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BackgroundKCNJ10 and CAPN1 variants have been shown to cause spinocerebellar ataxia (SCA) in Jack Russell, Parson Russell and Fox terriers (JRT, PRT and FT). However, their association with the clinical manifestation of myokymia and neuromyotonia (M/NM), often reported alongside SCA, remains unclear.AimsTo investigate the association between M/NM and SCA-related variants in 34 with SCA and/or M/NM affected dogs (30 JRTs; 1 PRT; 1 Yorkshire terrier, YT; 1 Dachshund; 1 crossbreed).MethodsKCNJ10 XM_038448705.1:c.627C>G (p.(Ile209Met)) and CAPN1 XM_038425033.1:c.344G>A (p.(Cys115Tyr)) variants, and the complete coding sequence (CDS) of KCNA1, KCNA2, KCNA6, KCNJ10 and HINT1, were analysed via Sanger sequencing.ResultsThe KCNJ10 c.627C>G variant was homozygously present in 16 JRTs, 1 Dachshund and 1 crossbreed with SCA and M/NM, and in 9 JRTs with SCA but without M/NM. The CAPN1 c.344G>A variant was homozygously present in 1 PRT with SCA but without M/NM. Both variants were not found in 2 JRTs with SCA but without M/NM, neither in 3 JRTs and 1 YT without SCA but with M/NM. No other causal variants were found in the coding sequence of the investigated candidate genes in these latter 6 dogs.ConclusionsThe KCNJ10 c.627C>G or CAPN1 c.344G>A variant was confirmed to be the causal variant in 28 of the 34 affected dogs (including 1 Dachshund with the KCNJ10 variant). The fact that 10 of these 28 dogs did not suffer from M/NM (all of them suffered from SCA) and that these variants were not found in 4 dogs suffering from M/NM without SCA, suggests that M/NM is caused by another genetic variant or that these patients suffer from an acquired (immune-mediated) syndrome, similar to humans. Another SCA-causing variant is probably also segregating in JRTs (but not in the CDS of the investigated candidate genes), because no causal variant was found in 2 JRTs suffering from SCA without M/NM.

A 9-month-old male entire Doberman Pinscher presented with acute onset of severe cervical hyperesthesia after a fall. Neurological examination revealed a normal gait with low head carriage and severe cervical hyperesthesia. A CT scan of the cervical vertebral column revealed the presence of a comminuted fracture at the dorsomedial aspect of the right occipital condyle and sclerosis of the underlying bone. Medical management was initiated consisting of an external bandage, strict rest, and pain medication. Due to the lack of clinical improvement, the dog was euthanized 2 months after diagnosis. Histopathology of the lesion was compatible with a healing fracture.

Status epilepticus (SE) or prolonged epileptic seizure activity is a common neurological emergency with a high mortality rate and, if left untreated, can lead to irreversible cerebral damage and systemic complications. Fast and effective first-line management is of paramount importance, particularly in the at-home management of seizures where drug administration routes are limited. Benzodiazepines (BZDs) have been exclusively used in veterinary medicine for decades as first-line drugs based on their high potency and rapid onset of action. Various administration routes exist in dogs, such as oral, intravenous, intramuscular, rectal, and intranasal, all with different advantages and limitations. Recently, intranasal drug delivery has become more popular due to its unique and favourable characteristics, providing potential advantages over other routes of drug administration in the management of canine SE. This narrative review provides an outline of the management of SE at home and in a hospital setting, discusses considerations and challenges of the various routes of BZD administration, and evaluates the impact of intranasal drug administration (nose-brain pathway) for controlling canine SE at home and within hospital settings.

Background Although repetitive transcranial magnetic stimulation (rTMS) has been assessed in epileptic humans, clinical trials in epileptic dogs can provide additional insight. Objectives Evaluate the potential antiepileptic effect of rTMS in dogs. Animals Twelve client‐owned dogs with drug‐resistant idiopathic epilepsy (IE). Methods Single‐blinded randomized sham‐controlled clinical trial (dogs allocated to active or sham rTMS) (I) and open‐labeled uncontrolled clinical trial (dogs received active rTMS after sham rTMS) (II). Monthly seizure frequency (MSF), monthly seizure day frequency (MSDF), and number of cluster seizures (CS) were evaluated for a 3‐month pre‐TMS and post‐rTMS period and safety was assessed. The lasting effect period of rTMS was assessed in each dog treated by active stimulation using the MSF ratio (proportion of post‐TMS to pre‐rTMS MSF) and treatment was considered effective if the ratio was 1. Conclusions and Clinical Importance Repetitive transcranial magnetic stimulation may be a safe adjunctive treatment option for dogs with drug‐resistant IE, but large‐scale studies are needed to establish firm conclusions.

