Objectives A previous single-country pilot study indicated serum anti-GM2 and anti-GA1 anti-glycolipid antibodies as potential biomarkers for acute canine polyradiculoneuritis. This study aims to validate these findings in a large geographically heterogenous cohort. Materials and Methods Sera from 175 dogs clinically diagnosed with acute canine polyradiculoneuritis, 112 dogs with other peripheral nerve, cranial nerve or neuromuscular disorders and 226 neurologically normal dogs were screened for anti-glycolipid antibodies against 11 common glycolipid targets to determine the immunoglobulin G anti-glycolipid antibodies with the highest combined sensitivity and specificity for acute canine polyradiculoneuritis. Results Anti-GM2 anti-glycolipid antibodies reached the highest combined sensitivity and specificity (sensitivity: 65.1%, 95% confidence interval 57.6 to 72.2%; specificity: 90.2%, 95% confidence interval 83.1 to 95.0%), followed by anti-GalNAc-GD1a anti-glycolipid antibodies (sensitivity: 61.7%, 95% confidence interval 54.1 to 68.9%; specificity: 89.3%, 95% confidence interval 82.0 to 94.3%) and these anti-glycolipid antibodies were frequently present concomitantly. Anti-GA1 anti-glycolipid antibodies were detected in both acute canine polyradiculoneuritis and control animals. Both for anti-GM2 and anti-GalNAc-GD1a anti-glycolipid antibodies, sex was found a significantly associated factor with a female to male odds ratio of 2.55 (P=0.0096) and 3.00 (P=0.0198), respectively. Anti-GalNAc-GD1a anti-glycolipid antibodies were more commonly observed in dogs unable to walk (odds ratio 4.56; P=0.0076). Clinical Significance Anti-GM2 and anti-GalNAc-GD1a immunoglobulin G anti-glycolipid antibodies represent serum biomarkers for acute canine polyradiculoneuritis.

BACKGROUND:Metronidazole is an antibacterial, antiprotozoal and anthelmintic medication commonly used in veterinary medicine. We describe cases of neurotoxicity associated with the drug's administration.METHODS:Medical records between 2004 and 2017 from four veterinary referral hospitals were reviewed. Inclusion criteria were the presence of neurological signs compatible with metronidazole toxicity, clinical history supporting recent metronidazole therapy and resolution of clinical signs upon discontinuation of metronidazole administration.RESULTS:A total of 26 dogs were identified with clinical signs supporting a diagnosis of metronidazole toxicity. Median age at presentation was 7.2 years (range, 0.1-12 years); median duration of treatment was 35 days (range, 5-180 days); median treatment dosage was 21 mg/kg BID (range, 13-56 mg/kg every 12 h); median resolution of the clinical signs upon discontinuation of metronidazole was 3 days (range, 1-26 days). Magnetic resonance imaging (MRI) of the brain was performed in 19 cases and only one dog had brain lesions affecting the dentate nuclei, which resembled the MRI appearance of this disease in humans.CONCLUSIONS:We found evidence of neurotoxicity in dogs at much lower doses than previously reported and we suggest caution when administering metronidazole at doses > 40 mg/kg every 24 h, regardless of the duration of the treatment.

Quality of life (QoL) plays a significant role in the treatment of dogs with idiopathic epilepsy (IE), yet is so far understudied. This study describes the outcome evaluation of an online questionnaire based on the carer's perception focusing on 62 QoL questions in 159 dogs with IE. Results showed that seizure frequency, but not seizure severity or presence of cluster seizures, was significantly associated with carer-perceived dog's QoL. Dogs receiving third-line antiepileptic drugs had a significantly lower perceived QoL than those that did not. Generalised linear mixed model analysis demonstrated that severity of the side effects sleeping more and ataxia were significantly associated with carer-perceived dog's QoL, with higher severities predicting lower QoL scores. The degree of carer acceptability of seizure frequency and severity was significantly associated with the dog's reported seizure frequency and severity. Moreover, there was a significant association between IE-related QoL changes of the dog and the carer, with reductions in perceived canine QoL scores associated with reductions in carer QoL, and vice versa. In conclusion, aspects of canine IE can affect both the carer and their dog's QoL. This has implications for the management and requires consideration when treatment options and outcomes are discussed.

