry panel from the
referring veterinarian revealed no abnormalities. Neurological 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 hypointensity and a moderate contrast enhancement was
visible. Differential diagnosis included makroadenoma/
carcinoma of the pituitary gland, germinoma meningioma, lymphoma and craniopharyngioma. The animal
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proceedings-movement-disorders-congres-2015

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