Background: Spinal cord dysfunction/compression and ataxia are common in horses. Presumptive diagnosis is most commonly based on neurological examination and cervical radiography, but the interest into the diagnostic value of transcranial magnetic stimulation (TMS) with recording of magnetic motor evoked potentials has increased. The problem for the evaluation of diagnostic tests for spinal cord dysfunction is the absence of a gold standard in the living animal. Objectives: To compare diagnostic accuracy of TMS, cervical radiography, and neurological examination. Animals: One hundred seventy-four horses admitted at the clinic for neurological examination. Methods: Retrospective comparison of neurological examination, cervical radiography, and different TMS criteria, using Bayesian latent class modeling to account for the absence of a gold standard. Results: The Bayesian estimate of the prevalence (95% CI) of spinal cord dysfunction was 58.1 (48.3%-68.3%). Sensitivity and specificity of neurological examination were 97.6 (91.4%-99.9%) and 74.7 (61.0%-96.3%), for radiography they were 43.0 (32.3%-54.6%) and 77.3 (67.1%-86.1%), respectively. Transcranial magnetic stimulation reached a sensitivity and specificity of 87.5 (68.2%-99.2%) and 97.4 (90.4%-99.9%). For TMS, the highest accuracy was obtained using the minimum latency time for the pelvic limbs (Youden's index = 0.85). In all evaluated models, cervical radiography performed poorest. Clinical Relevance: Transcranial magnetic stimulation-magnetic motor evoked potential (TMS-MMEP) was the best test to diagnose spinal cord disease, the neurological examination was the second best, but the accuracy of cervical radiography was low. Selecting animals based on neurological examination (highest sensitivity) and confirming disease by TMS-MMEP (highest specificity) would currently be the optimal diagnostic strategy.

Objectives Phenobarbital (PB) is the most common antiseizure drug (ASD) used for the management of feline epilepsy. In dogs, PB is known to cause serum liver enzyme induction and hepatotoxicity, especially after administration long term or in high concentrations. In cats, insufficient evidence is available to draw similar conclusions. The aim of this study was to evaluate the effect of PB administration on the serum biochemistry profile of epileptic cats. As an additional objective, other adverse effects arising, related to PB treatment, were recorded. Methods Medical records of four veterinary centres were retrospectively reviewed for epileptic cats receiving PB treatment. Cats were included if they had a diagnosis of idiopathic epilepsy or structural epilepsy; a normal baseline serum biochemistry profile; at least one follow-up serum biochemistry profile; no concurrent disease or had not received medication that could possibly influence liver function or lead to serum liver enzyme induction. Alkaline phosphatase, alanine aminotransferase (ALT), aspartate transaminase and gamma-glutamyl transferase activities, and total bilirubin, bile acids, glucose, albumin, total protein, urea and creatinine concentrations before and during PB administration were recorded. PB serum concentration was also recorded, when available. Results Thirty-three cats (24 males, nine females) with a median age of 3 years (range 2 months to 12 years) met the inclusion criteria. Idiopathic or structural epilepsy was diagnosed in 25 (76%) and eight (24%) cats, respectively. The follow-up period ranged from 9 to 62 months. This study found an increase in ALT in three cats, possibly related to a PB serum concentration >30 µg/ml. No statistically significant increase in serum liver enzymes or other evaluated biochemistry parameters was found by comparing pre- and post-treatment parameters. Conclusions and relevance PB administration did not result in hepatic enzyme induction or other biochemical abnormalities in cats. This strengthens the safety profile of PB as an ASD in cats.

Knowledge regarding the etiology and prognosis for canine megaesophagus (ME) is currently limited to small case series that may now be out of date in light of recent advances in the understanding of neurological syndromes and the availability of advanced diagnostic testing. Ninety-nine dogs diagnosed with nonstructural ME were included. Congenital idiopathic ME was present in 10 cases, with complete resolution of clinical signs in a single case. Eighty-nine cases were considered acquired, with most cases being either idiopathic (42.7%) or associated with myasthenia gravis (38.2%). Idiopathic cases represented a smaller percentage of acquired ME than previously reported. Death or euthanasia directly related to ME occurred in almost 50% of acquired cases, whereas clinical signs persisted in ∼20% of cases and resolved in 30% of cases. A diagnosis of an underlying etiology, in particular myasthenia gravis, was associated with a better outcome in acquired ME. ME continues to be a challenging condition to manage, with a guarded-to-poor prognosis, particularly when an underlying etiology is not identified. Thorough diagnostic testing for an underlying neurological disorder is important in cases with ME as this may allow institution of appropriate treatment and the potential for a better prognosis.

To date, motor evoked potential (MEP) recording in animals is often performed using intramuscular monopolar needle electrodes. Their placement and use has several disadvantages. Adhesive surface electrodes appear to be attractive because they are painless and easy to place. Because these are not used in horses, a scouting study is performed to (1) explore the applicability of surface electrodes in horses (2) determine the repeatability of motor latency times (MLTs) and amplitude measurements, and (3) to investigate if MLTs and amplitude values of surface electrode recordings were similar to intramuscular needle electrode recordings. Transcranial MEP recordings were performed by both coated needle and surface electrodes on ten sedated warmblood horses. Mean MLTs for the thoracic limbs were 20.8 ± 1.5 ms for needle and 21.2 ± 1.4 ms for surface electrode recording and 39.4 ± 3.8 ms and 39.2 ± 3.8 ms for the pelvic limbs, respectively. Mean amplitude values were 8.3 ± 4.1 and 7.2 ± 4.7 mV for the thoracic limbs and 4.2 ± 3.1 and 3.8 ± 2.4 mV for the pelvic limbs, respectively. A good agreement and repeatability for MLTs but insufficient agreement and repeatability for amplitude between both recording types were determined by Bland-Altman plots and Passing-Bablok regression and coefficients of variation calculation. In conclusion, this preliminary study shows that surface electrode recording of MEP is possible and well tolerated in horses. Surface recordings were repeatable and look similar to the intramuscular recordings when regarding MLTs, but overshadowing effects of large test-to-test variations precluded a conclusion concerning amplitude.