OBJECTIVES:To report the magnetic resonance imaging and clinical features of suspected idiopathic bilaterally symmetric hypertrophic ganglioneuritis affecting the C2 nerve roots.METHODS:Retrospective analysis of case records of dogs with imaging findings suggestive of idiopathic bilateral C2 neuritis. Data analysed included signalment, history, clinical signs, clinical pathology results and magnetic resonance imaging findings. Nerve root enlargement and spinal cord changes were classified as clinically significant or incidental, and further graded as mild, moderate or severe based on the degree of spinal cord distortion/compression. Imaging features were also correlated with severity of neurological deficits.RESULTS:Twelve dogs, including nine Staffordshire bull terriers showed magnetic resonance imaging features suggestive of idiopathic hypertrophic neuritis of C2 nerve roots. Findings were considered incidental (4/12) or clinically significant (8/12) based on prior neurological examination. Changes were best visualised on transverse images at the level of the C1-2 intervertebral foramina. The degree of associated spinal cord compression subjectively correlated with the severity of the neurological deficits. All cases with clinically significant lesions that were treated with corticosteroids responded favourably.CLINICAL SIGNIFICANCE:Bilaterally symmetric C2 neuritis likely represents idiopathic hypertrophic ganglioneuritis. Staffordshire bull terriers appear over represented. Immunosuppressive doses of corticosteroids should be considered for clinically significant lesions.

OBJECTIVES To develop and evaluate a method to quantify the T1-weighted magnetic resonance imaging signal intensity of the lentiform nuclei in dogs, and to determine if there is any significant difference in this signal intensity between dogs with portosystemic shunts and a control group. MATERIALS AND METHODS A retrospective blinded study was performed to investigate the reliability and use of a quantitative method for assessing the T1-weighted magnetic resonance imaging signal intensity of the lentiform nuclei in dogs with and without portosystemic shunts. The lentiform nuclei index (mean lentiform nucleus signal intensity/mean white matter signal intensity) was calculated for nine dogs with portosystemic shunts and a control group of 14 dogs. RESULTS The intra- and inter-observer intraclass correlation coefficients were considered excellent (>0 · 75), suggesting that the lentiform nuclei index is a reliable method. The dogs with portosystemic shunts had a higher lentiform nuclei index than the control group (P = 0 · 0127). CLINICAL SIGNIFICANCE This method of quantifying the T1-weighted magnetic resonance imaging signal intensity of the lentiform nuclei was reliable and showed that dogs with portosystemic shunts tend to have increased signal intensity. Further prospective studies are necessary to investigate the clinical significance and applications of these findings.

Background The impact of epilepsy and its treatment on the quality of life (QoL) is considered an important part of treatment supervision in human epilepsy. Objectives To develop a list of key questions evaluating QoL in dogs with idiopathic epilepsy (IE) and their carers. Animals One hundred fifty‐nine dogs with IE. Methods Cross‐sectional study. An online project questionnaire was developed containing 90 QoL‐associated questions that were initially allocated to 14 themes representing specific areas associated with the treatment and care of an epileptic dog. Principal component analysis was applied with the aim of refining the questionnaire to the least number of questions representing useful themes without loss of descriptive value. Carers were recruited by paper mail, primary practices, and canine epilepsy websites. Data were acquired from January to November 2011. Results Principal component analysis removed 54 questions, leaving 7 themes with 36 questions with a minimum Cronbach's alpha value of 0.7 indicating a good internal consistency: “Seizure severity and frequency”, “Adverse effects of antiepileptic drug (AED)”, “Restrictions on the carer's life”, “Frustrations over caring for a dog with IE”, “Carer distaste of AED adverse effects”, “Carer anxiety around the seizure event”, “Perceptions on rectal diazepam use”. Conclusions and Clinical Importance Principal component analysis successfully reduced the number of questions without loss in descriptive value. The remaining questions correlate well with each other in capturing valuable details about aspects of QoL and represent valuable key questions (EpiQoL) in the assessment of QoL for the carers of dogs with IE.

