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      Proceedings 29th Symposium ESVN‐ECVN Edinburgh, United Kingdom 16th–17th September 2016

      Journal of Veterinary Internal Medicine
      John Wiley and Sons Inc.

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          Selected research communications of the 29th Symposium of the ESVN‐ECVN Edinburgh, United Kingdom 16th to 17th September 2016 TIMETABLE OF THE SYMPOSIUM Friday 16th September 8.00 Registration APPLIED TRANSLATIONAL NEUROSCIENCE 8.15 Introduction/Welcome 8.30 INVITED SPEAKER SESSION Dominic Wells Stem cells research and Motor Neuron Disease and Amyotrophic Lateral Sclerosis (How basic science has informed change in clinical practice) 9.15 Joan Coates Canine Degenerative Myelopathy and Amyotrophic Lateral Sclerosis (from lab to practice – How basic science changed my understanding and clinical practice) 10.45 Coffee break, poster exhibition and sponsors 11.15 RESEARCH ABSTRACTS (1) Assessing the role of canine and feline ABCG2 as a mediator of pharmacoresistant epilepsy T. Jukier; S. Dassanayake; T. Coffey; A. Chen; K. Mealey (2) Clinical presentation, magnetic resonance imaging findings and outcome of dogs diagnosed with intracranial empyema A. K. Forward, I. N. Plessas, S. De Decker (3) The novel homozygous KCNJ10 c.986T>C (p.Leu329Pro) variant is pathogenic for the sesame/east homologue in malinois dogs K. Stee, M. Van Poucke, S. Bhatti, A. Vanhaesebrouck, L. Bosseler, L. Peelman, L. Van Ham (4) Juvenile polyneuropathy in American Staffordshire Terriers H. Vandenberghe, V. Mayousse, C. Escriou, S. Blot (5) Magnetic resonance elastography – towards a stiffness atlas of the canine brain for translational neurology N.M. Rzechorzek, L. Hiscox, E. Barnhill, S. Hirsch, P. Kennedy, J. Huston, T. Schwarz, I. Sack, S. Semple, K. Marioni‐Henry, N. Roberts (6) Therapeutic potential of ATP precursors in experimental stroke K. Faller, W. Holmes, C. McCabe, I. Macrae, B. Frenguelli (7) Analysis of blood degradation products and ferritin in the cerebrospinal fluid of dogs with acute thoracolumbar intervertebral disc extrusion S. Bittermann, E. Marti, J. Mirkovitch, C. Schild, D. Henke 13.00 Lunch, exhibition and poster session (Posters attended by authors) 14.15 INVITED SPEAKER SESSION Nina Rzechorzek Cold shock ‐ repurposing a single neuroprotective strategy into multiple therapeutic targets 14.45 Natasha Olby How to unravel the riddle of acute spinal cord diseases and novel treatment options (from lab to practice – How basic science changed my understanding and clinical practice) 16.15 Coffee break, poster exhibition and sponsors 16.45 FLASH PRESENTATIONS (F1) A canine brain template for image processing of clinical magnetic resonance imaging data S. Schulze, M.J. Schmidt, T. Flegel, E. Ludewig, M. Gounis, N. Ondreka, J. Boltze and B. Nitzsche (F2) Remote ischemic postconditioning in dogs undergoing elective spinal cord decompressive surgery V. Mortera, N. Granger (F3) Surgical treatment of chronic spinal cord compression in two coatis N. Meyerhoff, M. Fehr, J. Neßler, A. Maiolini, J. Tünsmeyer, P. Dziallas, V. Molnár, C. Ludwig, V. Stein, A. Tipold (F4) Facial nerve paralysis in dogs: a retrospective study of 69 cases C. Ricco, L. Giraud, L. Cauzinille (F5) Magnetic resonance imaging characteristics of cauda equina nerve roots in 50 dogs with degenerative lumbosacral stenosis D. Alder, S. Ohlert, F. Steffen (F6) Syringomyelia classification according to associated magnetic resonance imaging findings in French Bulldogs: 64 cases (2008–2016) A. Suñol Iniesta, M. López‐Font, C. Morales, J. Mascort, M. Manera, P. Montoliu (F7) Pathological circling patterns in dogs with brain lesions diagnosed D. Faissler, L. Grobicki (F8) Application of a functional brain atlas to interpret human epileptic seizure‐related FMRI maps and considerations for application in animals M. Charalambous, L. A. van Graan, A. Liston, L. Lemieux (F9) Species‐specific differences in cellular aggregation and localisation of virally‐transduced mutant and normal canine and equine superoxide dismutase 1 (SOD1) proteins A. Draper, Z. Windley, C. Maile and R.J. Piercy (F10) Intraoperative ultrasound elastography of the canine spinal cord J. Prager, A. Delaney, J. Rose, T. Harcourt‐Brown, D. Chari, N. Granger (F11) Inflamed intracranial meningioma mimicking brain abscess in a dog C. Tästensen, S. Hanemann, M.‐K. Müller, M. Rosati, K. Matiasek, T. Flegel (F12) Overshunting and subdural haemorrhage after implantation of a low‐pressure valve ventriculoperitoneal shunt in a dog with hydrocephalus internus, quadrigeminal cyst and high intracranial pressure S. Hanemann, I. Merseburger, V. Fromme, S. Piesnack, T. Flegel (F13) Cannabinoid receptor type 2 (CB2) expression in canine steroid‐responsive meningitis‐arteritis (SRMA) and intraspinal spirocercosis J. Freundt‐Revilla, F. Heinrich, M.H. Shamir, A. Oevermann, W. Baumgärtner, A. Tipold 17.36 AGM 20.00 Gala Dinner Saturday 17th September 8.00 Registration 8.30 INVITED SPEAKER SESSION Richard Piercy New insights into pathophysiology and treatment of laryngeal paralysis (from lab to practice – How basic science changed my understanding and clinical practice) 9.15 RESEARCH ABSTRACTS (8) The odds of demographic, social and environmental factors influencing the development of acute canine polyradiculoneuritis in the UK E. J. Laws, T. R. Harcourt‐Brown, N. Granger, J. H. Rose (9) Accuracy of a patient‐specific 3D‐printed drill guide for vertebral pedicle screw placement S. Bennett, S. Behr, B. Oxley (10) Clinical features and magnetic resonance imaging findings in 20 cats with confirmed neurological feline infectious peritonitis A. Crawford, A. Stoll, A. Shea, J. Michaels, A. Fraser, E. Beltran 10.00 Coffee break, poster exhibition and sponsors 10.30 RESEARCH ABSTRACTS (11) Safety and efficiency of an increased standardised protocol for the treatment of meningoencephalitis of unknown origin in dogs C. Ricco, L. Cauzinille (12) Genetically modifying canine olfactory ensheathing cells for spinal cord injury repair D. Carwardine, E. Muir, LF. Wong, N. Granger (13) Utility of the electronic von Frey aesthesiometer to quantify cervical skin sensitivity in dogs with syringomyelia H. Williams, S. Sanchis, H.A.Volk, L. Pelligand, J. Murrell, N. Granger (14) Kinematic measures for assessing gait in dogs with Degenerative Myelopathy J. Neeves, L.F. Wong, N. Granger (15) Canine Degenerative Myelopathy associated SOD1 gene mutation (E40K) alters the cellular behaviour and the steady state level of SOD1 protein Y. Qi, P. Montague, I.N.F. Shafie, P.E. Johnston, T.J. Anderson, M. McLaughlin (16) High prevalence of equine polysaccharide storage myopathy in horses with signs suggestive of equine motor neuron disease C. Massey, R.J. Piercy (17) Bovine dorsal root ganglia culture as an in vitro model for listeria monocytogenes brain invasion A. Fadda, M. Bärtschi, H.R. Widmer, A. Zurbriggen, A. Oevermann (18) The dog model of human brain aging and early Alzheimer's disease: a translational study of neuropathological markers T. Schütt, L. Helboe, L.Ø. Pedersen, G. Waldemar, M. Berendt, J.T. Pedersen 12.30 Lunch, exhibition and poster session (Posters attended by authors) 13.45 INVITED SPEAKER Richard Piercy Treatment for neuromuscular disease (How basic science has informed change in clinical practice) 14.25 RESEARCH ABSTRACTS (19) Bidirectional benefits of a naturally occurring canine model for testing and development of drugs for status epilepticus E. Patterson, I. Leppik, L. Coles, J. Cloyd (20) Environment in canine ambulatory electroencephalography F. James, K. Vurik, L. Gaitero, S. Nykamp, J. LaMarre, T. Jokinen, H. Lohi (21) Magnetic resonance (MR) imaging characteristics of histopathologically confirmed non‐functional sellar masses in dogs A. Chen, T. Owen, L Martin, A. Turner, S. Carrera‐Justiz, K. Karnik, D. Bruyette 15.10 Coffee break, poster exhibition and sponsors 15.40 RESEARCH ABSTRACTS (22) Why, when, how and post‐operative care of dogs undergoing transphenoidal hypophysectomy for large sellar masses T. Owen, A. Chen, L. Martin (23) Treatment of canine frontal and olfactory lobe meningioma with either surgical debulking alone, surgery and metronomic chemotherapy or surgery and definitive radiation therapy D. Faissler, T. Bentley, A. Bilderback, A. Sato (24) Paclitaxel releasing mesenchymal stromal cells treatment in canine gliomas O. Zeira, E. Ghezzi, M. Aralla, N. Asiag, M. Konar, A. Pessina, G. Alessandri (25) Evaluation of a modified transfrontal craniotomy technique in 8 dogs R.T. Bentley, S.A. Thomovsky (26) IL‐6 is increased in CSF and plasma of dogs with acute ischaemic stroke H. Gredal, B. Thomsen, A. Boza‐Serrano, L. Garosi, C. Rusbridge, D. Anthony, A. Møller, B. Finsen, T. Deierborg, K. L. Lambertsen, M. Berendt 16.55 Closing comments and competition winner ORAL PRESENTATIONS Assessing the Role of Canine and Feline ABCG2 as a Mediator of Pharmacoresistant Epilepsy T. Jukier 1, S. Dassanayake2, T. Coffey3, A. Chen1, K. Mealey2 1Department of Veterinary Clinical Sciences, Washington State University, Collage of Veterinary Medicine Pullman, Pullman, WA, USA2Program in Individualized Medicine, Washington State University, Collage of Veterinary Medicine Pullman, Pullman, WA, USA3Department of Statistics, Washington State University, Collage of Veterinary Medicine Pullman, Pullman, WA, USA Epilepsy is a chronic condition of recurring unprovoked epileptic seizures. Of the population of idiopathic epileptics, a subset of them fail to respond to medical management. This study investigated whether or not anti‐epileptic drugs (AED) are substrates for canine or feline orthologs of the drug efflux transporter ABCG2. Human embryonic kidney cells (HEK‐293) that had been stably transfected with plasmids containing either canine or feline ABCG2 cDNA were utilized for these experiments. Levetiracetam, phenobarbital, gabapentin, zonisamide, and lamotrigine were the AED evaluated with a flow cytometry‐based competitive transport assay. Mitoxantrone, a classic ABCG2 substrate, is an intrinsically fluorescent molecule. Transfected HEK‐293 cells expressing ABCG2 are expected to extrude mitoxantrone from the cell resulting in low intracellular fluorescence. Addition of another ABCG2 substrate results in competition for ABCG2 transport, decreasing mitoxantrone extrusion and increasing intracellular fluorescence. Analysis was performed separately for each AED with either canine or feline ABCG2‐transfected cells. One‐way ANOVA was used to assess a statistical difference between groups followed by Dunnett's test for comparisons against control. Statistical significance was achieved for one concentration in the canine zonisamide group. Because fluorescence actually decreased, indicating influx rather than efflux, the clinical significance is unknown. Results of this study suggest that ABCG2 does not contribute to pharmacoresistant epilepsy for the evaluated AED. Clinical Presentation, Magnetic Resonance Imaging Findings and Outcome of Dogs Diagnosed with Intracranial Empyema A. K. Forward 1, I. N. Plessas2, S. De Decker1 1Royal Veterinary College, University of London, Hatfield, UK2Davies Veterinary Specialists, Hertfordshire, UK Intracranial empyema is a rare neurological emergency that requires rapid and aggressive intervention. This case series aims to describe the clinical presentation, advanced imaging findings, and short and long term outcomes in dogs with intracranial empyema. Medical records from two referral hospitals were searched and identified dogs diagnosed with intracranial empyema. Inclusion criteria comprised of an MRI consistent with contiguous infection from adjacent structures, a CSF analysis suggestive of empyema or direct visualization of purulent material during intracranial surgery. Ten dogs were included, with a median age of 2 years (range 4 months–12.5 years). All presented as emergencies with 8/10 showing neurological abnormalities and 2/10 with retro‐bulbar swelling and exophthalmos. 6/10 had surgical intervention, 2/10 were medically managed and the remaining 2/10 were euthanised. Typical MRI findings included extra‐axial, T1‐weighted hypo‐ isointense, T2‐weighted hyperintense material with varying degrees of contrast enhancement, with 6/9 showing evidence of contiguous infection from adjacent structures on MRI. 6/10 had culture and sensitivity performed with 2/6 returning Enterococcus and Streptococcus species respectively. The median antimicrobial course length was 6 weeks (range 2–28 weeks). 8/10 survived to discharge, with a median hospitalisation time of 6.5 days (range 4–10 days). 5/8 are still alive at the time of writing (1 lost to follow up; 2 euthanised for other reasons) with all five considered neurologically normal with a successful long term outcome. Whilst intracranial empyema in dogs is a rare condition, excellent outcomes are possible in those cases treated appropriately. The Novel Homozygous KCNJ10 C.986T>C (P.LEU329PRO) Variant is Pathogenic for the Sesame/East HomOLOGUE in Malinois Dogs K. Stee 1, M. Van Poucke2, S. Bhatti1, A. Vanhaesebrouck3, L. Bosseler4, L. Peelman2, L. Van Ham1 1Department of Small Animal Medicine and Clinical Biology, Faculty of Veterinary Medicine, Ghent University, Belgium2Department of Nutrition, Genetics and Ethology, Faculty of Veterinary Medicine, Ghent University, Belgium3Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, UK4Department of Pathology, Bacteriology and Poultry Diseases, Faculty of Veterinary Medicine, Ghent University, Belgium SeSAME (Seizures, Sensorineural deafness, Ataxia, Mental retardation, and Electrolyte imbalance) or EAST (Epilepsy, Ataxia, Sensorineural deafness, Tubulopathy) syndrome is a multisystemic disorder in man. The condition is exclusively caused by homozygous or compound heterozygous variations in the KCNJ10 gene. Here we describe a similar syndrome in the Malinois dog breed. This mutation differs from the already identified KCNJ10 mutation in the Russell group of terriers responsible for spinocerebellar ataxia with myokymia, seizures, or both. Four 4‐month‐old Malinois of 2 unrelated families were presented for an uncoordinated gait since the age of 12 weeks. Neurological examination revealed severe generalized hypermetric ataxia in all dogs, involuntary vermicular muscle twitching (myokymia) triggered by excitement in 2 dogs and epilepsy in 2 dogs. Absent patellar reflexes were noted in all dogs. Complete blood count, serum biochemistry, urinalysis, magnetic resonance imaging of the brain and CSF analysis did not reveal any abnormalities. Electromyography showed neuromyotonic discharges in the clinically affected muscles. Results of motor nerve conduction and repetitive nerve stimulation did not differ from two age‐matched Malinois control dogs, however, brainstem auditory evoked potentials showed disappearance of wave components and mildly prolonged latencies in the affected dogs. Histopathology revealed bilateral myelopathy with predominant axonopathy and myelin vacuolization in the central nervous system. Genetic analysis detected a novel pathogenic KCNJ10 c.986T>C (p.Leu329Pro) variant, which is inherited in an autosomal recessive way. Conclusively, these mutant Malinois dogs may serve as a promising animal model to elucidate the pathogenesis and treatment of this disorder in man. Juvenile Polyneuropathy in American Staffordshire Terriers H. Vandenberghe 1, V. Mayousse1, C. Escriou2, S. Blot1 1Unité de neurologie, ChuvA, Université Paris‐Est, Ecole nationale vétérinaire d'Alfort, Maisons‐Alfort, France2Unité de neurologie, VetAgro‐Sup, Université de Lyon, Campus vétérinaire de Lyon, Marcy L'Etoile, France Inherited juvenile‐onset polyneuropathy with laryngeal paralysis has been reported in several breeds of dogs such as Dalmatian, Alaskan Malamute, Leonberger, Russian Black terrier, Rottweiler and Pyrenean mountain dogs, with a suspected autosomal recessive inheritance pattern. Eight young American Staffordshire Terriers were presented for inspiratory stridor and dyspnoea (7/8), locomotor weakness (8/8) with palmigrade and plantigrade stance (5/8), with an age of onset ranged from two to six months. Neurological evaluation revealed four limbs ataxia with high stepping pelvic limb gait (8/8), limb muscles atrophy (6/8), cutaneous hypoesthesia (5/8) and decreased spinal reflexes (5/8). Laryngeal paralysis was diagnosed during laryngoscopy in seven dogs. Electrophysiological investigations showed abnormal spontaneous electrical activities in the laryngeal muscles (7/8) and appendicular muscles (8/8), marked attenuation of compound muscle action potentials amplitude (8/8), reduced motor nerve