The purpose of the present study was to investigate if rectal administration of imepitoin in healthy dogs leads to plasma concentrations comparable to those after oral administration. Significantly lower systemic exposure and maximal plasma concentration (Cmax) of imepitoin was achieved after rectal compared to oral administration (P≤0.001). Therefore, this study does not support the rectal administration of imepitoin in dogs.

SeSAME/EAST syndrome is a multisystemic disorder in humans, characterised by seizures, sensorineural deafness, ataxia, developmental delay and electrolyte imbalance. It is exclusively caused by homozygous or compound heterozygous variations in the KCNJ10 gene. Here we describe a similar syndrome in two families belonging to the Malinois dog breed, based on clinical, neurological, electrodiagnostic and histopathological examination. Genetic analysis detected a novel pathogenic KCNJ10 c.986T>C (p.(Leu329Pro)) variant that is inherited in an autosomal recessive way. This variant has an allele frequency of 2.9% in the Belgian Malinois population, but is not found in closely related dog breeds or in dog breeds where similar symptoms have been already described. The canine phenotype is remarkably similar to humans, including ataxia and seizures. In addition, in half of the dogs clinical and electrophysiological signs of neuromyotonia were observed. Because there is currently no cure and treatment is nonspecific and unsatisfactory, this canine translational model could be used for further elucidating the genotype/phenotype correlation of this monogenic multisystem disorder and as an excellent intermediate step for drug safety testing and efficacy evaluations before initiating human studies.

Clinical, pathological, and genetic findings of a primary hereditary ataxia found in a Malinois dog family are described and compared with its human counterpart. Based on the family history and the phenotype/genotype relationships already described in humans and dogs, a causal variant was expected to be found in KCNJ10. Rather surprisingly, whole-exome sequencing identified the SLC12A6 NC_006612.3(XM_014109414.2): c.178_181delinsCATCTCACTCAT (p.(Met60Hisfs*14)) truncating variant. This loss-of-function variant perfectly segregated within the affected Malinois family in an autosomal recessive way and was not found in 562 additional reference dogs from 18 different breeds, including Malinois. In humans, SLC12A6 variants cause “agenesis of the corpus callosum with peripheral neuropathy” (ACCPN, alias Andermann syndrome), owing to a dysfunction of this K(+)–Cl(−) cotransporter. However, depending on the variant (including truncating variants), different clinical features are observed within ACCPN. The variant in dogs encodes the shortest isoform described so far and its resultant phenotype is quite different from humans, as no signs of peripheral neuropathy, agenesis of the corpus callosum nor obvious mental retardation have been observed in dogs. On the other hand, progressive spinocerebellar ataxia, which is the most important feature of the canine phenotype, hindlimb paresis, and myokymia-like muscle contractions have not been described in humans with ACCPN so far. As this is the first report of a naturally occurring disease-causing SLC12A6 variant in a non-human species, the canine model will be highly valuable to better understand the complex molecular pathophysiology of SLC12A6-related neurological disorders and to evaluate novel treatment strategies.

Background: When surgical treatment of cervical vertebral malformation is considered, precise localization of compression sites is essential, but remains challenging. Magnetic motor evoked potentials (mMEP) from paravertebral muscles are useful in localizing spinal cord lesions, but no information about cervical muscle mMEP in horses is available yet. Therefore, the aim of this study was to determine the possibility, normal values, inter-and intra-observer agreement and factors that have an effect on cervical mMEP in healthy horses. Methods: Transcranial magnetic stimulation was performed on 50 normal horses and 4 (2 left, 2 right) muscle responses were recorded at the middle of each cervical vertebra (C1-C7) and additionally just caudal to C7 to evaluate cervical nerves (Cn) Cn1 to Cn8. Latency time and amplitude of the recorded mMEP were defined by both an experienced and an unexperienced operator. Results: Latency increased gradually from 14.2 +/- 1.38 ms for Cn3 to 17.7 +/- 1.36 ms for Cn8, was significantly influenced by cervical nerve (P < 0.01), gender (P = 0.02) and height (P = 0.03) and had a good intra-observer agreement. The smallest mean amplitude (4.35 +/- 2.37 mV) was found at Cn2, the largest (5.99 +/- 2.53 mV) at Cn3. Amplitude was only significantly influenced by cervical nerve (P < 0.01) and had a low intra-observer agreement. No significant effect of observer on latency (P = 0.88) or amplitude (P = 0.99) measurements was found. Conclusion: mMEP of cervical muscles in normal horses are easy to collect and to evaluate with limited intra-and inter-observer variation concerning amplitude and should be investigated in future studies in ataxic horses to evaluate its clinical value.