The trigeminal nerve is involved in the opening of the pharyngeal orifice of the Eustachian tube by operating the tensor veli palatini muscle. The hypothesis was investigated that middle ear effusion occurs in a more severe disease phenotype of canine trigeminal nerve mass lesions compared with dogs without middle ear effusion. Three observers reviewed canine MRIs with an MRI-diagnosis of trigeminal nerve mass lesion from three institutions. Various parameters describing the musculature innervated by the trigeminal nerve were scored and compared between dogs with and without middle ear effusion. Nineteen dogs met the inclusion criteria. Ipsilateral middle ear effusion was observed in 63 per cent (95% CI 48.4 per cent to 77.6 per cent) of the dogs. The size of the trigeminal nerve mass lesions was positively correlated with the severity of masticatory muscle mass loss (Spearman r=0.5, P=0.03). Dogs with middle ear effusion had a significantly increased generalised masticatory muscle mass loss (P=0.02) or tensor veli palatini muscle loss score (P=0.03) compared with those without. Larger trigeminal nerve mass lesions were associated with a greater degree of masticatory muscle mass loss. Masticatory muscle mass and, importantly, tensor veli palatini muscle mass was more severely affected in dogs with middle ear effusion suggesting an associated Eustachian tube dysfunction.

Objectives To evaluate the accuracy of the cutaneous trunci reflex to localise thoracolumbar spinal cord injuries and to assess the correlation between focal loss (cut-off) of the reflex and clinical severity of thoracolumbar spinal cord injury. Methods Prospective study of 41 dogs with thoracolumbar spinal cord injuries investigated by magnetic resonance imaging. Linear regression analysis was performed to determine the relationship between the vertebral level of the cutaneous trunci reflex cut-off and the maximal and cranial lesion extent. The association between cutaneous trunci reflex cut-off and spinal cord injury severity was tested using a MannWhitney U test. Results Cutaneous trunci reflex cut-off was evident in 33 (80%) of dogs. The cut-off level was 0 to 4 vertebrae caudal to the maximal spinal cord lesion in all dogs. In 16 (48.5%) dogs the cut-off was either 2 or 3 vertebrae caudal to the lesion. The presence of a cut-off significantly correlated with increasing severity (P=0.0001). Loss of the reflex occurred at less severe grades than loss of ambulation and in dogs with ambulatory paresis it was significantly (P=0.0084) associated with increasing severity. Clinical Significance The cutaneous trunci reflex allows localisation of thoracolumbar spinal cord lesions within four vertebrae and facilitates clinical segregation of dogs with ambulatory paresis into mild and severe categories.

Multifocal haemorrhages associated with Angiostrongylus vasorum infection were observed in the central nervous system of four dogs with neurological signs including depression, seizures, spinal pain and paresis. In magnetic resonance images the majority of the lesions were isointense or slightly hyperintense in T1-weighted images, hyperintense in T2-weighted images and hypointense in T2*-weighted (gradient echo) images, compatible with haemorrhages more than seven days old. Lesions were found in the brain of three of the dogs and in the spinal cord of two. The cerebrospinal fluid contained high concentrations of protein and evidence of erythrophagia. All the dogs had coagulopathy and pulmonary haemorrhage of varying severity. A vasorum larvae were detected in the faeces of each of the dogs. Neural A vasorum was confirmed at postmortem examination in two dogs.