conduction velocities (7/8), decreased or absent sensory nerve action potentials (8/8). Muscle biopsies were performed in six cases and histologic analysis was consistent with neurogenic atrophy and intramuscular nerve branches myelinated fiber loss. Fibular nerve biopsy analysis, when performed (four cases), was consistent with chronic and severe extensive nerve fiber loss resulting from axonal degeneration. To the authors’ knowledge, this is the first report of a juvenile‐onset polyneuropathy with laryngeal paralysis in American Staffordshire Terrier. One of the dogs is a backcross and an autosomal recessive mode of inheritance is suspected. If pedigree analysis and genotyping are consistent with this hypothesis, the American Staffordshire Terrier polyneuropathy could be considered as a new spontaneous animal model of inherited axonal neuropathy (Charcot‐Marie‐Tooth disease). Genotyping could lead to the discovery of new genes involved in axonal degeneration. Magnetic Resonance Elastography – Towards a Stiffness Atlas of the Canine Brain for Translational Neurology N. M. Rzechorzek1,2, L. Hiscox3,4, E. Barnhill5, S. Hirsch5, P. Kennedy3, J. Huston6, T. Schwarz7, I. Sack5, S. Semple3, K. Marioni‐Henry1, N. Roberts3 1Neurology/Neurosurgery Service, Hospital for Small Animals, Royal Dick School of Veterinary Studies and Roslin Institute, University of Edinburgh, UK2Centre for Clinical Brain Sciences, University of Edinburgh, UK3Clinical Research Imaging Centre CRIC, Queen's Medical Research Institute, University of Edinburgh, UK4Alzheimer Scotland Dementia Research Centre, University of Edinburgh, UK5Institute of Medical Informatics, Charité, Universtätsmedizin, Berlin6Department of Radiology, Mayo Clinic, Rochester, MN7Diagnostic Imaging Service, Royal Dick School of Veterinary Studies and Roslin Institute, University of Edinburgh, UK Tissue mechanical properties vary over several orders of magnitude in the disease state and elude current veterinary neuroimaging modalities. Magnetic Resonance Elastography (MRE) combines conventional MRI with acoustic wave propagation to generate high‐resolution viscoelasticity or ‘stiffness’ data and is emerging as a valuable, non‐invasive diagnostic tool in human neurology. The purpose of this study was to establish whether MRE could be applied to the canine brain. Post‐mortem brain scans were performed on canines euthanized on welfare grounds with approval of the R(D)SVS Veterinary Ethical Review Committee. A standard cartesian Echo Planar Imaging sequence with additional motion encoding gradients was used for multiple frequency (30–100 Hz) acquisition on a 3T Verio MRI system (Siemens Medical Systems), with vibrations generated by the Resoundant actuator and head pillow (http://resoundant.com/). Raw phase images were analysed with the Elastography Software Pipeline to produce maps of viscoelastic parameters. Our protocol readily propagated waves into the specimens enabling construction of high‐resolution elastograms of the canine brain. Variation in tissue stiffness across different brain regions was observed, as noted in the human brain in vivo. Mean whole brain tissue viscoelasticity ± standard error was 2.99 ± 0.30 kPa (n = 3). This is the first demonstration that acoustic waves can be propagated into the canine brain in situ. Our follow‐on objective is to construct a reference atlas of canine brain stiffness against which to test the sensitivity of MRE for detecting and differentiating age‐related and pathological changes. ‘Virtual palpation’ of the brain with MRE has the potential to revolutionize veterinary neuroimaging. Therapeutic Potential of ATP Precursors in Experimental Stroke K. Faller 1,2, W. Holmes2, C. McCabe2, I. Macrae2, B. Frenguelli3 1School of Veterinary Medicine, College of Medical, Veterinary, and Life Sciences, University of Glasgow, Glasgow, UK2Institute of Neuroscience & Psychology, College of Medicine, Veterinary, and Life Sciences, University of Glasgow, Glasgow, UK3School of Life Sciences, University of Warwick, Coventry, UK Brain damage causes profound and prolonged ATP loss. Prior in vitro studies showed that supplementation of ischaemic brain slices with precursors of ATP synthesis, D‐ribose&Adenine (RibAde), restores ATP levels. We aimed to assess the therapeutic potential of RibAde ± Allopurinol in a rat model of transient focal cerebral ischaemia. Allopurinol should potentiate the effect of RibAde by preserving hypoxanthine, also used in the purine salvage pathway. This study conforms to the UK Animals (Scientific Procedures) Act. Male Wistar rats were randomised to three groups and the investigator was blinded to treatment. After 1‐h transient focal ischaemia, RibAde group received at reperfusion an intravenous infusion of ribose (200 mg/kg/h) and adenine (10 mg/kg/h) over 6 h. RibAde&Allopurinol group also received allopurinol (10 mg/kg, IP). Saline group received intravenous and intraperitoneal injections of saline. Acute ischaemic injury and subsequent infarction were assessed by MRI immediately prior to reperfusion (diffusion weighted imaging) and 7 days after reperfusion (T2‐weighted imaging). Functional outcome was assessed at days 1, 3 and 7 post‐stroke. RibAde ± Allopurinol had no significant side‐effect. A greatest reduction in lesion volume between day 0 and day 7 was observed in the RibAde ± Allopurinol (50 % reduction, n = 8) and RibAde groups (38 %, n = 8) compared to Saline group (18 %, n = 6). This did not achieve statistical significance but was accompanied by a trend for faster functional recovery. This pilot study suggests RibAde&Allopurinol as a potential therapy for stroke. Larger studies are required for confirmation of these preliminary results, before translation as a therapeutic option in clinical settings. Analysis of Blood Degradation Products and Ferritin in the Cerebrospinal Fluid of Dogs with Acute Thoracolumbar Intervertebral Disc Extrusion S. Bittermann 1,2, E. Marti3, J. Mirkovitch3, C. Schild4, D. Henke1,2 1Division of Neurological Sciences, Department of Clinical Veterinary Medicine, Vetsuisse Faculty, University of Bern, Switzerland2Division of Clinical Veterinary Neurology, Department of Clinical Veterinary Medicine, Vetsuisse Faculty, University of Bern, Switzerland3Department of Clinical Research and Veterinary Public Health, Vetsuisse Faculty, University of Berne, Vetsuisse Faculty, University of Bern, Switzerland4Institute of Clinical Chemistry, Inselspital, Bern University Hospital and University of Bern, Switzerland Intervertebral disc extrusion (IVDE) is a common cause of severe spinal cord injury, and an accurate prognosis remains challenging. Hemorrhage in the spinal cord or in the subarachnoidal space may have an important impact on damage of the spinal cord parenchyma and outcome, and thus, may be relevant for the prognosis of dogs with IVDE. Therefore, the aim of the study was to evaluate if blood degradation products and ferritin are measurable in the CSF of dogs with thoracolumbar IVDE, and if there is an association to clinical parameters. Measurements of net oxyhemoglobin absorption (NOA), net bilirubin absorption (NBA) and ferritin concentration were prospectively performed in the CSF of 34 dogs with thoracolumbar IVDE, 21 dogs with idiopathic epilepsy either native (IE) or artificially contaminated with blood (IEc), and 9 dogs with steroid responsive meningitis arteritis (SRMA). The NOA was significantly higher in the IVDE group compared to the IE (P < 0.001) and SRMA (P < 0.001), but not to the IEc group (P = 0.89). The NBA was significantly higher in the IVDE group compared to all control groups (P < 0.001, respectively). Ferritin concentration was significantly higher in the IVDE compared to the IE group (P = 0.03). In dogs with IVDE, there was no association between NOA, NBA and ferritin concentration and severity and duration of clinical signs, and outcome. It is possible to quantify blood degradation products and ferritin in the CSF. However, larger case numbers are needed to evaluate their relevance as prognostic indicator in dogs with thoracolumbar IVDE. The Odds of Demographic, Social and Environmental Factors Influencing the Development of Acute Canine Polyradiculoneuritis in the UK E. J. Laws, T. R. Harcourt‐Brown, N. Granger, J. H. Rose University of Bristol, Bristol, UK Immune‐mediated diseases, in animals and man, have been linked to factors and triggers that contribute to the pathogenesis of disease. The aim of this study was to identify if the development of acute canine polyradiculoneuritis (ACPRN) is associated with recent vaccination, breed, season, rural/urban habitation, sex, neuter status or age. A retrospective case‐control study with conditional logistic regression analysis was performed. Dogs were selected from a referral hospital population in the UK and controls were matched for year of presentation. Forty‐three cases were identified with ACPRN and 86 controls were selected. Jack Russell Terriers (P = 0.003) and West‐Highland White Terriers (P = 0.021) were found to have a significantly greater odds of developing ACPRN compared to ‘other breeds’ in our population of dogs. The odds of developing ACPRN were greater in the autumn (P = 0.043) and winter (P = 0.032) compared to spring. Vaccination, rural/urban habitation, sex, neuter status and age were not found to increase the odds of developing ACPRN. In conclusion breed and season were found to increase the odds of developing ACPRN. This may be important in further understanding the pathogenesis of disease. This may allow identification of triggers or genetics that play a role in ACPRN and allow us to develop breeding programs, avoid triggers or even produce preventative treatments to reduce the prevalence of the disease. Accuracy of a Patient‐Specific 3D‐Printed Drill Guide for Vertebral Pedicle Screw Placement S. Bennett, S. Behr, B. Oxley Department of Neurology and Neurosurgery, Willows Referral Service, Solihull, England The aim of this study was to develop a patient‐specific 3D‐printed drill guide for placement of caudal cervical bicortical pedicle screws as part of the treatment of disc‐associated wobbler syndrome and to validate its accuracy. CT scans of the cervical vertebrae from two patients were acquired. These data were exported to medical image processing software and virtual 3D models of the vertebrae created for processing in computer aided design (CAD) software. This was used to determine the optimal trajectory and size of the pedicle screws. For each patient virtual drill guides were created, 3D‐printed, and used intraoperatively. Locking titanium screws were used to reduce metal artifact on post‐operative CT; screw heads were bonded with polymethylmethacrylate cement to stabilise affected vertebral segments. Post‐operative CT was performed for each patient; the degree of vertebral canal violation was subsequently graded as 0 (no violation), 1 (<2 mm), 2 (2–4 mm) and 3 (>4 mm). For each screw CAD files were analysed to yield a screw‐diameter‐to‐pedicle‐width‐ratio (SDPWR) at the narrowest point of the pedicle; this was expressed as a percentage. A total of 22 screws were placed; 11 screws were 3.5 mm, nine were 2.7 mm and two were 2.4 mm. 20 screws (90.9%) were grade 0, 2 (9.1%) were grade 1 and no screws were grade 2 or 3. This was achieved despite a mean SDPWR of 73.6 % (range 57.9–93.3%). The use of a 3D‐printed patient‐specific drill guide permitted accurate placement of bicortical pedicle screws in the caudal cervical vertebrae. This technique has the potential to improve clinical outcome through increased osteosynthesis strength, reduced surgical time and reduced morbidity. Clinical Features and Magnetic Resonance Imaging Findings in 20 Cats with Confirmed Neurological Feline Infectious Peritonitis A. Crawford1, A. Stoll1, A. Shea2, J. Michaels3, A. Fraser4, E. Beltran1 1Department of Clinical Science and Services, Royal Veterinary College, London, UK2Animal Health Trust, Newmarket, UK3Department of Veterinary Medicine, University of Tennessee, USA4UVet, The University of Melbourne, Victoria, Australia Feline infectious peritonitis (FIP) is the most common infectious central nervous system disease in the cat, and is invariably fatal. Improved means of ante mortem diagnosis are required to facilitate clinical decision‐making. Information regarding the magnetic resonance imaging (MRI) findings in cases of FIP is currently limited, resulting in the need for better descriptions to optimize the use of this imaging modality as a diagnostic tool in suspected cases. The aim of this study was to describe the MRI findings in cases of confirmed neurological FIP. Archived records from 4 institutions were retrospectively reviewed to identify cases with confirmed neurological FIP that had undergone MRI of the brain and/or spinal cord. Signalment, clinical, clinicopathological, histopathological findings and outcome were evaluated. MRI abnormalities were detected in all 20 cases, including periventricular contrast enhancement (17), leptomeningeal contrast enhancement (18), ventriculomegaly (17), syringomyelia (14) and foramen magnum herniation (12). CSF was analysed in 10 cases, all of which demonstrated a marked increase in both total protein and total nucleated cell count. All 20 cases were euthanized due to the grave prognosis. The median survival time from onset of clinical signs to euthanasia was 14 days (range 2–105). Histopathological analysis revealed perivascular pyogranulomatous and/or lymphoplasmacytic infiltrates affecting the leptomeninges in 13 cases, the choroid plexus in 13 cases, periventricular infiltrates in 11, the spinal cord parenchyma in 7 and the brain parenchyma in 3. MRI provides a sensitive means of detecting neurological FIP, particularly in combination with consistent signalment, clinical presentation and CSF analysis. Safety and Efficiency of an Increased Standardised Protocol for the Treatment of Meningoencephalitis of Unknown Origin in Dogs C. Ricco, L. Cauzinille Centre Hospitalier Vétérinaire Frégis, Arcueil France Despite being a common diagnosed disease in veterinary neurology, treatment options in literature for méningo‐encephalo‐myelitis of unknown origin are quite variable and poorly standardised. The use of Cytarabine Arabinoside (CA) (50 mg/m2 at repeated injections) in combination with prednisolone has been previously reported with variable success rates. The aim of the paper was to determine the efficiency and safety of high dosage CA (100 mg/m2) protocol in conjunction with prednisolone and the outcome for dogs according to previously reported variables. These were assessed through a repeated cerebrospinal fluid collection obtained around the 6th CA administration (average – 3, 4 months) after the initiation of protocol, records of survival, relapse rates and side effects. The Chihuahua appeared statistically over‐represented in this study in regard to our regular hospital population. Eighty seven percent of dogs (77/89) were alive by the completion of the protocol, 81% were considered to have a positive outcome and 46% of dogs did not require any further CA administration. Thirty percent of dogs (27/89) relapsed during the protocol period and 15% after its completion. Cerebrospinal fluid analysis did not allow to predict relapse in this study. Dogs with a forebrain lesions and a higher initial dose of glucocorticoids had increased odds of a positive outcome. Brainstem lesions appear to carry a worse outcome. The degree of pleocytosis and protein contents at the first CSF collection was not a prognostic factor of outcome. This (100 mg/m2 SQ for 48 h every 3 weeks, 6 times) protocol of CA appears safe and enabled to reduce faster the initial immumusuppressive dosage of prednisolone with lower risks of heavy side effects and a better short term outcome. Genetically Modifying Canine Olfactory Ensheathing Cells for Spinal Cord Injury Repair D. Carwardine 1, E. Muir3, L. F. Wong2, N. Granger1 1School of Veterinary Sciences, University of Bristol2School of Clinical Sciences, University of Bristol3Department of Physiology, Development and Neuroscience, University of Cambridge A multitude of factors must be overcome following spinal cord injury. Chondroitin sulphate proteoglycans (CSPGs) of the glial scar present a significant block to axonal regeneration. Digestion of CSPGs by the bacterial enzyme chondroitinase ABC (ChABC) leads to axonal regeneration, neuronal plasticity and functional improvement in rodent spinal cord injury models. However, the enzyme degrades within 24–72 h at body temperature, limiting its application. Another therapy for spinal cord repair, the olfactory ensheathing cell (OEC) transplant, has