Objective: To describe a modified implantation procedure of a vagus nerve stimulation (VNS) device in dogs and to report short- and long-term complications. Study Design: Descriptive, experimental study. Animals: Healthy, adult Beagle dogs (n=10). Methods: A VNS Therapy((R)) System was implanted in the left cervical region of anesthetized dogs. During and within 48hours after surgery, electrocardiography (ECG) and impedance testing of the system were performed. Dogs were monitored daily and the impedance of the system was determined regularly until VNS devices were surgically removed 3 years after implantation. Results: The implantation procedure was successful in all dogs without intraoperative complications. ECG monitoring and impedance tests were within normal limits during and within 48hours after surgery. Postoperative seroma formation was common (70%). One dog developed an irreversible Horner's syndrome leading to removal of the device 5 months after implantation. Another dog developed trauma-induced damage of the lead requiring surgical revision. The device could be safely removed in all dogs; however, electrodes were left in place to avoid nerve damage. At removal, the anchor tether was dislodged in 40% of dogs and the lead was twisted in 50% of dogs. Conclusion: Implantation of a VNS Therapy((R)) System is safe and feasible in dogs; however, seroma formation, twisting of the lead, and dislodgement of the anchor tether were common. Practical improvements in the technique include stable device placement, use of a compression bandage, and exercise restriction. Regular evaluation of lead impedance is important, as altered values can indicate serious complications.

Alexander disease (AxD) is a fatal neurodegenerative disorder of astrocyte dysfunction in man, for which already a number of causal variants are described, mostly de novo dominant missense variants in the glial fibrillary acidic protein (GFAP). A similar disorder was already phenotypically described in animals but without the identification of causal variants. We diagnosed a Labrador retriever with a juvenile form of AxD based on clinical (tetraparesis with spastic front limbs mimicking ‘swimming puppy syndrome') and pathological (the detection of GFAP containing Rosenthal fibers in astrocytes) features. In order to identify a causal variant, the coding sequences of the four detected GFAP transcript variants (orthologues from human transcript variants α, γ, δ/ɛ and κ) were sequenced. From the five detected variants, a heterozygous c.719G>A nucleotide substitution resulting in a p.Arg240His substitution was considered to be causal, because it is orthologous to the heterozygous de novo dominant c.716G>A (p.Arg239His) hotspot variant in man, proven to cause a severe phenotype. In addition, the variant was not found in 50 unrelated healthy Labrador retrievers. Because the condition in dogs is morphologically similar to man, it could be a promising animal model for further elucidating the genotype/phenotype correlation in order to treat or prevent this disease.

Epilepsy is the most common chronic neurological disorder in both humans and dogs. The effect of sex hormones on seizures is well documented in human medicine. Catamenial epilepsy is defined as an increase in frequency and severity of seizures during certain periods of the menstrual cycle. Oestradiol increases seizure activity and progesterone is believed to exhibit a protective effect. The role of androgens is controversial and there is a lack of research focusing on androgens and epilepsy. Indeed, little is known about the influence of sex hormones on epilepsy in dogs. Sterilisation is believed to improve seizure control, but no systematic research has been conducted in this field. This review provides an overview of the current literature on the influence of sex hormones on seizures in humans. The literature on idiopathic epilepsy in dogs was assessed to identify potential risk factors related to sex and sterilisation status. In general, there appears to be an over-representation of male dogs with idiopathic epilepsy but no explanation for this difference in prevalence between sexes has been reported. In addition, no reliable conclusions can be drawn on the effect of sterilisation due to the lack of focused research and robust scientific evidence.

Refractory epilepsy is a common disorder both in humans and dogs and treatment protocols are difficult to optimise. In humans, different non-pharmacological treatment modalities currently available include surgery, the ketogenic diet and neurostimulation. Surgery leads to freedom from seizures in 50-75% of patients, but requires strict patient selection. The ketogenic diet is indicated in severe childhood epilepsies, but efficacy is limited and long-term compliance can be problematic. In the past decade, various types of neurostimulation have emerged as promising treatment modalities for humans with refractory epilepsy. Currently, none of these treatment options are used in routine daily clinical practice to treat dogs with the condition. Since many dogs with poorly controlled seizures do not survive, the search for alternative treatment options for canine refractory epilepsy should be prioritised. This review provides an overview of non-pharmacological treatment options for human refractory epilepsy. The current knowledge and limitations of these treatments in canine refractory epilepsy is also discussed.

Idiopathic head tremor (IHT) syndrome is a recognized but poorly characterized movement disorder in English bulldogs (EBs). The data analyzed were collected via a detailed online questionnaire and video recordings. Thirty-eight percent of the population demonstrated IHT. The first presentation was early in life. There was no sex or neutered status predisposition. The condition disappeared with time in 50% of the cases. The direction of the head movement was vertical or horizontal. The number of episodes per day and the duration of the episodes were greatly variable. The majority of episodes occurred at rest. Most of the episodes were unpredictable. And there was no alteration of the mental status for most dogs during the episodes. Stress has been reported as a suspected trigger factor. IHT in EBs can be considered an idiopathic paroxysmal movement disorder.