Journal of Veterinary Internal MedicineVolume 20, Issue 4 p. 1042-1044 Open Access Portosystemic Shunt Associated with Severe Episodic Weakness A. Wessmann, Corresponding Author A. Wessmann North Downs Specialist Referrals, Caterham, Surrey, UK Dr. med. vet. MRCVS, North Downs Specialist Referrals the Village, Guards Avenue, Coulsdon Road, Caterham, Surrey CR3 5ZD, UK; e-mail: awessmann@vetneurologist.com.Search for more papers by this authorH.A. Volk, H.A. Volk Department of Veterinary Clinical Sciences, The Royal Veterinary College, North Mymms, Hertfordshire, UKSearch for more papers by this authorG.D. Shelton, G.D. Shelton Department of Pathology, School of Medicine, University of California-San Diego, La Jolla, CASearch for more papers by this authorK.E. Chandler, K.E. Chandler Department of Veterinary Clinical Sciences, The Royal Veterinary College, North Mymms, Hertfordshire, UKSearch for more papers by this authorS. Baines, S. Baines Department of Veterinary Clinical Sciences, The Royal Veterinary College, North Mymms, Hertfordshire, UKSearch for more papers by this authorR. Cappello, R. Cappello Department of Veterinary Clinical Sciences, The Royal Veterinary College, North Mymms, Hertfordshire, UKSearch for more papers by this author A. Wessmann, Corresponding Author A. Wessmann North Downs Specialist Referrals, Caterham, Surrey, UK Dr. med. vet. MRCVS, North Downs Specialist Referrals the Village, Guards Avenue, Coulsdon Road, Caterham, Surrey CR3 5ZD, UK; e-mail: awessmann@vetneurologist.com.Search for more papers by this authorH.A. Volk, H.A. Volk Department of Veterinary Clinical Sciences, The Royal Veterinary College, North Mymms, Hertfordshire, UKSearch for more papers by this authorG.D. Shelton, G.D. Shelton Department of Pathology, School of Medicine, University of California-San Diego, La Jolla, CASearch for more papers by this authorK.E. Chandler, K.E. Chandler Department of Veterinary Clinical Sciences, The Royal Veterinary College, North Mymms, Hertfordshire, UKSearch for more papers by this authorS. Baines, S. Baines Department of Veterinary Clinical Sciences, The Royal Veterinary College, North Mymms, Hertfordshire, UKSearch for more papers by this authorR. Cappello, R. Cappello Department of Veterinary Clinical Sciences, The Royal Veterinary College, North Mymms, Hertfordshire, UKSearch for more papers by this author First published: 28 June 2008 https://doi.org/10.1111/j.1939-1676.2006.tb01827.xCitations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. References 1 Maddison JE. Hepatic encephalopathy. Current concepts of the pathogenesis. J Vet Intern Med 1992; 6: 341– 353. 2 Loebert V., Mischke R., Tipold A. Lactate and pyruvate levels in blood and cerebrospinal fluid in dogs. In: 16th Annual Symposium "Neurosurgery", Prague, Czech Republic European Society of Veterinary Neurology; 2003. 3 Rothuizen J., van den Ingh T., Voorhout G., et al. Congenital porto-systemic shunts in sixteen dogs and three cats. J Small Anim Pract 1982; 23: 67– 81. 4 Krotje LJ, Fix AS, Potthoff AD. Acquired myasthenia gravis and cholangiocellular carcinoma in a dog. J Am Vet Med Assoc 1990; 197: 488– 490. 5 Shelton GD, Schule A., Kass PH. Risk factors for acquired myasthenia gravis in dogs: 1,154 cases (1991–1995). J Am Vet Med Assoc 1997; 211: 1428– 1431. 6 Kelly M. Myasthenia gravis—A receptor disease. Compend Contin Educ 1981; 3: 544– 551. 7 Chaudhry V., Corse AM, O'Brian R., et al. Autonomic and peripheral (sensorimotor) neuropathy in chronic liver disease: A clinical and electrophysiologic study. Hepatology 1999; 29: 1698– 1703. 8 Chopra JS, Samanta AK, Murthy JM, et al. Role of porta systemic shunt and hepatocellular damage in the genesis of hepatic neuropathy. Clin Neurol Neurosurg 1980; 82: 37– 44. 9 McDougall AJ, Davies L., McCaughan GW. Rapid improvement of autonomic and peripheral neuropathy after liver transplantation: A single case report. Liver Transpl 2002; 8: 164– 166. 10 Hindfelt B., Holmin T. Experimental porta-caval anastomosis and motor nerve conduction velocity in the rat. J Neurol 1980; 223: 171– 175. 11 Cauch-Dudek K., Abbey S., Stewart DE, et al. Fatigue in primary biliary cirrhosis. Gut 1998; 43: 705– 710. 12 Huet PM, Deslauriers J., Tran A., et al. Impact of fatigue on the quality of life of patients with primary biliary cirrhosis. Am J Gastroenterol 2000; 95: 760– 767. 13 Kumar D., Tandon RK. Fatigue in cholestatic liver disease—A perplexing symptom. Postgrad Med J 2002; 78: 404– 407. 14 Sumida S., Tanaka K., Kitao H., et al. Exercise-induced lipid peroxidation and leakage of enzymes before and after vitamin E supplementation. Int J Biochem 1989; 21: 835– 838. 15 Ettinger S. J., Feldman EC. Textbook of Veterinary Internal Medicine, 6th ed. St Louis , MO : Elsevier Saunders; 2005: 522– 574. 16 Gubler C. Handbook of Vitamins. New York : Marcel Dekker, Inc; 1984: 246– 297. 17 Chaudhry V., Umapathi T., Ravich WJ. Neuromuscular diseases and disorders of the alimentary system. Muscle Nerve 2002; 25: 768– 784. 18 Read DH, Harrington DD. Experimentally induced thiamine deficiency in Beagle Dogs: Clinical observations. Am J Vet Res 1981; 42: 984– 991. 19 Hazlett MJ, Smith-Maxie LL, de Lahunta A. A degenerative encephalomyelopathy in 7 Kuvasz puppies. Can Vet J 2005; 46: 429– 432. 20 McLellan GJ, Cappello R., Mayhew IG, et al. Clinical and pathological observations in English Cocker Spaniels with primary metabolic vitamin E deficiency and retinal pigment epithelial dystrophy. Vet Rec 2003; 153: 287– 292. Citing Literature Volume20, Issue4July 2006Pages 1042-1044 ReferencesRelatedInformation