been shown to be beneficial in numerous rodent spinal cord injury paradigms and in naturally occurring spinal cord injury in canine patients. OECs support and guide axonal regeneration across the lesion gap. We have genetically modified canine OECs to produce a mammalian ChABC using a lentiviral vector thereby combining these two promising therapies. We have demonstrated digestion of CSPGs with OECs expressing ChABC in vitro using an enzyme assay and western blotting. In nude rats with dorsal column crush injury, we also observed digestion of CSPGs following transplantation of OECs expressing ChABC. To improve the safety and clinical applicability of the system, we have developed a tetracycline regulated lentiviral vector (Tet‐On) capable of switching ChABC production ‘on’ when oral doxycycline is given to the animal. We have achieved efficient lentiviral transduction of neurons and regulatable digestion of CSPGs in vitro and in vivo with the addition or removal of doxycycline. In conclusion, we have generated a novel cell therapy that we plan to develop further using dogs with naturally occurring spinal cord injury. Utility of the Electronic Von Frey Aesthesiometer to Quantify Cervical Skin Sensitivity in Dogs with Syringomyelia H. Williams 1, S. Sanchis2, H. A. Volk2, L. Pelligand2, J. Murrell1, N. Granger1 1The School of Veterinary Sciences, University of Bristol, Bristol, UK2Queen Mother Veterinary Hospital, The Royal Veterinary College, Hatfield, UK Only 35% of Cavalier King Charles Spaniels (CKCS) with syringomyelia display pain‐associated behaviours, but we suspect that a greater proportion experience pain. An objective means of detecting pain in these dogs is lacking. Electronic von Frey aesthesiometer (eVF) testing consists of applying pressure onto the skin via a plastic tip. The pressure value is displayed electronically. Exceeding a certain pressure, defined as the skin sensitivity threshold, triggers a behavioural response from the dog. We conducted an ethically‐approved, two‐centre prospective observational study to assess whether the eVF could differentiate, based on cervical skin sensitivity threshold, CKCS with: (i) syringomyelia and clinical signs (syringomyelia‐symptomatic – SM‐S); (ii) syringomyelia without clinical signs (syringomyelia‐asymptomatic – SM‐A); and (iii) no syringomyelia (syringomyelia‐free ‐ SM‐F). All dogs had cervical and caudal fossa magnetic resonance imaging. Following acclimatisation, the eVF was applied by an investigator blinded to the eVF display and skin sensitivity threshold recorded at C2 and C4 vertebrae bilaterally (three measures per site) and at the right dorsal metatarsal (RH). Data were analysed with multiple analysis of variance including fixed factors (centre, medication, group) and covariates (RH, age, clinical signs duration). Seventy CKCS were recruited into: SM‐S (37), SM‐A (15), SM‐F (18). No difference in sensitivity was found between groups, except for the RH when analysed as a covariate (P = 0.031) but not post‐hoc as a dependent variable (P = 0.885). Split plot analysis of variance demonstrated differences between cervical sites, independently of syringomyelia group (P < 0.001). In conclusion, eVF assessment of skin sensitivity does not differ significantly by syringomyelia status. Kinematic Measures for Assessing Gait in Dogs with Degenerative Myelopathy J. Neeves 1, L. F. Wong2, N. Granger1 1School of Veterinary Sciences, University of Bristol2School of Clinical Sciences, University of Bristol Canine degenerative myelopathy (DM) is a progressive, adult‐onset, neurodegenerative disease of the spinal cord with features similar to amyotrophic lateral sclerosis (ALS) in humans. Some forms of human ALS / canine DM are associated with mutations of the superoxide dismutase‐1 (SOD1) gene. As such, dogs with DM might serve as a model population to test new therapies for SOD1‐ALS. However, we are lacking objective measures in DM dogs to quantify their locomotor deficits. To fill this gap, we recorded the gait of 10 DM dogs with 3D motion capture technology during treadmill locomotion and quantified pelvic/thoracic limb coordination in each inter‐girdle pair of limbs (described as right and left diagonal coupling intervals) and pelvic limb lateral stability. We compared these to 15 neurologically healthy controls and 10 dogs diagnosed with intervertebral disc herniation. Dogs were diagnosed with MRI and tested for SOD1 mutation. We also sequenced C9orf72, TARDBP, FUS, and VCP genes linked to human ALS. One DM dog was negative for the SOD1 mutation but bore a FUS mutation. Marked kinematic differences were revealed between DM and control dogs for pelvic/thoracic limb coordination (P < 0.001) and pelvic limb lateral stability (P = 0.015). Dogs with DM had significantly greater difference between right and left diagonal coupling intervals (P = 0.046) compared to disc cases. This supported the known clinical finding that DM dogs are usually asymmetrically affected during the course of their disease. These preliminary data altogether provide baseline kinematic measures for DM dogs that might serve as a benchmark for future studies. Canine Degenerative Myelopathy Associated SOD1 Gene Mutation (E40K) Alters the Cellular Behaviour and the Steady State Level of SOD1 Protein Y. Qi1, P. Montague2, I. N. F. Shafie3, P. E. Johnston1, T. J. Anderson1, M. McLaughlin 1 1School of Veterinary Medicine, College of MVLS, University of Glasgow2Institute of Infection, Inflammation & Immunity, College of MVLS, University of Glasgow, Glasgow, Scotland3Faculty of Veterinary Medicine, University Putra Malaysia, Serdang, Malaysia Canine degenerative myelopathy (DM) is a progressive neurological disorder associated with a 118G>A mutation of the SOD1 gene and is inherited in an autosomal recessive manner. The impact of this mutation on the dynamics of the wild type and mutant forms of the SOD1 proteins is largely unknown. Here we investigated the steady state levels of the SOD1 in the thoracic spinal cord of homozygotes. The cellular behaviour of SOD1 proteins was explored using an in vitro transfection system to track the distribution of wild type and mutant SOD1 fusion proteins containing either a Cherry or EGFP fluorescent tag. We report that the spinal cord level of SOD1 is significantly reduced in DM and SOD1 solubility properties are altered. The in vitro studies confirmed the fusion proteins had enzymatic activity using a native gel system. SOD1 aggregates accumulate in cells expressing mutant but not wild type Sod1 cDNA recombinants. Wild type and mutant fusion proteins with different fluorescent tags co‐localise in co‐transfectants suggesting a direct interaction and also form aggregates. This study suggests that the Sod1 mutation affects the turnover dynamics of SOD1 and aggregate formation in vitro. Evidence for a direct association between wild type and the DM mutant forms of SOD1 together with aggregate formation suggests a potential for a toxic mechanisms in the heterozygous scenario. This experimental paradigm will assist in identifying the mechanisms affecting SOD1 dynamics and explain why heterozygotes, in general, do not develop DM. Ethical approval was granted for the collection of tissue. High Prevalence of Equine Polysaccharide Storage Myopathy in Horses with Signs Suggestive of Equine Motor Neuron Disease C. Massey, R. J. Piercy Department Clinical Science and Services, Royal Veterinary College, London, UK Equine motor neuron disease (EMND), a degenerative polyneuropathy, is characterised by an insidious onset of generalised muscle atrophy, and mild elevations in plasma muscle enzyme activities. Affected horses are paretic and present with an ‘elephant on a drum’ stance and intermittent muscle fasciculation. Ante‐mortem, gold standard diagnosis is achieved by biopsy of the sacrocaudalis dorsalis muscle. In this study, we hypothesised that these classic clinical signs are a manifestation of various neuromuscular problems, rather than being specific for EMND. We retrospectively examined muscle biopsy submissions from horses with suspected EMND and compared them with the final diagnosis. Of a total of 85 biopsy samples from horses with possible EMND, 24 had neuropathic histological features, of which EMND was diagnosed in 18 (21%). 28 (33%) had various myopathic features, of which 9 (11%) had polysaccharide storage myopathy (PSSM). 24 (28%) biopsy submissions were considered normal and 9 (11%) had an open diagnosis. Of the 9 PSSM cases, 3 were homozygous for the R309H GYS1 mutation responsible for PSSM1, 2 were heterozygotes, 1 was wild type and therefore diagnosed with PSSM2. Genotyping was unavailable for the remaining 3. This study reveals the high prevalence of primary myopathies in horses suspected to have EMND, in particular of PSSM. It emphasizes the need for additional testing, because the final result would likely influence prognosis and disease management. Bovine Dorsal Root Ganglia Culture as an In Vitro Model for Listeria Monocytogenes Brain Invasion A. Fadda1,2, M. Bärtschi1, H. R. Widmer3, A. Zurbriggen1, A. Oevermann1 1Division of Neurological Sciences, Vetsuisse Faculty, University of Bern, Switzerland2Graduate School for Cellular and Biomedical Sciences, University of Bern, Bern, Switzerland3Neurocenter and Regenerative Neuroscience Cluster, University Hospital and University of Bern, Bern, Switzerland Listeria monocytogenes (LM) causes rhombencephalitis in humans and ruminants associated with high mortality rates. Previous studies indicated that Schwann cells are a port of entry for brain invasion of LM. The aim of this study was to characterize primary dorsal root ganglia (DRG) cultures from calves slaughtered for food consumption and to assess their suitability as a host specific model for LM infection of peripheral nerves and brain invasion. Dissociated DRG cultures consisted of neurons, Schwann cells and satellite cells. Neurons survived for more than 4 weeks. Growth factor (GF) supplementation was not required for neuronal survival but promoted neurite outgrowth and branching. Cultures were susceptible to infection with a LM bovine rhombencephalitis isolate (JF5203) from sequence type 1 (lineage I). Bacterial invasion of DRG cells was similarly efficient as that of cell lines, but replication was lower and reached an early plateau phase. Bacteria showed tropism for Schwann and satellite cells and were rarely observed in neurons and axons. Inactivated bacteria were not internalized indicating that infection of satellite cells involves an active receptor‐mediated invasion mechanism rather than phagocytosis. The isogenic InlA‐deletion mutant of JF5203 was less efficient in invasion than the parental strain JF5203 suggesting that the bacterial virulence factor Inl‐A is involved in satellite cell invasion. DRG cultures from slaughtered calves represent a useful host specific model for the mechanistic study of peripheral nervous system invasion by LM. Results indicate that neurons are not the primary target and are invaded by non‐receptor dependent spread from Schwann/satellite cells. The Dog Model of Human Brain Aging and Early Alzheimer's Diesase: A Translational Study of Neuropathological Markers T. Schütt 1, L. Helboe2, L. Ø. Pedersen2, G. Waldemar3, M. Berendt1, J. T. Pedersen2 1Department of Veterinary Clinical and Animal Sciences, University of Copenhagen, Denmark2Department of Neurodegeneration, H. Lundbeck A/S, Valby, Denmark3Danish Dementia Research Centre, Rigshospitalet, University of Copenhagen, Denmark Canine cognitive dysfunction (CCD) or “canine dementia” is a neurobehavioural syndrome in aged dogs characterized by varying degree of progressive cognitive decline and with certain similarities to the clinical and neuropathological changes associated with Alzheimer's disease (AD) in humans. The present study investigated specific markers of brain pathology related to aging and cognitive dysfunction in dogs and compared these findings to human AD neuropathology. The neuropathological investigations included evaluation of amyloid‐β (Aβ) plaque deposition (including N‐terminally truncated and pyroglutamyl‐modified Aβ) and tau pathology in the prefrontal cortex from fifteen aged dogs with normal cognitive function, mild cognitive impairment or CCD and compared with findings in the prefrontal cortex from two young control dogs and sections from human AD subjects. Cortical Aβ deposition was found to be only of the diffuse subtype as no dense‐core or neuritic plaques were found. The Aβ deposition followed a progressive pattern in four maturation stages. Accumulation of the Aβ peptide was also extensively observed in the vessel walls. Both immunohistochemically and biochemically measured levels of Aβ pathology in the prefrontal cortex showed a consistent positive correlation to age but not to cognitive decline. No evidence of neurofibrillary tau pathology was found. In conclusion, the findings support the senescent dog with spontaneous cognitive dysfunction as a valuable non‐transgenic model for further investigations of the molecular events involved in the neurodegenerative processes associated with aging and early stage AD, especially the Aβ‐related pathology. Bidirectional Benefits of a Naturally Occurring Canine Model for Testing and Development of Drugs for Status Epilepticus E. Patterson 1, I. Leppik2,3, L. Coles2, J. Cloyd2 1University of Minnesota – College of Veterinary Medicine2College of Pharmacy, St. Paul and Minneapolis Minnesota3Department of Neurology – Medical School, St. Paul and Minneapolis Minnesota Compounds for status epilepticus (SE) have exclusively been developed from drugs for chronic therapy. With 20–40% mortality for SE in both people and dogs, there is a need to develop novel drugs with unique properties. The purpose of these studies have been to validate the canine model of SE via RCTs, and to utilize 4–6 research dog with naturally occurring epilepsy to initially test compounds. Pharmacokinetic analysis of IV levetiracetam, and IV fosphenytoin was performed in 4–6 research dogs with modeling simulations that led to RCTs for SE of 30–60 mg/kg of IV levetiracetam and 15 mg/kg phenytoin equivalent of fosphenytoin in 19 and 31 client owned dogs respectively. 