Case Description—A 4-year-old sexually intact male mixed-breed dog was evaluated because of clinical signs of acute-onset pelvic limb ataxia, rapidly progressing to paraplegia with severe spinal hyperesthesia. Clinical Findings—General physical examination revealed pyrexia, tachycardia, and tachypnea. Neurologic examination demonstrated severe spinal hyperesthesia and paraplegia with decreased nociception. Magnetic resonance imaging revealed extradural spinal cord compression at T13-L1 and hyperintense lesions on T1- and T2-weighted images in the epaxial musculature and epidural space. Treatment and Outcome—Decompressive surgery, consisting of a continuous dorsal laminectomy, with copious lavage of the vertebral canal was performed. Cultures of blood, urine, and surgical site samples were negative. Histologic examination results for samples obtained during surgery demonstrated suppurative myositis and steatitis. These findings confirmed a diagnosis of sterile idiopathic inflammation of the epidural fat and epaxial muscles with spinal cord compression. The dog's neurologic status started to improve 1 week after surgery. After surgery, the dog received supportive care including antimicrobials and NSAIDs. The dog was ambulatory 1 month after surgery and was fully ambulatory despite signs of mild bilateral pelvic limb ataxia 3 years after surgery. Clinical Relevance—Although idiopathic sterile inflammation of adipose tissue, referred to as panniculitis, more commonly affects subcutaneous tissue, its presence in the vertebral canal is rare. Specific MRI findings described in this report may help in reaching a presumptive diagnosis of this neurologic disorder. A definitive diagnosis and successful long-term outcome in affected patients can be achieved by decompressive surgery and histologic examination of surgical biopsy samples.

Objective—To determine magnetic resonance imaging (MRI) vertebral ratio values representing vertebral canal height, vertebral canal shape, and vertebral body shape in Doberman Pinschers with and without disk-associated cervical spondylomyelopathy (DACSM) and clinically normal English Foxhounds. Animals—Doberman Pinschers with (n = 18) and without (20) DACSM and clinically normal English Foxhounds (18). Procedures—All dogs underwent low-field MRI of the cervical vertebral column. From 5 specific measurements made at C3 through C7, 4 linear vertebral ratios were calculated and assessed for correlation: vertebral canal height-to-body height ratio (CBHR), vertebral canal height-to-body length ratio (CBLR), caudal canal height-to-cranial canal height ratio (CCHR), and vertebral body length-to-height ratio (BLHR). The CBHR and CBLR described vertebral canal height, CCHR described vertebral canal shape, and BLHR described vertebral body shape. A midvertebral canal-occupying ratio (mVCOR) for the spinal cord was calculated at C5. Results—Compared with both groups of unaffected dogs, CBHR, CBLR, and BLHR for Doberman Pinschers with DACSM were significantly smaller. The C7 CCHR was significantly larger in DACSM-affected Doberman Pinschers, compared with clinically normal English Foxhounds. Ratios did not differ significantly between unaffected Doberman Pinschers and clinically normal English Foxhounds. Correlation coefficients between CBHR, CBLR, and mVCOR were low and not significant. Conclusions and Clinical Relevance—Doberman Pinschers with DACSM had significantly smaller vertebral canal heights and more square-shaped vertebral bodies, compared with unaffected Doberman Pinschers, combined with a funnel-shaped vertebral canal at C7. Breed-specific differences were not evident. Linear MRI vertebral canal-to-body ratios do not appear to predict relative vertebral canal stenosis.

The clinical and clinicopathological characteristics, treatment and outcome of vermicular muscle contractions (myokymia) and generalized muscle stiffness (neuromyotonia) in 37 Jack Russell terriers were evaluated retrospectively. Thirty dogs were affected by both disorders, whereas seven were presented with myokymia and never developed neuromyotonia. Clinical signs started at the mean age of 8 months. Except for signs of myokymia and neuromyotonia, clinical and neurological examination was normal in all dogs. Thirty dogs demonstrated typical signs of hereditary ataxia. Changes in serum chemistry included increased creatine kinase, aspartate aminotransferase and alanine aminotransferase concentrations. Electromyographic abnormalities, especially in muscles showing macroscopically visible myokymia, consisted of semirhythmic bursts of doublet, triplet, or multiplet discharges of a single motor unit. The amplitudes varied between 80 μV and 1 mV and occurred with an interburst frequency between 10 and 40 Hz and an intraburst frequency between 150 and 280 Hz. Most dogs were treated with a sodium channel blocker with variable results. Seven dogs died (most likely because of hyperthermia) or were euthanased during a neuromyotonic attack; 15 dogs were euthanased due to worsening of clinical signs, or lack of or no long-lasting effect of medication, and three were euthanased for unknown or unrelated reasons. Nine dogs were lost to follow-up and three were still alive 5-10.5 years after the start of clinical signs. In conclusion, young Jack Russell terriers with myokymia and neuromyotonia should undergo a complete blood and electrophysiological examination. Long-term prognosis is not favourable.