Hereditary ataxia in the Jack Russell Terrier (JRT) is characterized by a gait disturbance with symmetric generalized ataxia and hypermetric and spastic movements. Histopathology shows a disease of the entire central nervous system, predominantly an axonopathy. In the present study, 35 clinically affected dogs were examined. Gait abnormalities began at 2-9 months of age. Generalized seizures occurred in 13 dogs in addition to the ataxia, and 7 dogs developed respiratory distress. Brain stem auditory-evoked potentials (BAEPs) were abnormal in 4 of 8 examined dogs, in which only waves I and II were detected. Abnormal BAEPs suggest the possibility of hereditary ataxia in the JRT. Investigations regarding the mode of inheritance were performed by complex segregation analyses on 3 pedigrees with a total of 115 JRTs (27 clinically affected dogs and 88 unaffected littermates and ancestors). Different modes of inheritance were tested, including monogenic, mixed, and polygenic models, as well as a model with environmental effects only. Models with genetic effects explained the data significantly better than the environmental model. The monogenic model had to be rejected in this study because of an insufficient match of data when compared to that of the most general model. The polygenic and mixed major gene models explained the pedigree data best and therefore have to be regarded as possible hypotheses for the mode of inheritance of hereditary ataxia in the JRT. The polygenic model proved best suited to explain the segregation pattern in the JRT, because it had the fewest number of parameters.

A case of discospondylitis in a dog secondary to Bordetella species, diagnosed early with the assistance of magnetic resonance imaging (MRI), is reported. The history and clinical signs were suggestive of possible discospondylitis. MRI identified changes and allowed a presumptive diagnosis of discospondylitis, which was subsequently confirmed by bacterial culture of biopsy material. Discospondylitis associated with Bordetella species infection has not, to the authors' knowledge, been previously reported in the dog.

A 10-month-old female Parson Jack Russell Terrier was euthanatized because of therapy-resistant ataxia, hypermetria, and deafness that had first been observed at 10 weeks of age. Severe, bilateral, symmetrical neuronal degeneration and mineralization of the brain were found in the cochlear and cerebellar nuclei, dorsal areas of the medulla oblongata, the vestibulocochlear nerve, plexus choroideus, and within the granule cell layer of the ventral cerebellar hemispheres. The mineralized deposits were located free in the parenchyma, around intact or degenerate neurons, in myocytes of small- and medium-sized arteries, and around capillaries. Hepatocytes and cardiac myocytes showed oncocytotic change with increased numbers of enlarged or misshapen mitochondria filled with densely packed cristae and electron-dense inclusions. Skeletal myocytes had only minor increases in the number of mitochondria. The microscopic and ultrastructural lesions were consistent with mitochondrial encephalopathy with similarities to mitochondrial encephalomyopathy with lactic acidosis and strokelike episodes in humans.

Four lack Russell Terriers with Hereditary Alaxia were examined. They showed typical generalized ataxia with hypermetric movements. Further investigations, such as routine haematological and biochemical analyses and examination of the cerebrospinal fluid (total cell count, protein), myelography and computertomography (thekography), revealed no abnormalities. Histopathology performed an one of the examined dogs confirmed the clinical diagnosis. An abnormal measurement of brainstem auditory-evoked potentials (BAEP) was found in two dogs, since only wave I and II could be detected. Since studies on the mode of inheritance of this specific disease in the lack Russell Terrier were not yet performed, we collected additional data in order to build up a pedigree. This pedigree includes 76 lack Russell Terriers exhibiting hereditary ataxia, their ancestors and their littermates. A predisposition of the disease for certain families could be detected. Further investigations are necessary to clarify the mode of inheritance of this specific disease.