10–20 mg/kg of a novel formulation of IV topiramate was studied for pharmacokinetic and EEG pharmacodynamic parameters. The RCT for levetiracetam resulted in a response rate of 56% vs 10% for placebo, and for fosphenytoin of 63% vs 23%. Pharmacokinetic modeling of topiramate indicated that 20 mg/kg IV for dogs not on phenobarbital, and 25–30 mg/kg for dogs on chronic phenobarbital might potentially be effective for SE. EEG analysis during topiramate administration indicated it had similar spectral changes to 0.5 mg/kg IV diazepam. We will be performing similar studies of up to 4 mg/kg IV of allopregnanolone, a novel neurosteroid, over the summer of 2016. In conclusion, pharmacokinetic and EEG pharmacodynamic testing of established drugs validated the utility of the canine model. In addition, in testing novel IV formulations in the canine model, there is hope for new future therapies of SE for both species. Environment in Canine Ambulatory Electroencephalography F. James 1, K. Vurik2, L. Gaitero1, S. Nykamp1, J. LaMarre1, T. Jokinen3, H. Lohi4 1Ontario Veterinary College, University of Guelph, Guelph, Ontario, Canada2Veterinary Neurology Center, Tustin, California, USA3Department of Clinical Veterinary Sciences, University of Helsinki, Helsinki, Finland4Department of Medical Genetics, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland Ambulatory electroencephalography (EEG) is a technique used to diagnose epilepsy in humans. Canine ambulatory EEG involves the application of new wireless, portable video equipment while recording EEG in unsedated dogs. This technology has yet to be evaluated outside the clinical environment. It was hypothesized that recording ambulatory video EEG (vEEG) would be equally achievable in three distinct environments: the intensive care unit (ICU), the neurology examination room, and the home, as measured by physiologic and non‐physiologic artifacts. Six healthy dogs were randomized by modified latin square to undergo 2 h vEEG recording in each of the three environments. Twenty minute vEEG epochs (early, middle, and late) were scored in blinded fashion for artifact. Artifact scores were compared for each environment. Instrumental artifact was significantly different between the home kennel and the neurology examination room (P = 0.044) as well as the ICU (P = 0.008). There was no significant difference found between environments for all other artifacts. Based on these findings, three client‐owned dogs were instrumented and sent home for ambulatory vEEG recording. The first was accompanied home by the researchers where recording was discontinued after the events of interest occurred. The second and third dogs were sent home in the care of their owners and returned after 24 h of recording. One case was found to have had premature termination of recording before 14 h had elapsed due to drained batteries. This proof of concept study highlights the feasibility of in‐home ambulatory vEEG for dogs. Magnetic Resonance (MR) Imaging Characteristics of Histopathologically Confirmed Non‐Functional Sellar Masses in Dogs A. Chen 1, T. Owen1, L. Martin1, A. Turner1, S. Carrera‐Justiz2, K. Karnik2, D. Bruyette2 1Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University, Pullman, Washington2West Los Angeles Animal Hospital, Los Angeles, California Limited information is available regarding the MR imaging characteristics of non‐functional sellar masses. The purpose of this study was to determine whether pituitary adenomas can be distinguished from other sellar masses based on MR imaging characteristics since these tumors carry variable prognosis with treatment. MR images were retrospectively reviewed for ten histologically confirmed non‐functional sellar masses. Histopathology revealed chromophobe pituitary adenomas (n = 4), meningiomas (n = 2), and one each of the following tumor types: pars intermedia adenoma, chromophobe pituitary adenocarcinoma, ependymoma, and craniopharyngioma. All masses were ≥ 2 cm at the largest margin except for 1. All masses were predominately T2 and FLAIR hyperintense with 8/10 masses having some variable intensities within. Both pituitary adenomas and other sellar masses had hemorrhage based on GRE images (7/10). Mild peri‐lesional edema was seen with one pituitary adenoma and the pituitary adenocarcinoma. On T1‐weighted post‐contrast images, all masses were round and discrete and showed moderate to strong contrast enhancement. Bilateral lateral ventricular dilation was seen secondary to one pituitary adenoma and the ependymoma. Fifty percent of non‐functional sellar masses were pituitary adenomas. Pituitary adenomas have similar MR imaging characteristics as other sellar masses. Regardless of histopathology, all sellar masses had a tendency to be large and contained hemorrhage. Sellar masses rarely had concurrent perilesional edema, hydrocephalus, or herniation. Why, When, How and Post‐Operative Care of Dogs Undergoing Transphenoidal Hypophysectomy for Large Sellar Masses T. Owen, A. Chen, L. Martin Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University, Pullman, Washington Sellar‐based masses including pituitary tumors are common in veterinary medicine. Large pituitary masses with a high pituitary/brain (P/B) ratio have historically been difficult to remove and have poorer outcome as compared to tumors with lower P/B ratios. This retrospective and ongoing clinical series is evaluating the intra‐operative complications, post‐operative care and long‐term follow‐up of dogs with large sellar masses. The goal is to assimilate this information into an algorithm to aid in surgical decision‐making. The surgical protocol is based on Meij's original work with the addition of a novel telescope and high‐definition camera for excellent magnification and illumination of the surgical field. Our pituitary team consists of a surgeon, neurosurgeon and critical care specialist which all play an integral part in each aspect of the patient's care. Twenty‐two of 34 dogs (65%) evaluated have a P/B ratio of > 0.70 (normal canine P/B ratio < 0.32) with a mean P/B ratio of 0.95. Preliminary results have been very encouraging with some dogs living greater than 2 and 3 years after surgery, either with complete or incomplete resection of their tumor. Those dogs surviving surgery have improvement in their neurologic status and those with hormonally functional tumors show improvement in their hormonal status. Surgical debulking has been followed with radiation therapy in some dogs with promising results. Median long‐term survival is currently being investigated. Our ongoing evaluation has been encouraging for those dogs with large sellar masses and we have had success removing tumors with a P/B ratio of >0.70. Treatmnent of Canine Frontal and Olfactory Lobe Meningioma with Either Surgical Debulking Alone, Surgery and Metronomic Chemotherapy or Surgery and Definitive Radiation Therapy D. Faissler 1, T. Bentley2, A. Bilderback3, A. Sato1 1Cummings School of Veterinary Medicine at Tufts University, North Grafton, MA, USA2Perdue University, College of Veterinary Medicine, West Lafayette, IL, USA3Long Island Veterinary Specialists, Plainview, NY, USA The goal of this retrospective study was to examine outcome in dogs with frontal lobe meningiomas undergoing transfrontal craniectomy alone (group 1), surgery and metronomic chemotherapy (group 2) or surgery followed by definitive radiation therapy (group 3). In order to examine the influence of tumor location a control group with temporal, parietal, occipital and cerebellar meningiomas treated with surgery alone was enrolled. Criteria of inclusion were access to complete medical history and information of final outcome. Only dogs discharged from the hospital and free of concurrent disease at the time of diagnosis were included. Forty dogs with a median age of 9.9 years were enrolled. Seizures (n = 36) were the most frequent clinical sign. Eight dogs were assigned to group 1, 8 to group 2, and 18 to group 3. The control group included 6 dogs. In group 2 CCNU (n = 3) and hydroxyurea (n = 5) was used. The median total radiation dose was 48 gray. Life‐threatening perisurgical complications (n = 3) included pneumoencephalus, brain herniation and aspiration pneumonia. Two dogs developed histologically proven radiation necrosis. Four dogs are alive, 15 were euthanized for disease progression and 21 for other reasons. Median survival times were the following; Group 1: 9.5 months, group 2: 14.9 months, group 3: 27.6 months and control group: 30.5 months. In frontal lobe meningiomas surgery and radiation therapy have the best survival (P = 0.049) similar to non‐frontal cases treated with surgery alone, most likely due to the more complete tumor removal in this group. Metronomic chemotherapy does not significantly extend survival time. Paclitaxel Releasing Mesenchymal Stromal Cells Treatment in Canine Gliomas O. Zeira 1, E. Ghezzi1, M. Aralla1, N. Asiag1, M. Konar1, A. Pessina2, G. Alessandri3 1San Michele Veterinary Hospital, Tavazzano, Italy2Dept. of Medical Science, University of Milan, Italy3Stroke Unit, Ist. Neurologico Besta, Milan, Italy Mesenchymal stromal cells (MSCs) are able to upload and release drugs. MSCs preloaded by paclitaxel (MSCsPTX) have a strong anti‐tumor activity, both in vitro and in vivo, due to their homing capacity towards the tumor and its microenvironment. Our study evaluates safety, feasibility and efficacy of MSCsPTX as growth inhibitor of canine gliomas. After harvesting bone marrow (BM) from dogs and generating BM‐MSCsPTX, we evaluated, in vitro, their activity on canine gliomas by means of binding the tumoral cells and their anti‐angiogenesis activity. Three dogs with brain gliomas, diagnosed by clinical signs, MRI characteristics and histologic exam, underwent treatment schedule consisting of: day 0‐ MSCsPTX administrated intrathecally; day 5‐temozolomide (100 mg/m² for 5 days every 28 days); day 15‐ MSCsPTX administrated intravenously. Schedule has been repeated for 5 months. Other three dogs were treated with temozolomide only. All patients had no other treatments. Follow‐up included neurologic exam and MRI 3 months after the beginning of treatment. In vitro results showed a considerable killing activity of BM‐MSCsPTX; no adverse effects followed BM‐MSCsPTX administration. Neurologic exams were normal. MRI showed no further tumor development in the first group. The results suggest that BM‐MSCsPTX may be a safe and feasible optional treatment for canine gliomas. Evaluation of a Modified Transfrontal Craniotomy Technique in 8 Dogs R. T. Bentley, S. A. Thomovsky Department of Veterinary Clinical Sciences, Purdue University College of Veterinary Medicine, West Lafayette, IN, USA The study purpose was to evaluate a modified transfrontal surgical approach providing greater rostral cerebral and falcine access. Medical records were searched for dogs undergoing transfrontal craniotomy, and data retrieved regarding signalment, surgical procedure, complications, histopathologic diagnosis and outcome. Patients were predominantly large mixed‐breed dogs, median age 9.5 years (range 3.6–14.3), including 7 spayed females and 1 castrated male. A sagittal saw used to create a diamond‐shaped opening in the frontal sinus. The rostral portion of the diamond was conventional in shape and design. Caudally, the bony opening was enlarged laterally compared to the conventional approach, via exposure enhanced by temporalis elevation. This afforded 68% (95% CI, 42–93%) wider access to the mid‐frontal lobes when pre‐operative imaging was assessed. The procedure was easily combined with rostrotentorial craniectomy (n = 2). Median surgical time was 280 minutes (first 4 cases) or 170 minutes (subsequent 4 cases). Five dogs suffered complications but recovered fully: CSF rhinorrhea, cutaneous infection, subcutaneous emphysema, aspiration pneumonia, prolonged neurological recovery. There was 1 peri‐operative death. Median hospitalization was 6 days. Magnetic resonance imaging confirmed complete resection (n = 5). Diagnoses were meningioma (n = 4), oligodendroglioma (n = 3) and granuloma (n = 1). Euthanasia occurred due to recurrence (n = 2; 9 and 12 months) and unrelated disease (n = 1; 8 months). Four patients remain alive (1–10 months). Median survival (Kaplan‐Meier analysis) was 22 months. A diamond‐shaped opening of the frontal sinus, made wider caudally via elevating temporalis musculature, provides excellent access to the mid‐caudal frontal lobes. Despite short‐term complications, long‐term outcome can be excellent. IL‐6 is Increased in CSF and Plasma of Dogs with Acute Ischaemic Stroke H. Gredal 1, B. Thomsen1, A. Boza‐Serrano2, L. Garosi3, C. Rusbridge4, D. Anthony5, A. Møller6, B. Finsen7, T. Deierborg2, K. L. Lambertsen7,8, M. Berendt1 1Department of Veterinary Clinical and Animal Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg, Denmark2Experimental Neuroinflammation Laboratory, Department of Experimental Medical Science, BMC, Lund University, Lund, Sweden3Davies Veterinary Specialists, Manor Farm Business Park, Higham Gobion, Hitchin, UK4Fitzpatrick Referrals, Halfway Lane, Eashing, Godalming, Surrey, UK5Department of Pharmacology, University of Oxford, Mansfield Road, UK6Centre of Functionally Integrative Neuroscience, Aarhus University, Aarhus C, Denmark7Department of Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, J.B. Winsloewsvej, Odense, Denmark8Department of Neurology, Odense University Hospital, Odense C, Denmark Inflammatory cytokines are potential modulators of infarct progression in acute ischaemic stroke. They are therefore possible targets for new treatment strategies in humans. From a translational research perspective, dogs with spontaneous ischaemic stroke offer an opportunity of studying the cytokine response in a non‐invasive setup, and thus may complement current experimental stroke models. The aim of our study was to investigate cytokine concentrations in plasma and cerebrospinal fluid (CSF) in dogs with acute ischaemic stroke, and to search for correlations between infarct volume and cytokine concentrations. Blood and CSF were collected from dogs less than 72 h after a spontaneous ischaemic stroke. Infarct volumes were estimated on magnetic resonance images. IL‐2, IL‐6, IL‐8, IL‐10 and TNF in plasma, CSF and brain homogenates from the infarct core were measured employing a canine‐specific multiplex immunoassay and compared to healthy control dogs. IL‐6 was significantly increased in plasma (P = 0.04) and CSF (P = 0.04) in stroke dogs compared to healthy controls. The concentrations of other cytokines, such as TNF and IL‐2, were unchanged. Plasma IL‐8 levels correlated significantly with infarct volume (Spearman r = 0.8, P = 0.013). The findings of increased concentrations of IL‐6 in CSF and plasma in dogs compare to previous findings in humans. This suggests that the inflammatory response in dogs with spontaneous stroke resembles that in humans, and that dogs could provide alternative opportunities for studies of the inflammatory processes that accompany stroke. POSTER PRESENTATIONS Canine Peripheral Nerve Sheath Tumors: Clinical Aspects, MRI Findings and Comparision of Palliation Surgery and Stereotactic Radiotherapy M. Dolera 1, L. Malfassi1, S. Marcarini1, S. Pavesi1, G. Mazza1, M. Sala1, N. Carrara1, S. Finesso1, G. Urso1,2 1La Cittadina Fondazione Studi e Ricerche Veterinarie, Romanengo, Italy2Azienda Socio Sanitaria Territoriale di Lodi, Lodi, Italy No updates for canine peripheral nerve sheaths tumor (PNST) appeared in recent literature. The aim of this study was to evaluate the correlation between clinical aspects and MRI findings of tumors involving a major peripheral nerve, plexus or root and to determine the survival time in dogs treated with palliation, surgery or stereotactic radiotherapy (SRT). Records of dogs with PNST evaluated from 2000 to 2014 were reviewed to determine signalment, duration of clinical signs, neurological examination, MRI features, treatment option (palliation, surgery, stereotactic hypo 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. Brain‐Sparing Irradiation of Stage IV Canine Nasal Tumors: A Feasibility Study and First Clinical Experiences M. Dolera, L. Malfassi, S. Pavesi, M. Sala, G. Mazza, S. Marcarini, N. Carrara, S. Finesso La 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 VMAT 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 CT/ MRI examination were performed. Disease control and toxicity effects were evaluated according to RECIST and VRTOG 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 RT 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. Contrast‐Enhancing Extra‐Axial Central Nervous System Masses in Dogs: Magnetic Resonance Imaging Differential Diagnoses for Meningioma R. T. Bentley 1, S. Carrera‐Justiz2, S. A. Thomovsky1 1Department of Veterinary Clinical Sciences, Purdue University College of Veterinary Medicine, West Lafayette, IN, USA2Department of Small Animal Clinical Sciences, University of Florida College of Veterinary Medicine, Gainesville, FL, USA Limited information is available to inform differential diagnoses for meningiomas on canine magnetic resonance imaging (MRI). A retrospective study and a literature review of lesions with similar imaging appearance to meningioma was performed. Inclusion criteria were contrast‐enhancing intra‐dural extra‐parenchymal MRI mass lesions and histologic confirmation. Brain and spinal lesions were eligible. Meningiomas and ventricular lesions were excluded. We investigated radiologic criteria that could aid in differentiating other etiologies from meningiomas. Nineteen cases were retrospectively identified. Brain histological diagnoses included: histiocytic sarcoma (n = 2), granuloma (n = 2), glioma (n = 2), and craniopharyngioma (n = 2). There were single cases of granular cell tumor, hemangioblastoma, hematoma, esthesioneuroblastoma, gliomatosis cerebri and germ cell tumor. Spinal lesions included two intradural‐extramedullary nerve sheath tumors, two nephroblastomas and an undifferentiated sarcoma. Irregular or indistinct margins were useful in discriminating from meningioma. Craniopharyngiomas and germ cell tumors were seen in the sella turcica region only. Otherwise, these lesions could not be readily distinguished from meningioma. Literature review identified 93 cases, highlighting the frequency with which the following lesions are described as contrast‐enhancing extra‐axial masses or preliminarily diagnosed as meningiomas: pituitary adenoma, nerve sheath tumors (trigeminal and spinal), granular cell tumor, lymphoma, glioma, fungal granuloma and histiocytic sarcoma. Sarcoma, metastasis and various sporadic pathologies were rare. Many neoplasms and granulomas can have similar or identical MRI appearance to meningioma. A poorly defined or irregular margin on MRI might decrease the suspicion of meningioma. Differential diagnoses for sella turcica masses should include craniopharyngioma and germ cell tumor. Morphological and Immunohistochemical Study of the Vascular Components in Spontaneous Canine Gliomas