Objective—To determine intraobserver, interobserver, and intermethod agreement for results of myelography, computed tomography-myelography (CTM), and low-field magnetic resonance imaging (MRI) in dogs with disk-associated wobbler syndrome (DAWS). Design—Prospective cross-sectional study. Animals—22 dogs with DAWS. Procedures—All dogs underwent myelography, CTM, and low-field MRI. Each imaging study was interpreted twice by 4 observers who were blinded to signalment and clinical information of the patients. The following variables were assessed by all 3 techniques: number, site, and direction of spinal cord compressions; narrowed intervertebral disk spaces; vertebral body abnormalities; spondylosis deformans; and abnormal articular facets. Intervertebral foraminal stenosis was assessed on CTM and MRI images. Intraobserver, interobserver, and intermethod agreement were calculated by κ and weighted κ statistics. Results—There was very good to good intraobserver agreement for most variables assessed by myelography and only moderate intraobserver agreement for most variables assessed by CTM and low-field MRI. There was moderate to fair interobserver and intermethod agreement for most variables assessed by the 3 diagnostic techniques. There was very good or good intraobserver, interobserver, or intermethod agreement for the site and direction of the worst spinal cord compression as assessed by all the imaging modalities; abnormal articular facets and intervertebral foraminal stenosis were the least reliably assessed variables, with poor interobserver agreement regardless of imaging modality used. Conclusions and Clinical Relevance—There was considerable variation in image interpretation among observers and between use of various imaging modalities; these imaging techniques should be considered complementary in assessment of dogs with DAWS.

Objective: To evaluate a distractable titanium cage for the treatment of disk-associated wobbler syndrome (DAWS). Study Design: Prospective study. Animals: Dogs (n=7) with DAWS. Methods: After total discectomy of C5–C6 and C6–C7, the median part of the vertebral body of C6 was removed with preservation of the lateral walls and dorsal cortex. The removed cancellous bone was collected. The implant was placed in the bony defect of C6. After placement, the titanium cage was distracted and affixed by 4 screws. Finally, the implant was filled and covered with cancellous bone. Dogs had follow-up examinations at 1, 3, 6, 12, and 24 months. Six months after surgery, cervical radiographs and computed tomography (CT) were performed. Results: Although no intraoperative complications occurred, correct placement of the cage was technically challenging. Revision surgery was necessary in 2 dogs because of implant loosening and aggravation of vertebral tilting. All dogs improved after discharge from the hospital. In 1 dog, recurrence of clinical signs caused by articular facet proliferation at an adjacent intervertebral disk space occurred. Radiographs at 6 months demonstrated cage subsidence in 4 dogs. In all dogs, CT was suggestive for fusion of the bone graft with the vertebral body. Conclusions: Although results are promising, technical adaptations will be necessary to make this specific surgical technique, designed for humans, suitable for routine use in dogs.

Objective—To evaluate the use of transcranial magnetic stimulation for differentiating between clinically relevant and clinically irrelevant cervical spinal cord compression on magnetic resonance imaging (MRI). Design—Validation study. Animals—Clinically normal Doberman Pinschers without (n = 11) and with (6) spinal cord compression on MRI and 16 Doberman Pinschers with disk-associated wobbler syndrome (DAWS). Procedures—After dogs were sedated, transcranial magnetic motor evoked potentials were recorded from the extensor carpi radialis muscle (ECRM) and cranial tibial muscle (CTM). Onset latencies and peak-to-peak amplitudes were measured. Magnetic resonance imaging was performed to identify spinal cord compression. Results—There were significant differences in ECRM and CTM onset latencies between Doberman Pinschers with DAWS and each of the 2 groups of clinically normal dogs, but there were no significant differences in ECRM and CTM onset latencies between the 2 groups of clinically normal dogs. There were significant differences in CTM peak-to-peak amplitudes between Doberman Pinschers with DAWS and each of the 2 groups of clinically normal dogs, but there were no significant differences in ECRM peak-to-peak amplitudes among groups or in CTM peak-to-peak amplitudes between the 2 groups of clinically normal dogs. There was a significant correlation between severity of spinal cord compression and ECRM onset latency, CTM onset latency, and CTM peak-to-peak amplitude. Conclusions and Clinical Relevance—Results suggested that transcranial magnetic stimulation may be a useful diagnostic tool to differentiate between clinically relevant and clinically irrelevant spinal cord compression identified on MRI alone.

We evaluated the feasibility of interictal single photon emission computed tomography (SPECT) to detect alterations in regional cerebral blood flow and neuronal activity in dogs with idiopathic epilepsy. Twelve dogs with idiopathic epilepsy underwent interictal technetium-99m-ethyl cysteinate dimer SPECT of the brain. Different cortical regions of interest (ROIs), 1 ROI at the cerebellum and 1 ROI at the subcortical area were evaluated by semiquantitative analysis and compared with a control group (18 dogs). Significant hypoperfusion (P = 0.02) was present in the subcortical area of epileptic dogs. This hypoperfusion was not associated with seizure frequency, age at onset of seizures, duration of epilepsy, or time since the last seizure. Interictal SPECT did not reveal cortical or cerebellar perfusion alterations. The subcortical area may play an important role in the pathophysiology of canine idiopathic epilepsy.

The aim of this study was to determine the electrocardiographic characteristics of whippets and to compare the results with published reference values for a general dog population. Electrocardiographic parameters from 105 healthy whippets were used to establish reference values for the breed. The most important differences compared to published reference values were the higher median R-wave amplitudes in leads II, CV6LL and CV6LU. For some parameters (P-wave amplitude, ST-segment deflection and T-wave amplitude in lead II; R-wave amplitude in CV5RL), a marked percentage of the whippet values were above the published maximum reference data. The results confirmed that whippets have electrocardiographic characteristics similar to those reported in athletic heart syndrome in humans. Some of these characteristics could be erroneously taken as evidence of cardiac disease and clinicians should be aware of these factors to prevent unnecessary investigations in healthy dogs.

Objective— To report the clinical signs, diagnosis, and surgical treatment of an intranasal meningoencephalocele in a dog. Study Design— Case report. Animal— Female Border collie, 5 months old. Methods— A right intranasal meningoencephalocele was identified by computed tomography and magnetic resonance imaging. Results— The lesion was approached by a modified transfrontal craniotomy. Surgical closure of the defect at the level of the cribriform plate and removal of extruded brain tissue resulted in regression of lacrimation and coincided with absence of seizuring. Treatment with phenobarbital was gradually reduced and stopped at 7 months after surgery. At 28 months the dog remained free of seizures. Conclusion— Meningoencephalocele, although rare, can cause seizures in dogs and can be treated surgically. Clinical Relevance— A transfrontal craniotomy with excision of the meningoencephalocele and closure of the defect can be an effective treatment for an intranasal meningoencephalocele in dogs.

Een jonge, mannelijke rottweiler werd aangeboden met neurologische symptomen die sinds zijn geboorte aanwezig waren. De hond vertoonde hypermetrie op de voorhand, ataxie op de achterhand en zijn proprioceptie was achteraan duidelijk vertraagd. Computertomografisch onderzoek na myelografie en een MRI-onderzoek toonden een lang dorsaal subarachnoïdaal diverticulum aan, dat zich uitbreidde van craniaal C2 tot craniaal C5. Dit diverticulum veroorzaakte een ruggenmergcompressie, die de neurologische symptomen verklaarde. De hond werd geopereerd via een cervicale dorsale laminectomie, gevolgd door durotomie en marsupialisatie. Postoperatief waren er complicaties, waardoor de hond opnieuw geopereerd moest worden. Hierna was nog een vijftal dagen mechanische ventilatie nodig, waarna de hond weer zelfstandig kon ademen. De neurologische toestand van de hond verbeterde postoperatief geleidelijk. Hij herstelde volledig en deed het elf maanden postoperatief nog altijd goed.

Endogenous progesterone and synthetic progestins may induce hypersecretion of growth hormone (GH) of mammary origin, hyperplastic ductular changes in the mammary gland, and the development of cystic endometrial hyperplasia (CEH) in dogs. It was investigated whether progestin-induced mammary GH plays a role in the pathogenesis of CEH in the bitch. During 1 year, bitches with surgically excised mammary glands and healthy control bitches received medroxyprogesterone acetate (MPA). Before and after MPA treatment, uterine and mammary tissues were collected for histological, immunohistochemical, and RT-PCR examination. After MPA administration, the mammary tissue in the control dogs had differentiated into lobulo-alveolar structures and CEH was present in all uteri of both dog groups. In the MPA-exposed mammary tissue of the control dogs, GH could only be demonstrated immunohistochemically in proliferating epithelium. After treatment with MPA the dogs of both groups had immunohistochemically demonstrable GH in the cytoplasm of hyperplastic glandular uterine epithelial cells. RT-PCR analysis of the mammary gland tissue after MPA administration demonstrated a significant higher GH gene, and lower GHR gene expression than before treatment. In the uterus, the expression of the gene encoding for GH was significantly increased in the mastectomized dogs, whereas in the control dogs the expression of the gene encoding for insulin-like growth factor-I had significantly increased with MPA administration. MPA treatment significantly down regulated PR gene expression in the uterus in both dog groups. These results indicate that progestin-induced GH of mammary origin is not an essential component in the development of CEH in the bitch.