F. Fernández‐Flores1, J. Soto1, E. Blasco1,2, M. Pumarola1,2 1Department of Animal Medicine and Surgery, Universitat Autònoma de Barcelona, Barcelona, Spain2Mouse and Comparative pathology Unit UPMiC, Universitat Autònoma de Barcelona, Barcelona, Spain Gliomas are among the most vascularized human solid tumours and are related with their poor prognosis. While neovascularization occurs by vasculogenesis in embryonic stages, angiogenesis is mostly related with adult tissue development. However, there are five different mechanisms by which gliomas achieve neovascularisation: vascular co‐option (CO), angiogenesis, vasculogenesis, vascular mimicry (VM) and glioblastoma endothelial cell transdifferentiation. The objective of this study is to evaluate the neovascularization features of spontaneous canine gliomas. Eighteen spontaneous canine gliomas were retrospectively selected from the databases of the Mouse and Comparative Pathology Unit of the Universitat Autònoma de Barcelona, including 12 anaplastic oligodendrogliomas, 3 oligodendrogliomas and 3 glioblastomas. Vascular features were evaluated by slides stained with Hematoxylin‐Eosin. The immunohistochemical study was performed by a semiquantitative evaluation of representative fields using CD31 as a mature endothelial cell adhesion protein marker and VEGFR‐2 as an angioblast plasmatic membrane receptor cell marker. The morphological study showed that low‐grade gliomas (LGG) mostly display a generalized capillary proliferation and high‐grade gliomas (HGG) mostly contains capillary glomeruloid formations (GC) in peripheral areas. Self‐organization of neoplastic cells with presence of CO mechanisms were present in LGGs while MI was only present in HGGs. No expression of vascular markers was observed in CO or VM areas, confirming that they occur independently of endothelial proliferation. GC showed a variable CD31+/VEGFR‐2+ cells, indicating their high angiogenic potential in HGG. These results are similar than those described in human gliomas indicating that vascular markers are useful for to localize neurogenic areas as therapeutical targets. Clinical Characteristics and Outcome in Dogs Treated with Transsphenoidal Hypophysectomy for Non‐Functional Sellar Masses L. Martin 1, T. Owen1, A. Chen‐Allen1, A. Turner1, S. Carrera‐Justiz2, D. Bruyette2 1Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University, Pullman, Washington, USA2VCA West Los Angeles Animal Hospital, Los Angeles, California, USA Transsphenoidal hypophysectomy (TSH) is an effective therapy for functional pituitary corticotroph adenomas; however, little is known about the clinical presentation and outcome of non‐functional sellar masses following TSH. The purpose of this study was to characterize the clinical features and outcome post‐TSH in dogs with non‐functional sellar masses. Medical records were retrospectively reviewed for historical and neurological findings, histopathological diagnosis, and outcome. Ten dogs had TSH performed as therapy for their non‐functional sellar masses. The Bulldog was the most common breed represented (4 dogs) and all but one breed represented were brachycephalic. Median body weight was 22.5 kg and median age at time of diagnosis was 8.8 years. Six dogs had a history of progressive dullness, 3 dogs had behavior or personality changes, 2 dogs had head or generalized tremors, and 2 dogs had vision loss. Neurologic findings included: dull mentation (7 dogs) with the other 3 dogs reported to be obtunded, delayed or absent conscience proprioception (5 dogs), and ataxia (3 dogs). Histopathology revealed that 4 dogs had chromophobe pituitary adenomas, 2 dogs had meningiomas, and one each of the following tumor types was seen: pars intermedia adenoma, ependymona, craniopharyngioma, and chromophobe pituitary adenocarcinoma. Overall median survival post‐TSH was 232 days (range 0–1190 days). Median survival for dogs with adenomas was 487 days (range 182–1190 days). Non‐functional sellar masses were commonly identified in brachycephalic breeds and dull or obtunded mentation was commonly identified on neurologic examination. TSH may be an effective therapy for dogs with non‐functional pituitary adenomas. Volumetric Modulated ARC Radiotherapy for Canine Trigeminal Nerve Tumors M. Dolera 1, L. Malfassi1, M. Sala1, S. Marcarini1, G. Mazza1, S. Pavesi1, N. Carrara1, C. Bianchi1, L. Corbetta1, S. Finesso1, G. Urso1,2 1La Cittadina Fondazione Studi e Ricerche Veterinarie, Romanengo, Italy2Azienda Socio Sanitaria Territoriale di Lodi, Lodi, Italy Peripheral nerve sheath tumors (PNST) affecting the trigeminal nerve are relatively uncommon in dogs and few literature data regarding the best treatment are available. The aim of this work was to evaluate the feasibility and effectiveness of curative high dose hypo fractionated frameless Volumetric Modulated Arc Radiotherapy (VMAT). The primary endpoints were the recurrence or the progression of the tumor, the death from any cause and the death from the considered disease. A prospectic clinical trial was conducted from February 2010 to December 2013 on client‐owned dogs with presumptive imaging‐based diagnosis of trigeminal PNST. The treatment was performed using a 6 MV linear accelerator equipped with an external beam micro‐multileaf collimator. The plans were computed with Montecarlo algorithm. Overall survival was estimated using the Kaplan–Meier product method. Seven dogs were enrolled and treated with 37 Gy in 5 fx. MRI follow‐up examinations revealed complete response in 1 dog, partial response in 4 dogs, stable disease in 2 dogs as the best treatment results. No major complications occurred. One dog develop disease progression at 483 days and deceased for proven relapse at 523 days. Considering all deaths, mean and median overall survival were, respectively, 609 days (range, 313–952) and 952 days. Comparing the obtained survival with previously published studies, VMAT appears to be safe, effective and offer the best median survival time in dogs suffering from trigeminal PNST. Due to the rarity of intracranial canine PNST, further multi center cooperative trials are advisable. Multislice Computed Tomography for the Detection of Compressive Hydrated Nucleus Pulposus Extrusion in Dogs E. Royaux1, I. Gielen2, K. Kromhout2, E. Van der Vekens2, B. J. G. Broeckx3, L. Van Ham1, V. Martlé 1 1Department of Small Animal Medicine and Clinical Biology, Faculty of Veterinary Medicine, Ghent University, Belgium2Department of Veterinary Medical Imaging and Small Animal Orthopedics, Faculty of Veterinary Medicine, Ghent University, Belgium3Laboratory of Pharmaceutical Biotechnology, Faculty of Pharmaceutical Sciences, Ghent University, Belgium Compressive hydrated nucleus pulposus extrusion (HNPE) is defined as an acute extradural compressive lesion consisting of hydrated nucleus pulposus material, occurring at the level of the associated intervertebral disc in dogs. Magnetic resonance imaging (MRI) is the imaging modality of choice to diagnose HNPE. This study examines the possibility to detect compressive HNPE with computed tomography (CT). A first objective of the study was to determine the capability of CT to detect HNPE and to describe the CT characteristics. The second objective of the study was to determine the sensitivity and specificity of CT to detect HNPE. A retrospective analysis of the clinical and imaging data of dogs diagnosed with compressive HNPE on MRI was performed. Both CT and MR images had to be available to be included. The CT images of MRI confirmed cases were assessed by a non‐blinded image reader to define the CT characteristics. The sensitivity and specificity of CT to detect a cervical HNPE was determined by 2 blinded observers using a control group of dogs with acute type 1 disc disease. HNPE was characterized on CT as a hypodense extradural compressive lesion dorsal to the intervertebral disc space with rim enhancement on postcontrast images. The sensitivity and specificity to detect HNPE with CT was respectively very good (91%) and excellent (100%). CT is a useful technique to detect compressive HNPE in dogs. However, if no clear lesion is identified with CT or if information about intramedullary changes is needed, MRI still needs to be performed. Engineering Canine Olfactory Cell Grafts using Magnetic Particle Mediated Delivery of Therapeutic Genes: Implications for Canine Spinal Injury C. Adams1, A. Delaney1, D. Carwardine2, A. Fernandes1, A. Al‐Shakli1, N. Granger 2, D. Chari1 1Cellular and Neural Engineering Group, Institute of Science and Technology in Medicine, Keele University, Keele, UK2School of Veterinary Sciences, University of Bristol, Bristol, UK A clinical trial in spinal cord injured dogs demonstrated that implantation of autologous canine olfactory mucosa cells (cOMCs) lead to recovery of some motor function. However, not all dogs responded to cOMCs and there was no improvement in long‐tract functionality. One strategy to enhance transplant‐mediated regeneration is genetically engineering cOMCs to release therapeutic biomolecules. To achieve this clinically, magnetic particle (MP) based vectors are emerging as key non‐viral alternatives for genetically engineering therapeutic cell populations. In particular, magnetofection with various magnetic fields has been shown to safely and efficiently transfect a range of neural cells. Here, we optimised MP mediated gene delivery to cOMCs and demonstrated delivery of Brain Derived Neurotrophic Factor (BDNF; shown to promote repair in spinal injury) encoded by the advanced minicircle vector platform. Along with MPs, minicircles have significant advantages for translation compared to conventional plasmids, resulting from bacterial backbone removal. Therefore, they can incorporate larger genes, do not undergo transcription silencing and do not elicit immune responses, leading to higher safety. Under the no‐field condition, 86 ± 0.8% of cells displayed MP uptake and 34.9 ± 2.9% expressed the reporter gene. These values were significantly enhanced by application of all tested magnetic fields to ca. 95% (MP uptake) and 55% (transfection efficiency) whilst maintaining high cOMC viability. Minicircle encoded BDNF was successfully delivered to cOMCs (transfection efficiency of 8.1 ± 0.3%) resulting in a fourfold concentration increase of BDNF in conditioned media (transfected cells versus controls). This is a major refinement of the cOMC therapy now requiring testing in the clinic. Urodynamic Characteristics of Neurogenic Bladder Dysfunction in the Canine Clinical Model of Spinal Cord Injury N. Granger 1, H. Z. Hu2, V. Kichler2, C. Marko2, N. D. Jeffery2 1School of Veterinary Sciences, University of Bristol, Bristol, UK2Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, USA Supra‐sacral spinal cord injury, common following intervertebral disc herniation in dogs, causes dysfunction of urine storage and voiding leading to urinary incontinence and retention. Severe dysfunction of this nature is currently incurable and may lead to serious, even fatal, secondary complications. Our objectives in this study were to characterise lower urinary tract dysfunction in chronic supra‐sacral spinal cord injury in dogs and analyse the relationship of bodyweight, chronicity and severity of injury with bladder compliance, to serve as baseline data for future clinical trials using this natural animal model. After receiving ethical permission, we prospectively recruited dogs as part of randomized clinical trials on treatment for severe chronic (>6 weeks) thoracolumbar spinal cord injury for cystometric evaluation. Relationships of bodyweight, chronicity and severity of injury with compliance were analysed using logistic regression. In 84 dogs, mean bladder capacity was 73% of that expected for bodyweight. 58 dogs (69%) had premature urine leakage. Of 38 dogs in which it was measured, 21 (55%) had unprovoked involuntary detrusor contractions (median = 3 contractions/cystometry – range = 1–11) during bladder filling with bladder pressure reaching a mean of 32.2 cmH2O (range = 10–54 cmH2O). 58/84 dogs had reduced bladder compliance (defined as <12.5 mL/cmH2O) with a median of 5.8 mL/cmH2O (range = 2.8–16.5 mL/cmH2O). Compliance was not associated with bodyweight, chronicity or severity of injury. This population of spinal cord‐injured dogs exhibited many features of lower urinary tract dysfunction also found in injured humans. It constitutes an available model to test putative therapies for abrogating the loss of bladder control caused by severe spinal cord injury. Electrophysiological Evidence of Spinal Cord Plasticity in Dogs with Chronic Severe Spinal Cord Injury N. Granger 1, H. Z. Hu2, N. D. Jeffery2 1School of Veterinary Sciences, University of Bristol, Bristol, UK2Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, USA Estimation of the severity of thoracolumbar spinal cord injury (SCI) following canine intervertebral disc herniation relies on neurological examination. Cases lacking conscious pain perception (CPP) are problematic because: (i) many will recover but predicting an individual's prognosis is not possible; and (ii) assessing CPP is not standardised or truly objective. Having a means of objectively teasing out different severities of SCI within the ‘deep pain negative’ group would be useful. Our objective in this study was to describe the presence/absence of ascending somatosensory evoked potentials (SSEPs) and descending transcranial magnetic motor evoked potentials (TMMEPs) in the chronic phase of SCI in dogs. After receiving ethical permission, we prospectively recruited 82 dogs as part of randomized clinical trials on treatment for severe (lacking CPP) chronic (>6 weeks) thoracolumbar SCI for electrophysiological evaluation under sedation. In 31 dogs in which brain recording was done, SSEPs could be detected over the left cortex in 9 (29%) (latency = 25.5 ± 2.9 ms, amplitude = 0.318 ± 0.196 μV) and over the right cortex in 5 (16%) (latency = 27.9 ± 3.0 ms, amplitude = 0.523 ± 0.323 μV) with 5 dogs having detectable waves bilaterally. In 51 dogs, we attempted to record sensory evoked spinal potentials but no wave could be recorded above the lesion. Of 82 dogs, TMMEPs could be detected in the left pelvic limb in 16 (19%) (latency = 57.4 ± 23.0 ms), in the right pelvic limb in 13 (16%) (latency = 54.0 ± 16.7 ms), and bilaterally in 9 dogs. Dogs lacking CPP can be divided into 2 groups based on the presence/absence of SSEPs/TMMEPs. This distinction might help case selection to test putative therapies for SCI repair. Ultrasonographic Imaging of Atlantoaxial Subluxation in a Pediatric Canine Patient D. W. Hague, A. C. Billhymer, M. E. Howes, L. Underwood, S. Joslyn Veterinary Clinical Medicine Dept., University of Illinois, Urbana, Illinois An 8‐week‐old intact female Chihuahua was evaluated for acute tetraparesis progressing to non‐ambulatory paraparesis. On neurologic examination, the patient was non‐ambulatory tetraparetic with subtle motor and ataxia in the thoracic limbs and mild motor in the pelvic limbs. There was increased extensor tone with normal reflexes in all four limbs. Placing responses were absent in all four limbs and hopping was decreased to absent in all four limbs. The dog demonstrated discomfort over the calvarium and cervical spine. The neuroanatomic localization was to the cervical spine, with or without the involvement of the brain, based on the hyperesthesia. Ultrasound assessment of the cranium ruled out hydrocephalus and was used further to assess the craniocervical junction. A small curvilinear ultrasound probe was applied to the cranial neck and the C1 and C2 vertebrae were visualized in extension and with mild flexion. There was repeatable distraction of these bony landmarks and visualization of the spinal cord revealed kinking at the level of the atlanto‐axial articulation. Radiographs and CT were performed to corroborate the suspected ultrasound diagnosis of atlantoaxial subluxation. The relative safety of this procedure makes it more favorable than traditional radiography that usually requires flexion of the neck and can require general anesthesia. This imaging modality may be limited in its success to very young animals which are skeletally immature. Ultrasound can also potentially provide a more cost‐effective preliminary diagnostic tool prior to pursuing more expensive diagnostics such as CT and MRI. Phenobarbital or Potassium Bromide as an Add‐On Anti‐Epileptic Drug for the Management of Canine Idiopathic Epilepsy Refractory to Imepitoin E. Royaux1, L. Van Ham1, B. Broeckx2, I. Van Soens3, I. Gielen4, D. Deforce2, S. Bhatti1 1Department of Small Animal Medicine and Clinical