Background The macroscopic appearance of cutaneous adverse drug reactions can be similar to a plethora of skin diseases and in particular may resemble autoimmune and immune-mediated disorders. The reaction can occur after single or multiple administrations, with the latter varying in durations of up to years of treatment. These reactions are mostly self-limiting with cessation of the offending drug. Objectives To report a cutaneous adverse drug reaction associated with chronic administration of imepitoin. Case report A 4-year-old, Jack Russell terrier dog was presented with progressive skin lesions of 1-week duration. The dog had a 6 month history of idiopathic epilepsy treated with imepitoin for the previous 5 months. Imepitoin is an anti-epileptic drug that acts as a low-affinity partial agonist of the benzodiazepine site at the GABAA receptor. The dosage of imepitoin was increased from 20 mg/kg twice daily to 30 mg/kg twice daily, 3 days before the onset of skin lesions, due to uncontrolled seizures. [Correction added on 15 February 2016 after first online publication: In the preceding sentence, the dosage of imepitoin was previously incorrect and has been amended in this current version.] Dermatological examination revealed erythema and exfoliation at the mucocutaneous junctions of the lips, lip folds, philtrum, ears, axillae and the ventral abdomen. Small erosions and depigmentation were visible on the oral mucosa, lip folds and philtrum. Histopathology was supportive of a lupoid drug reaction. Complete resolution of skin lesions was seen after discontinuation of imepitoin and low dose of prednisolone during a period of 4 weeks. No recrudescence of skin lesions was observed during a 6 month follow-up period. Conclusion and clinical importance Imepitoin may result in cutaneous adverse drug reactions in dogs.

The effects of three growth hormone secretagogues (GHSs), ghrelin, growth hormone-releasing peptide-6 (GHRP-6), and growth hormone-releasing hormone (GHRH), on the release of adenohypophyseal hormones, growth hormone (GH), adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), luteinising hormone (LH), prolactin (PRL) and on cortisol were investigated in young and old healthy Beagle dogs. Ghrelin proved to be the most potent GHS in young dogs, whereas in old dogs GHRH administration was associated with the highest plasma GH concentrations. The mean plasma GH response after administration of ghrelin was significantly lower in the old dogs compared with the young dogs. The mean plasma GH concentration after GHRH and GHRP-6 administration was lower in the old dogs compared with the young dogs, but this difference did not reach statistical significance. In both age groups, the GHSs were specific for GH release as they did not cause significant elevations in the plasma concentrations of ACTH, cortisol, TSH, LH, and PRL. It is concluded that in young dogs, ghrelin is a more powerful stimulator of GH release than either GHRH or GHRP-6. Ageing is associated with a decrease in GH-releasing capacity of ghrelin, whereas this decline is considerably lower for GHRH or GHRP-6.

Magnetic stimulation of radial (RN) and sciatic (SN) nerves was performed bilaterally in 40 healthy cats. Reference values for onset latency and peak-to-peak amplitude of magnetic motor evoked potentials (MMEPs) were obtained and compared with values of electric motor evoked potentials (EMEPs) in 10/40 cats. Onset latencies and peak-to-peak amplitudes of the MMEPs of three cats with polyneuropathy (PNP) were compared to the reference values. Magnetic motor evoked responses were easily recorded in all normal cats. Significant differences were found in onset latencies between MMEPs and EMEPs, but peak-to-peak amplitudes were equal. The MMEPs of three cats with PNP can be seen as outliers in comparison to the reference values. MMEPs from the RN and SN were easily obtained and reproducible in normal cats. The technique could represent a useful adjunct in the assessment of peripheral nerve disorders. (C) 2011 Elsevier Ltd. All rights reserved.

Background Vagus nerve stimulation (VNS) is an established treatment for refractory epilepsy in humans, but the precise mechanism of action (MOA), predictive responsive factors and the optimal stimulation parameters remain to be elucidated. Objective We aimed to investigate the effect of two rapid cycling VNS paradigms on CSF monoamine levels and the seizure threshold in the canine pentylenetetrazole (PTZ) model. Methods Eight Beagle dogs, implanted with a VNS Therapy ® System, participated in a cross-over study. Levels of serotonin (5HT), norepinephrine (NE) and dopamine (DA) were quantified in the CSF after 1 h of sham, standard and microburst VNS with a wash-out period of 1 month. One week after the CSF experiment, the PTZ seizure threshold was determined after the same stimulation paradigm. As a positive control, the PTZ seizure threshold was determined after a single oral dose of phenobarbital. Results Rapid cycling standard and microburst VNS caused a significant increase of NE levels in the CSF ( P = 0.03 and P = 0.02 respectively). No significant changes in 5HT or DA levels were detected. Rapid cycling standard and microburst VNS did not cause significant changes in the PTZ seizure threshold compared to sham. Conclusions VNS induces an increase of NE in the canine brain, which supports previous findings indicating that VNS influences the locus coeruleus-NE (LC/NE) system. Importantly, this study demonstrates that this increase in NE is measurable in the CSF. One hour of VNS did not affect seizure threshold in the canine PTZ model. Therefore, the role of NE in the antiepileptic effect of VNS in dogs remains to be elucidated.

Two male neutered domestic shorthair cats were evaluated for generalised tremors. On neurological examination both cats showed whole-body tremors, worsening with stress. A mainly cerebellar disorder was suspected. Blood examination, cerebrospinal fluid analysis and electrophysiological examination of both cats and magnetic resonance imaging of the brain in one cat were normal. Idiopathic generalised tremor syndrome (IGTS) was suspected owing to the exclusion of underlying causes and the clinical similarities with the syndrome in dogs. Treatment as recommended for dogs was initiated and resulted in improvement. This report describes the first cases of IGTS in cats.