Biology, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium2Laboratory of Pharmaceutical Biotechnology, Faculty of Pharmaceutical Sciences, Ghent University, Ghent, Belgium3Companion Animal Internal Medicine Section, Faculty of Veterinary Medicine, Liège University, Liège, Belgium and Orion Veterinary Clinic, Noorderwijk, Belgium4Department of Medical Imaging of Domestic Animals and Orthopaedics of Small Animals, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium Imepitoin has recently been registered for the management of dogs with idiopathic epilepsy (IE). Currently, there is no evidence‐based information available on which antiepileptic drug (AED) to add to the treatment of dogs with IE that are not well controlled with imepitoin. The goal of this study was to evaluate the efficacy of phenobarbital (PB) or potassium bromide (KBr) as an add‐on AED for controlling dogs refractory to a maximum dose of imepitoin. The study was performed as a prospective, randomized, controlled clinical trial. The efficacy of PB or KBr was evaluated by comparing monthly seizure frequency (MSF), monthly seizure day frequency (MSDF) and the presence of cluster seizures during a retrospective 2‐month period with a prospective follow‐up period of 6 months. Also the 50% responder rate (RR) was investigated. Twenty‐seven dogs were included in the study, 14 dogs in the PB group and 13 dogs in the KBr group. A significant decrease in median MSF and MSDF was found in the PB group (P = 0.001 and P = 0.001, respectively) and in the KBr group (P = 0.004 and P = 0.003, respectively). Overall, the number of dogs with cluster seizures decreased significantly (P = 0.0005). The RR was 79% vs. 69% in the PB and KBr group, respectively. We conclude that PB or KBr add‐on treatment efficiently decreases median MSF and MSDF in dogs refractory to a maximum dose of imepitoin. Combination therapy was generally well tolerated and resulted in an improvement in seizure management in the majority of the dogs. The MR Volumetric Brain Assessment in Canine Epileptic Patients – A Pilot Study M. Wrzosek, P. Podgórski, P. Drobot, W. Bodys, J. Nicpoń Department of Internal Medicine and Clinic for Horses, Dogs and Cats, Center of Experimental Diagnostics and Innovative Biomedical Technology, The Faculty of Veterinary Medicine, Wrocław University of Environmental and Life Sciences, Poland Canine epilepsy MR imaging is still a diagnostic challenge for veterinary professionals. MR volumetry is technique of non‐invasive volume measurement of the selected anatomical structures, that could allow to determine a possible structural changes in a CNS. Quantitative MR imaging in humans exceeds the findings of visual inspection of clinical MR imaging studies. The aim of the work is to study the canine brains in terms of its volumetric construction designed to demonstrate the possible brain volume changes in canine epileptic patients as a possible model for human patients. The study was carried out on 22 MRI scans (1.5T Ingenia Philips), 13 dogs with diagnosed idiopathic epilepsy (according to IVETF guidelines), 9 normal control. All dogs were patients of the Department of Internal Medicine and Clinic for Horses, Dogs and Cats, Faculty of Veterinary Medicine, Wrocław University of Environmental and Life Sciences, Poland. Analyzed MRI research dimensional sequence were T1‐weighted (sT1W_3D, TE 5.2, TR: 25.0, FOV: 220, layer thickness: 0.8 mm, GAP: −0.4 mm, voxel size: 0.75 × 0.75 × 0.375). The analysis was conducted by using Slicer software (version 4.5.0). A ratio of ventricular system to brain tissue (V‐B) was counted with special reference for white to gray matter (W‐G) comparison. There was a significant difference in a V‐B ratio in between the IE and control groups (respectively 0.0056–0.0153) found, and no difference in the W‐G ratio (0.261–0.232). These preliminary results suggest a possible reduce of the brain volume in epileptic patients with a preservation of the white‐to gray matter ratio. Epilepsy and Compulsive Disorders in Dogs C. Escriou, M. Garrone Unité de neurologie, VetAgro‐Sup, Université de Lyon, Campus vétérinaire de Lyon, Marcy L'Etoile, France There is a long‐recognized association between obsessive–compulsive disorder (OCD) and chronic epilepsy in humans, most notably refractory temporal lobe epilepsy (TLE). In dogs, neurobehavioral comorbidities associated with development of epilepsy have been recently demonstrated. Compulsive disorder (CD) are well described in dogs with breed specific CD like breed specific idiopathic epilepsy. Our aim was to assess the association between CD and idiopathic epilepsy in a comparative design. Fifty dogs diagnosed with idiopathic epilepsy in the neurology unit of a universitary referral center between the 01/01/2010 and the 31/12/2014 were enrolled. All dogs completed tier 1 and tier 2 diagnostic approach proposed by the “international veterinary epilepsy task force”. 100 healthy non‐epileptic dogs (2 healthy dogs (same breed, same age) for one epileptic dog) chosen in the referral center clinical database were enrolled as control. Owners were asked to complete a questionnaire designed to assess the presence or absence of all CD described in dogs during a telephone conversation conducted by always the same investigator. Significant association were found between the CD pacing, head bobbing, self‐biting, face‐ rubbing, self‐licking, inanimate objects aggression, whining, chewing or eating objects, and polyphagia – polydipsia. Head bobbing and inanimate objects aggression was neither reported in control dogs. Although antiepileptic drugs can induce some CD like polyphagia‐polydipsia, our study is the first to assess comorbidities between CD and idiopathic epilepsy in dogs. As some CD remains infrequent behavior, our results probably underestimate their link with idiopathic epilepsy and increasing statistical strength of the study with larger population is mandatory. An Assessment of Neuronal Cell Body and Synaptic Terminal Density in the Spinal Cord and Red Nucleus of Canine Degenerative Myelopathy L. Henderson, P. E. Johnston, L. Stevenson, J. Leach, T. J. Anderson, M. McLaughlin School of Veterinary Medicine, College of MVLS, University of Glasgow Canine degenerative myelopathy (DM) is a late onset disorder characterised by progressive general proprioceptive ataxia and paresis of the pelvic limbs which progresses to affect the thoracic limbs. A missense mutation (118G>A) in the superoxide dismutase 1 gene (Sod 1) is associated with DM but it is unclear how this mutation leads to the disease. The purpose of this study was to determine if pathology in specific anatomical regions could account for clinical features of the disease. Specifically, we investigated whether the accumulation of SOD‐1 in neurons impacted on the density of neuronal cell body and synaptic terminals in the thoracic and cervical regions of the spinal cord and the red nucleus. Immunohistochemistry was performed on paraffin embedded sections from both control and DM cases and staining intensity was quantified using Image J software. SOD1 staining was higher in spinal cord regions of DM dogs compared with controls but the density of neuron cell bodies was comparable. The synaptic density was unchanged in both the thoracic or cervical spinal cord. However, in the red nucleus, SOD1 staining was comparable between control and DM but synaptic density was significantly decreased in DM. In conclusion, the results of this study suggest the accumulation of SOD1 does not alter neuronal density, however it has an impact on synaptic density in the red nucleus, one of the brainstem nuclei involved with motor co‐ordination and may relate to clinical features associated with DM. Ethical approval was granted for use of all tissues in this study. Visualization of Intracranial Vessels in Toy‐Breed Dogs using Three Dimensional Time‐of‐Flight Magnetic Resonance Angiography C. Ishikawa, D. Ito, N. Tanaka, S. Ohta, M. Kitagawa School of Veterinary Medicine, Nihon University, Kanagawa, Japan Accurate visualization of canine intracranial vessels using three dimensional time‐of‐flight magnetic resonance angiography (3D TOF MRA) have been reported, which were evaluated dogs with more than 9 kg. We hypothesize that image quality of intracranial vessels between small‐sized (toy‐breed) dogs and large‐sized dog might be different, as vessels in small‐sized dog would be thinner than those in large‐sized dog. Therefore, the aim of this study was to evaluate image quality of intracranial vessels in small‐sized dogs using 3D TOF MRA. This study was approved by Nihon University Animal Medical Center ethical committee. Five small‐sized dogs (mean body weight 2.8 kg) were enrolled, which were diagnosed as idiopathic epilepsy using 1.5T MRI. A total of 13 intracranial arteries were evaluated on MIP images. For each vessel, image quality was reviewed by three veterinarians, and divided into four categories: excellent, good, fair and poor. Excellent and good were assessed as worth of diagnostic image. Segment of the internal carotid artery in three of five (3/5) dogs and the rostral cerebellar artery in 2/5 dogs were evaluated as fair or poor. Most of remaining vessels was evaluated as excellent or good. In conclusion, segment of intracranial carotid artery and rostral cerebellar artery in small‐sized dogs might not be clearly identified using 1.5T 3D TOF MRA. As they were identified in previous studies using 3T, visualization of them might be affected by not only body size but field strength of MRI. Intracranial vessels in toy‐breed dogs could be evaluated using this method, although further studies are necessary to evaluate about image quality of vessel on 3D TOF MRA. Cerebrospinal Fluid Movement using Magnetic Resonace Spin Labeling in 3 Dogs with Congenital Hedrocephalus N. Tanaka 1,2, D. Ito1, C. Ishikawa1, S. Ohta1, M. Kitagawa1 1School of Veterinary Medicine, Nihon University, Kameino, Fujisawa, Kanagawa, Japan2Grace animal hospital, Ogikubo, Suginamiku, Tokyo, Japan Diagnosis of hydrocephalus is to obtain image observation of the ventriculomegaly. In human, time spatial labeling inversion pulse (time‐SLIP) is used to research about cerebrospinal fluid (CSF) dynamics. In dogs, it is thought that common causes of congenital hydrocephalus are flow obstacles of CSF, but actual CSF dynamics in dogs was not understand. Therefore, we investigate CSF dynamics in dogs with hydrocephalus using time‐SLIP. This study was approved by Nihon University Animal Medical Center ethical committee. Two dogs that diagnosed stenosis/obstruction at outlet of the forth ventricle on conventional MRI and one dog with aqueduct stenosis/obstruction was underwent further images, time‐SLIP. We observed CSF dynamics at the aqueduct and pre‐pontine cisterns on mid‐sagittal brain. In all dogs, CSF flow (one direction movement) was observed in the aqueduct and the pre‐pontine cisterns. It is conceivable that CSF flow in the aqueduct and CSF circulation of outside of the ventricular system would stop when CSF flow in the aqueduct is obstructed completely. However CSF flow was observed in the aqueduct and the pre‐pontine cisterns. Therefore the cause of hydrocephalus might be stenosis of the aqueduct, not obstruction. CSF flow at the pre‐pontine cisterns might be affected in dogs with stenosis/obstruction at outlet of the forth ventricle. Because dilation of the fourth ventricle compress the brain stem and space of the cistern would be getting thinner. But again, CSF flow was observed at both pre‐pontine cistern and aqueduct, this mean the isle of CSF at exit of the fourth ventricle was not closed. CSF flow was visualized by time‐SLIP in all dogs with congenital hydrocephalus. This method might be help for explication of CSF dynamics in hydrocephalus. CSF Aquaporin‐4,‐1 and Interleukin‐6 in Dogs with Naturally Occurring Communicating Internal Hydrocephalus before and after Ventriculoperitoneal Shuntig M. J. Schmidt 1, C. Rummel1, J. Hauer1, M. Kolecka1, N. Ondreka1, V. McClure2, J. Roth3 1Small Animal Clinic Department Of Small Animal Surgery, JL University, Giessen, Germany2Institute for Veterinary Physiology and Biochemistry, Justus‐Liebig‐University, Giessen, Germany3Department of Companion Animal Clinical Studies, Faculty of Veterinary Science, University of Pretoria, Onderstepoort, Republic of South Africa Studies in animal models, in which internal hydrocephalus has been induced by obstructing the cerebrospinal fluid pathways, have documented an up‐regulation of the concentrations of aquaporin‐4 (AQP4) in the brain. In this study, the concentrations of aquaporin‐1 (AQP1), AQP1, AQP4 and Interleukin‐6 (IL‐6) were determined in the CSF of dogs with idiopathic communicating hydrocephalus before and after the reduction of intraventricular volume following ventriculo‐peritoneal shunt (VP‐shunt) treatment. The concentrations of AQP4 and IL‐6 were increased in the cerebrospinal fluid of dogs with hydrocephalus compared to controls. Both parameters significantly decreased after surgical treatment, accompanied by decrease of ventricular size and the clinical recovery of the dogs. AQP1 was not detectable in CSF. Brain AQP4 up‐regulation might be a compensatory response in dogs with hydrocephalus. Future determination of AQP4 at the mRNA and protein level in brain tissue is warranted to substantiate this hypothesis. Sound Localisation in Dogs with Vestibular Disease: A Preliminary Study P. Gardiner, P. Freeman Department of Veterinary Medicine, University of Cambridge, UK Vestibular disease is a common neurological presentation in small animal practice and has many possible aetiologies. An important step in the investigation of vestibular disease is to determine whether the signs are caused by a peripheral or central lesion, as this informs both the prognosis and the most appropriate diagnostic investigations. In human medicine determining whether there is any hearing loss associated with the vestibular signs is part of the initial assessment. This information aids in localisation of the lesion as unilateral deafness is common in peripheral vestibular disease but rare in central disease. Demonstrating unilateral deafness in dogs relies on specialist equipment to investigate brainstem auditory evoked potentials (BAEP), and the equipment required for this is not widely available in first opinion practice. This study used a simple test involving a squeaky toy suitable for use in first opinion practice to demonstrate localisation of sound in dogs. The preliminary component of the study establishes a baseline of responsiveness in 39 healthy dogs with which to compare animals with vestibular disease. It also establishes and validates the test protocol as a practical way of measuring this response to sound. Noise Inducted Hearing Loss in a Police Dog D. W. Hague Veterinary Clinical Medicine Dept., University of Illinois, Urbana, Illinois A 4 year old intact male Belgium Malinois was evaluated for acute hearing loss. The dog was a working police dog involved in a training exercise where a gun was fired five times on his right side. The estimated noise level was approximately 140 decibels. Later that day, the dog was involved in bite work and the handler noted the dog was not responding to verbal commands. He presented three days later for evaluation of hearing. There was no evidence of any abnormalities on neurologic or physical examination. Brainstem auditory evoked response (BAER) testing was performed in both ears with a 70 and 90 decibel click stimulus using a mastoid reference and masking tone in the opposite ear. There was evidence of an absence of waveforms. Based on the history, the patient was diagnosed with a noise‐induced hearing loss. Two weeks later, a repeat BAER test showed evidence of intact waveforms (I‐V) in both ears. The handler reported the dog was responsive to oral commands. This case represents the risk of noise‐induced hearing loss in working dogs. Therefore, hearing protective devices should be considered in working dogs exposed to episodic or chronic loud noises. Autophagy Versus Apoptosis – Myofibre Death in Canine Immune Mediated Myositis (CIMM) M. Rosati, M. Leipig, K. Matiasek Section of Clinical & Comparative Neuropathology, Ludwig‐Maximilians University, Munich, Germany Muscle fibre death in immune‐mediated inflammatory myopathies is poorly understood. MHC‐II myocytic expression in CIMM represents a shift towards an antigen presenting cell phenotype and breaking of immuno‐tolerance. Autophagy can impact the immune response through its role on antigen delivery to the MHC. In order to unravel myofibre death mechanisms we investigated autophagy and apoptosis in CIMM. Thirty four CIMM dogs (11 MMM and 23 PM), 10 dogs with non‐inflammatory myopathy, 10 dogs with neurogenic muscle atrophy and 4 dogs without neuromuscular disorders were evaluated immunohistologically for the expression of MHC‐II, LC3 and Cleaved Caspase‐3 in muscle biopsies. Their expression was semiquantitatively scored and sorted for subcellular distribution (MHC‐II) after which group specific data were obtained according to standard algorithms. CIMM presented with significantly higher (P < 0.05) scores for MHC‐II and LC3 if compared to the other diseases and controls, while Cleaved Caspase‐3 was not expressed by myocytes throughout the groups. There was no difference in MHC‐II and LC3 expression in MMM and PM. No correlation could be found between MHC‐II and LC3 in CIMM. MHC‐II regulation seems to be driven by inflammation rather than be triggered by autophagy with subsequent exposure of self‐antigens to T helper cells. However increased expression of LC3 with activation of macroautophagy might be responsible for sarcopenia in course of CIMM together with direct destruction of myofibres by inflammatory infiltrates. Lack of Cleaved Caspase‐3 expression on the other hand suggests that myocytes do not undergo apoptosis and T‐cells exert their lethal hit by a different mechanism. 1H NMR Cerebrospinal Fluid Profile in Dogs with Polyradiculoneuritis – Case Series M. Musteata 1, A. Nicolescu2, G. Solcan1, C. Deleanu2 1Department of Clinical Sciences – Internal Medicine, Faculty of Veterinary Medicine Iasi, Romania2“Petru Poni” Institute of Macromolecular Chemistry, Romanian Academy, Iasi, Romania The aim of this study was to describe the cerebrospinal fluid (CSF) metabolites identified and quantified by 1H NMR spectroscopy in four dogs with polyradiculoneuritis (PRN). The diagnosis was fixed based on clinical appearance (acute flaccid tetraparesis, dysphonia) and electrodiagnostic tests (positive sharp waves and complex repetitive discharges on EMG, and slow NCS). The CSF samples were harvested from altantoccipital space under general anaesthesia and they were analyzed for proteins and cells. The 1H NMR spectra were recorded from four dogs with PRN and were compared with those obtained from 10 healthy dogs, 13 metabolites being identified and quantified. The data were analyzed with PASW Statistics 18. On routine examination, the CSF samples were characterized by a normal number of cells (<5 cells/μL) with normal or a moderate increase of protein amount (<40 mg/L). Using 1H NMR examination, a decreased concentration of pyruvate (0.058 ± 0.361 nmol/L vs 0.234 ± 0.011 nmol/L, P < 0.001) and myo‐inositol (0.408 ± 0.023 nmol/L vs. 0.499 ± 0.017 nmol/L, P = 0.012) and an increase concentration for glucose (0.467 ± 0.028 nmol/L vs 0.398 ± 0.013 nmol/L, P = 0.03) were observed when compared with normal group. Citrate was found in ¼ dogs and ascorbic acid was absent in all PRN cases. Our results may suggest that in PRN CSF reflects a major alteration in the energetic metabolism of the neurons, similar with those reported in humans’ central nervous system chronic demyelinating diseases. Alpha‐Chloralose Poisoning in a Cat L. Grau‐Roma1, A. Stephens1, A. Wessmann 2, N. Carmichael3, S. de Brot1 1School of Veterinary Medicine and Sciences, University of Nottingham2Pride Veterinary Centre, Neurology3Carmichael Torrance Veterinary Diagnostic Laboratory A 5‐year‐old domestic cat presented with acute onset of ataxia, depressed mentation, hyperaesthesia, hypothermia, and continuous twitching/seizure activity in the morning after having been outside overnight. Despite immediate treatment, the cat progressed within 24 h to a comatose state, opisthotonus and severe miosis unresponsive to light. Given a poor prognosis, euthanasia was elected. Gross findings were disappointing and consisted of a non‐specific lung oedema and congested lungs and spleen. Surprisingly, within the stomach and intestines, fragments of cockshafers were found. Histologic examination confirmed the gross findings and additionally showed evidence of mild brain oedema, but failed to identify a cause for the severe clinical symptoms. In a final attempt to solve the case, a urine sample was tested for toxic substances and it was found to contain a significant amount of alpha‐chloralose. Alpha‐chloralose (AC), a chlorinated acetal derivative of glucose, is used as a rodenticide, avicide and repellent, often in form of hypnotic baits to immobilize and live‐capture pest animals. It is moderately toxic to mammals and fish, and highly toxic to birds. In animals, accidental AC poisoning is only poorly reported. The most common clinical signs are seizures, muscle tremor, hyperaesthesia, hypothermia, salivation, miosis, stupor, coma and ataxia. Coma and hypothermia was more common in cats, whereas salivation, ataxia and hyperthermia was more frequently seen in dogs. AC poisoning in pet animals within Europe or the United States is poorly reported and no case has been described within the UK, as far as the authors are aware. Genome Sequencing Reveals a Splice Donor Site Mutation in the SNX14 Gene Associated with a Novel Cerebellar Cortical Degeneration in the Hungarian Vizsla Dog Breed J. Fenn 1, M. Boursnell2, R. J. Hitti2, C. A. Jenkins2, R. L. Terry3, S. L. Priestnall3, P. J. Kenny1, C. S. Mellersh2, O. P. Forman2 1Department of Clinical Science and Services, Animal Health Trust, Kentford, Newmarket, Suffolk, UK2Kennel Club Genetics Centre, Animal Health Trust, Kentford, Newmarket, Suffolk, UK3Department of Pathology and Pathogen Biology, Royal Veterinary College, Hawkshead Lane, North Mymms, Hertfordshire, UK Cerebellar cortical degeneration (CCD) is a neurodegenerative disease affecting many dog breeds. Typical presentation consists of progressive cerebellar ataxia, with variable onset ages and rates of progression. Causative genes have been identified associated with CCD in several breeds, allowing screening for selective breeding to reduce disease prevalence. There have been no previous reports of CCD in Hungarian Vizslas. Two full‐sibling Hungarian Vizsla puppies from a litter of nine presented with progressive ataxia, starting around three months old. Clinical signs included cerebellar ataxia, truncal sway, intention tremors, absent menace responses and nystagmus in one dog. Routine diagnostic investigations were unremarkable, and magnetic resonance imaging in one dog demonstrated cerebellar atrophy. Euthanasia was elected shortly after the onset of signs. Histopathological examination revealed primary Purkinje neuron loss consistent with CCD. Whole genome sequencing identified a disease‐associated splice donor site variant in the sorting nexin 14 gene (SNX14) as a strong causative candidate. An altered SNX14 splicing pattern was demonstrated by RNA analysis, and no SNX14 protein could be detected in CCD case cerebellum by western blotting. Genetic screening of 133 unaffected Hungarian Vizslas revealed three heterozygotes, supporting the presence of carriers in the wider population. SNX14 is involved in maintaining normal neuronal excitability and synaptic transmission, and a mutation causes autosomal recessive cerebellar ataxia and intellectual disability syndrome in humans. This is the first report of CCD in Hungarian Vizsla dogs and identifies a splice donor site mutation in SNX14 as the likely cause, with an autosomal recessive mode of inheritance suspected. Aspartoacylase Deficiency in a Domestic Cat with Leukodystrophy M. Kohyama 1,2, T. Fujimura3, N. Matsuki4, K. Uchida5, A. Yabuki1, M. Shima‐Sawa1,2, O. Yamato1 1Laboratory of Clinical Pathology, Joint Faculty of Veterinary Medicine, Kagoshima University, Kagoshima, Japan2Research Fellow of Japan Society for the Promotion of Science, Tokyo, Japan3Minnie Animal Hospital, Chiba, Japan4Laboratory of Veterinary Clinical Pathology, the University of Tokyo, Tokyo, Japan5Laboratory of Veterinary Pathology, the University of Tokyo, Tokyo, Japan Aspartoacylase (ASPA) deficiency, also called Canavan disease in humans, is a rare autosomal recessive neurodegenerative disease and is a type of leukodystrophy. The deficiency is caused by mutations in the ASPA gene. Absence of ASPA activity results in accumulation of N‐acetylaspartate (NAA) in the brain, visceral organs, and urine. In animals, naturally occurring ASPA deficiency has not been reported yet. Recently, ASPA deficiency was diagnosed in a domestic cat with leukodystrophy, and a candidate causative mutation was identified in the feline ASPA gene. A 4‐month‐old female domestic cat weighting 1 kg was presented with frequent vomiting, head tremors, and frequent falling due to body imbalance. Magnetic resonance imaging showed T2‐weighted hyperintensity and T1‐weighted hypointensity in the brain stem and cerebellum. Gas chromatography‐mass spectrometry analysis of the urine revealed unusual excretion of NAA, which is indicative of ASPA deficiency. The cat finally died at 7 months of age, and histopathological spongy degeneration was observed in the cerebrum and cerebellar region. Direct sequence analysis identified a homozygous missense mutation in the coding region of the feline ASPA gene. A genotyping survey using real‐time PCR did not detect this mutation in approximately 1,000 domestic cats, thereby suggesting that this mutation is most possibly a causative mutation in this disease. Ethical approval for this study was obtained from the Animal Research Committee at Kagoshima University (approval number VM15041). In conclusion, this is the first report of naturally occurring ASPA deficiency in animals, and the cat represents a model of human Canavan disease. Hypophysitis in a Scottish Terrier with Associated Panhypopituitarism and Hypothalamitis Mimicking a Pituitary Gland Neoplasia M. Oliveira 1, L. Polledo2, J. Adamany2, A. Wessmann1, P. Graham3, M. Dhumeaux2, K. Baiker3 1Department of Neurology and Neurosurgery, Pride Veterinary Centre, Derby, UK2Department of Internal Medicine, Pride Veterinary Centre, Derby, UK3School of Veterinary Medicine and Science, University of Nottingham, UK A 6‐year‐old, neutered male Scottish Terrier was referred for progressive lethargy and anorexia of a week duration. Neurological examination revealed a low head carriage, hind limb ataxia, and decreased bilateral nasal sensation localising the lesion to the forebrain. MRI of the brain revealed a rounded, well‐defined, central mass measuring 12 mm in diameter located dorsally and slightly rostrally to the pituitary fossa. The mass was slightly hyperintense to cortical grey matter on T2W, hypointense on T1W and without T2* signal void. There was a central fusiform enhancement of the mass after contrast administration suggestive of neoplasia. T4 and TSH levels raised the suspicion of secondary hypothyroidism. The cortisol ACTH ratio was < 0.0132 suggestive of primary hypoadrenocorticism. During hospitalisation, the dog developed an acute severe hypernatremia and died. Post mortem examination showed a severe lymphocytic panhypophysitis with extension to the hypothalamus; most lymphocytes were CD3 positive T‐cells. Immunohistochemistry for Neospora caninum antigen was negative. To the authors’ knowledge, a lymphocytic panhypophysitis with extension to the hypothalamus has never been reported. Hypothalamic involvement in autoimmune hypophysitis has rarely been described in people and usually manifests with central Diabetes Insipidus as suspected in our case due to the sudden onset of severe hypernatremia. This is the first MRI description of autoimmune hypophysitis in a dog. Like in humans, the clinical and MRI findings can be difficult to differentiate from other more common pituitary masses. Therefore, transphenoidal biopsies may be required for conclusive histopathological diagnosis and prompt institution of adequate treatment. Computer Tomography (CT) Guided Drainage of a Brainstem Abscess in a Cat as a Life Saving Procedure E. Bersan, T. W. Maddox, G. Walmsley, R. Burrow School of Veterinary Sciences, University of Liverpool, Small Animal Teaching Hospital, Neston, UK A 3‐year‐old male neutered domestic short haired cat was presented with progressive lethargy and abnormal behaviour. Clinical exam found cardiovascular signs suggestive of raised intracranial pressure. Neurological examination found obtunded mentation, non‐ambulatory tetraparesis with left sided pleurothotonus and intermittent decerebellate rigidity. The postural responses were reduced in all four limbs, worse on the right. Cranial nerve evaluation found absent menace response and reduced facial sensation on the right, vertical positional nystagmus, anisocoria (right sided mydriasis) and an absent pupillary constriction on the right in response to direct and indirect PLR. Neurolocalisation was to multifocal lesions involving the right brainstem and forebrain. Magnetic resonance imaging of the brain revealed a large, well‐defined, predominantly fluid‐filled extra‐axial mass causing severe dorsal displacement of the pons and the medulla oblongata and cerebellar vermis herniation through the foramen magnum. These findings were most consistent with an intracranial abscess. Emergency CT‐guided needle drainage of the space‐occupying lesion was performed through the soft palate and basioccipital bone. Bacteriology revealed heavy growth of Arcanobacterium haemolithicum and mixed growth of pleomorphic, mainly Gram‐negative rods (Cl.hastiforme, Cl.Septicum, Cl.perfringens and Treponema/Serpulina spp). At discharge the cat had normal mentation and mild ambulatory tetraparesis. Broad‐spectrum antibiotics based on culture and sensitivity were continued for 8 months and repeat imaging prior to withdrawal found complete resolution. Follow‐up examination 16 months later found only mild right sided postural reaction deficits that did not affect quality of life. CT guided drainage of a brainstem abscess is not without risk however in this case it reduced intracranial pressure and provided a diagnostic sample. Evaluation of the Proprioceptive Positioning Response and Patellar Tendon Reflex in Dogs with no Neurological Clinical Signs E. Daniell 1, S. Gomes1, A. Jeandel2, P. Freeman1 1The Queen's Veterinary School Hospital, Department of Veterinary Medicine, University of Cambridge, UK2Davies Veterinary Specialists, Hitchin, UK The proprioceptive positioning response (PPR) and patellar tendon reflex (PTR) are clinical tests commonly used to assess and localise neurological conditions in dogs. The primary aim of this study was to investigate the specificity of these tests by evaluating test outcomes in the hindlimbs of a population of dogs showing no overt signs of neurological disease. The secondary aim was to investigate the influence of age on these tests. Twenty‐nine dogs without evidence of neurological or hindlimb orthopaedic disease were selected and divided into two groups: A (<10 years‐old, n = 20) and B (≥10 years‐old, n = 9). A European Specialist in Veterinary Neurology, blinded to the age of the dogs, performed the tests. The PTR was considered normal in all of the study population, while the PPR was abnormal in 17% of the dogs. The proportion of dogs with an abnormal PPR in one or more hindlimb was 10% in group A and 33% in group B; this difference was not statistically significant (P = 0.29). Only dogs in group B had bilateral PPR deficits (22%), but this difference between groups was not statistically significant (P = 0.089). The finding that some dogs had PPR deficits despite having no overt neurological disease has implications for neurological examination interpretation: deficits should be interpreted with caution. There was no statistically significant difference in the proportion of PPR deficits between the two age groups. The PTR was normal in all cases, suggesting a lower prevalence of absent patellar reflexes in the general population than recorded in previously published literature. Species‐Specific Differences in Cellular Aggregation and Localisation of Virally‐Transduced Mutant and Normal Canine and Equine Superoxide Dismutase 1 (SOD1) Proteins A. Draper, Z. Windley, C. Maile, R. J. Piercy Department of Clinical Science and Services, Royal Veterinary College, London, UK Canine Degenerative Myelopathy (DM) is associated with a substitution mutation of a glutamic acid (E) to lysine (K) residue in SOD1 (E40K) which increases its tendency to aggregate in cells. E40 is highly conserved across mammalian species with the exception of horses, which naturally express a K residue. We hypothesised that normal horse SOD‐1 has the same tendency to aggregate as mutant DM‐affected dog SOD1 in contrast to its E40 counterpart. cDNAs from wild‐type (E40) and mutant (K40) canine SOD1 and wild‐type (K40) equine SOD1 were amplified by PCR and cloned with N‐terminal GFP‐tags. PCR‐mutagenesis was used to create an equivalent equine E40 SOD1 variant. Inserts were sub‐cloned and transduced, alongside a GFP‐only vector as lentiviral particles into human neuroblastoma cells (SHSY‐5Y). Aggregates (nuclear or cytosolic) were quantified following fluorescence microscopy, in a blinded fashion (n = 3 coverslips per variant, on 3 separate occasions; minimum of 1500 cells counted per condition). There were significantly more cytoplasmic SOD1 aggregates in the GFP‐mutant dog SOD1 expressing cells (mean %±SEM; 23%±5), compared to the wild‐type dog (6.7%±1.3) or GFP‐only vector (1.7%±0.5) (P < 0.05); there were significantly more nuclear aggregates in both GFP‐horse SOD‐1 variants (K40: 50.4%±5.2, E40: 68.1%±4.9) compared to the GFP‐only vector (8.2%±1.2) (P < 0.05). These results suggest that there are species‐differences in vitro in the tendency of mutant and normal SOD1 proteins to aggregate and localise. Cognitive Deficits and Pathological Features of Cerebral Amyloid Angiopathy in 27 Elderly Dogs R. A. Marcasso1, J. R. Moreira2, M. V. Bahr Arias 3, A. P. F. R. L. Bracarense2 1Laboratory of Animal Pathology, UNOPAR, Arapongas, Paraná, Brazil2Laboratory of Animal Pathology, Universidade Estadual de Londrina, Paraná, Brazil3Department of Veterinary Clinics, Universidade Estadual de Londrina, Paraná, Brazil Cerebral amyloid angiopathy (CAA) is defined as the deposition of beta amyloid proteins within leptomeningeal and cortical vessels, being associated to Alzheimer disease and canine cognitive disease. This study aimed to evaluate in elderly dogs the association between cerebral amyloid deposition and pathologic lesions in the development and clinical manifestation of cerebral dysfunction. Local ethical permission was obtained for this study. Gross evaluation of 44 brains of elderly dogs revealed cortical atrophy and ventricular widening in 22.7% (10/44) specimens. Congo red stain was utilized to classify the 61.4% (27/44) positive dogs (9–19 years old, mean 13.9 years old) to CAA. CAA were graded in mild (13/27 dogs), moderate (3/27 dogs) and severe (11/27 dogs). In all groups the most common clinical sign was disorientation. By the immunohistochemistry using polyclonal anti‐beta amyloid 1–42 antibody, the average of positive vessels to beta‐amyloid increased with age. Association of cortical atrophy, neuron loss and micro hemorrhages contribute to the developing of cognitive deficits. The consistent presence of this change in a variety of dogs above the age of 13 years, the correlation with intracerebral hemorrhage, and the similarity of the affected regions between dogs and humans, all uphold the utility of aged dogs as a natural model for studies about cerebral amyloid angiopathy. Three Years after Clinical Onset of Cerebellar Cortical Degeneration in a Juvenile Coton De Tulear – What Comes after Inflammation? C. Ricco 1, A. Fouhetti1, M. Rosati2, K. Matiasek2, L. Cauzinille1 1Centre Hospitalier Vétérinaire Frégis, Arcueil, France2Ludwig‐Maximilians‐University, Munich, Germany Cerebellar disorders in dogs can be subclassified into congenital, developmental and abiotrophic/degenerative types. Among the abiotrophies, the term cerebellar cortical degeneration (CCD) has been introduced lately, which includes an uncommon form mainly affecting granular cells. This variant has been described in several breeds including the Coton de Tulear. In this specific breed an immune‐mediated disease process has been suggested. In this case report we describe a late stage presentation of a cerebellar granuloprival degeneration. A 7‐month‐old, Coton de Tuléar was presented with a history of progressive ataxia. The puppy was clear of the breed specific neonatal cerebellar ataxia. Neurological examination revealed generalised ataxia, hypermetric gait, head tremors, decreased proprioception in the hind limbs and an inconstant bilateral menace response. MRI revealed a cerebellum mildly decreased in size and a normal cerebrospinal fluid analysis. Clinical signs progressed over time and the dog was euthanized at the age of 3 years. Histopathology confirmed diffuse, chronic and severe granuloprival cerebellar cortical degeneration accompanied by severe gliosis of the cerebellum. Signs of inflammatory infiltrates were not detected on conventional stains and immmunohistochemistry. This Coton de Tulear appears as the first report of a chronic form of granuloprival CCD in this breed. Although the lack of inflammatory cells could suggest the absence of an immune mediated disease, these findings are most likely stage related and might reflect successful removal of the immunogenic target. Further studies should focus on the research of a genetic mutation associated with these histologic findings. Evaluation of GFAP Levels in Serum and Cerebrospinal Fluid in Dogs D. Kostic, R. Carlson, S. Wicha, A. Tipold Department Small Animal Medicine and Surgery, University of Veterinary Medicine Hannover, Germany Glial fibrillary acidic protein (GFAP) is the main intermediate filament protein in astrocytes and a potential biomarker for intracranial disorders. The hypothesis should be proven that severe brain tissue destruction leads to measurable GFAP serum levels independent of the cause of the disease. Furthermore, it should be proven that GFAP levels in cerebrospinal fluid (CSF) are reflecting disease categories. Six healthy Beagles and patients (n = 198) with the clinical diagnoses idiopathic epilepsy, brain tumor, inflammation, spinal cord injury (SCI) and traumatic brain injury (TBI) were included. GFAP concentrations were determined by ELISA. In serum, GFAP was only measurable in single cases. However, all CSF samples were positive for GFAP. Using Wilcoxon test, significant differences were found between GFAP CSF levels of dogs with tumor and epilepsy (P < 0.0004) and between inflammatory diseases and epilepsy (P < 0.0408). There was no correlation between GFAP values and severity, type and seizure frequency and severity of neuroparenchymal damage. In TBI patients high serum GFAP levels had a strong correlation with the Glasgow Coma Scale score. In dogs with SCI no significant difference between chronic and acute cases and severity of clinical signs could be detected. In conclusion, GFAP cannot be recommended as a marker for a specific disease. However, serum levels in TBI patients may have predictive value for the outcome. Eight Cases of Eosinophilic Meningoencephalitis (EME) in Dogs from 2009 to 2015 S. Guo, D. Lu Peace Avenue Veterinary Clinic, Hong Kong Idiopathic eosinophilic meningoencephalitis (EME) is a rare condition of unknonw etiology and has been described in different breeds such as Golden Retriever, Rottweiler, Yorkshire Terrier, etc1. When the eosinophils in the cerebrospinal fluid (CSF) is <5%, this finding is considered nonspecifit; it is recommended that an eosinophilia of 10% of the total white cells in the CSF should be used as a minimum criteria for the diagnosis of EME in people2. This retrospective study described 8 cases of EME seen in a private referral practice in Hong Kong from 2009 to 2015, affecting several breeds of dogs. EME is a rare condition and makes up to 4.6% of all the MUE cases seen in a Hong Kong referral clinic from 2009 to 2015. The clinical presentation and MR images were variable and diagnosis was mainly made by the presence of eosinophilic pleocytosis of CSF. In general they carry good prognosis following immunosuppresive treatment, with 5 out of 8 cases (62.5%) in remission (off treatment) and 1 (12.5%) only needed AED due to persistent seizure. Cannabinoid Receptor Type 2 (CB2) Expression in Canine Steroid‐Responsive Meningitis‐Arteritis (SRMA) and Intraspinal Spirocercosis J. Freundt‐Revilla 1, F. Heinrich2, M. H. Shamir3, A. Oevermann4, W. Baumgärtner2, A. Tipold1 1Department Small Animal Medicine and Surgery, University of Veterinary Medicine Hannover, Germany2Department of Pathology, University of Veterinary Medicine Hannover, Germany3Korea School of Veterinary Medicine, The Hebrew University of Jerusalem, Israel4Department Clinical Research and Veterinary Public Health, Vetsuisse, University of Bern, Switzerland Increased levels of endocannabinoids were recently found in CSF of dogs suffering from Steroid‐Responsive Meningitis‐Arteritis (SRMA) and Intraspinal Spirocercosis (IS) (Abstract ECVN 2013). These endogenous ligands interact with two main types of cannabinoid receptors (CB1 and CB2). The CB2 receptor is highly expressed in inflammatory cells and is up‐regulated in early phases of inflammation in cells of the CNS. In the present study, CB2 receptor expression was evaluated in spinal cord lesions of dogs with SRMA (n = 8) and IS (n = 2) and compared to healthy control dogs (n = 6). Therefore, a rabbit polyclonal anti‐human CB2 antibody (LSBio®) was established on canine paraffin‐embedded tissue samples using routine immunohistochemistry. In cervical, thoracic, and lumbar spinal cord sections of dogs with SRMA and IS, CB2 was strongly expressed on the cellular surface of infiltrating leukocytes (i.e. neutrophils, eosinophils, lymphocytes, plasma cells, and macrophages). In SRMA, CB2‐positive inflammatory cells were located within the adventitia of vessels, perivascular, subdural, subarachnoidal, and within white and grey matter. Moreover, moderate to strong CB2‐positive endothelial cells and arachnoid mesothelial‐like cells were present. In IS, CB2‐expressing leukocytes were found adjacent to the parasite accompanied by severe necrosis and haemorrhage. Both diseases showed CB2‐positive glial cells exhibiting a moderate to strong membranous signal. Likewise, scattered myelinophages and spheroids stained intensely positive with CB2. Dorsal and ventral neurons showed inhomogeneous slight to strong cytoplasmic immunoreactivity. The present study demonstrates CB2 expression in inflammatory lesions of SRMA and IS and highlights the endocannabinoid system as a potential target for treatment of inflammatory CNS diseases. Inflamed Intracranial Meningioma Mimicking Brain Abscess in a Dog C. Tästensen 1, S. Hanemann1, M.‐K. Müller1, M. Rosati2, K. Matiasek2, T. Flegel1 1Department of Small Animal Medicine, University of Leipzig, Germany2Clinical and Comparative Neuropathology, Centre for Clinical Veterinary Medicine, LMU Munich, Germany An 11‐year‐old mixed breed dog was presented with an acute onset of cluster seizures. At presentation, the dog showed a status epilepticus, which could be interrupted with anticonvulsive medication. Due to the stuporous state of the patient the following day, a thorough neurological examination could not be performed. MRI of the head revealed an inhomogeneously contrast enhancing mass within the right frontal lobe adjacent to the cribriform plate and extending caudally to the rostral thalamus. CSF analysis showed a severe pleocytosis of 11540 cells/µL with 70% neutrophils and 30% monocytes and a protein of 2.63 g/L. Based on MRI findings and CSF analysis main differentials were intracranial abscess versus neoplasia. Surgery was performed and a major part of the intracranial mass was removed through a bilateral transfrontal approach. Histological examination revealed a WHO grade I conforming meningothelial meningioma with multiple intratumoural microabscesses. Neither the CSF nor the mass itself showed bacterial growth. The dog recovered well over the following 7 days and was discharged for radiotherapy at which time the dog was neurological unremarkable. This case report illustrates that even a severe neutrophilic pleocytosis in the CSF cannot rule out an intracranial neoplasia. To our knowledge this is the first report of a meningioma with sterile microabscesses in a dog. Clinical and Epidural Histopathological Differences Observed in Cervical and Thoracolumbar Intervertebral Disc Extrusion in Dogs L. Züger 1,2, A. Fadda1,2, A. Oevermann1,3, F. Forterre4,2, D. Henke1,2 1Division of Neurological Sciences, Vetsuisse Faculty, University of Bern, Switzerland2Department of Clinical Veterinary Medicine, Vetsuisse Faculty, University of Bern, Switzerland3Department of Clinical Research and Veterinary Public Health, Vetsuisse Faculty, University of Bern, Switzerland4Division of Veterinary Surgery, Vetsuisse Faculty, University of Bern, Switzerland Marked differences in clinical presentation and outcome between cervical and thoracolumbar disc extrusions have only been partially explained. We have recently shown that the inflammatory response in the epidural space has an impact on the outcome in thoracolumbar IVD extrusions. The aims of the present study were to evaluate clinical data and histopathological parameters of epidural material from 55 dogs with cervical IVD extrusion, and to compare these data to those from 80 dogs with thoracolumbar IVD extrusion from a previous study. Cervical epidural material was histologically examined, and associations between severity of inflammation and selected clinical and pathological parameters, impact of chondrodystrophic phenotype, and anatomic localization were evaluated statistically. Dogs with a cervical IVD extrusion were significantly older (P < 0.001), had less severe and a longer duration of neurological signs (both P < 0.001), were more painful (P = 0.038), had a better outcome (P = 0.005), and revealed less severe calcification (P = 0.002) and inflammation (P < 0.001) in histopathology than dogs with a thoracolumbar IVD extrusion. No significant differences regarding chondrodystrophic phenotype were found. In conclusion, the present study revealed obvious differences in clinical presentation and epidural space pathology between cervical and thoracolumbar IVD extrusions. Notably, there was a significantly less intensive epidural inflammatory response in the former. This correlated positively with a significantly lower degree of nucleus pulposus calcification in cervical extrusions indicating biochemical/ metabolic and biomechanical differences between the two locations which remain to be characterized in future studies. Somatosensory and Motor Evoked Potentials Under General Anesthesia in Dogs with Thoracolumbar Intervertebral Disc Extrusion M. C. C. M. Inglez de Souza 1, R. J. R. Ferreira2, G. C. F. Patricio1, J. M. Matera1 1School of Veterinary Medicine ‐ University of São Paulo, São Paulo, Brazil2Institute of Orthopaedics and Traumatology, University of São Paulo, São Paulo, Brazil Somatosensory evoked potentials (SEPs) and transcranial motor evoked potentials (TMEPs) provide information regarding sensory and motor pathways, and dogs are considered translational models for naturally‐occurring spinal cord injury. Our aim was to describe SEPs and TMEPs technique in uninjured and in affected chondrodystrophic dogs (CD). Paraplegic CD (5 with pain perception, 5 with loss of pain perception) due to thoracolumbar disc extrusions confirmed by computed tomography; and 5 neurologic normal CD were anesthetized with Fentanyl and Propofol in a continuous infusion rate. SEPs were recorded with electrodes positioned subcutaneously on scalp following median and tibial nerves stimulation. TMEPs were obtained by electrical stimulation applied transcranially and captured via electrodes inserted into extensor carpi radialis and cranial tibial muscles. SEPs waves were identified in all dogs after median nerve stimulation, and 5 dogs had no SEPs recordings on pelvic limbs, and they were clinically without pain perception. TMEPs were recorded on thoracic limbs in all dogs, but were severe attenuated in 7 dogs and absent in 3 dogs. Even if no voluntary movement could be detected clinically, electrophysiological responses were present caudal to spinal cord lesion, i.e., these patients may be paraplegic from clinical assessment, but not concerning electrophysiological function. All neurologically normal CDs presented SEPs and TMEPs on pelvic limbs. Combined SEPs and TMEPs techniques appear to be reliable for spinal cord lesion evaluation under general anesthesia. TMEPs could be detected caudal to the lesion even in severely affected patients, possibly being a useful tool for spinal cord therapies evaluation. Comparison of Pre‐Operative Quantitative MRI and Clinical Assessment of Deep Pain Perception as Prognostic Tools for Recovery of Motor Function in Paraplegic Dogs A. Wang‐Leandro, M. K. Hobert, P. Dziallas, V. M. Stein, A. Tipold Department of Small Animal Medicine and Surgery, University of Veterinary Medicine Hannover, Germany Development of objective prognostic tools for paraplegic dogs suffering from spinal cord injury (SCI) is mandatory for novel treatment selection and implementation. Th