Description and clinical relevance of the variable conformation of canine spinal arachnoid diverticula.

The conformation of spinal arachnoid diverticula (SAD) and their clinical implications are poorly characterized in dogs. This retrospective cross-sectional study describes different SAD conformations in dogs and aims to identify if there is an association between SAD conformation and clinical features, localization, syringomyelia (SM) presence, concurrent vertebral condition, treatment option, and short as well as long-term outcome. Sixty-two dogs were included (12 cervical and 50 thoracolumbar SAD). All dogs with a cervical SAD had a cranial tethered conformation and were not included in the statistical analysis. Half of the dogs with a thoracolumbar SAD were cranial tethered, and the other half were caudal tethered. SM associated with SAD had a moderate prevalence in the cervical region (58.3%) and a high prevalence in the thoracolumbar region (82%). All dogs with the presence of SM and caudal tethered SAD had a cranial positioned SM, and all dogs with SM and a cranial tethered SAD had a caudal positioned SM. The SM absolute length and SM length/L2 ratio were significantly higher (P = .018, respectively) in the caudal tethered SAD compared with the cranial tethered SAD. The short-term outcome was statistically different (P = .045) between caudal and cranial tethered thoracolumbar SAD, but not the long-term outcome (P = .062). Multivariable logistic regression identified thoracolumbar caudal tethered SAD conformation had a better short-term outcome (P = 0.017, OR: 0.043, CI: 0.003-0.563), independently of SM length measurements. SAD conformation in dogs can influence SM formation. A possible link between short-term outcome and SAD conformation was found, but further research is warranted.

A case series of 37 surgically managed, paraplegic, deep pain negative French bulldogs, with thoracolumbar intervertebral disc extrusion, from two English referral centres.

Background: Thoracolumbar intervertebral disc extrusions (TL-IVDEs) are a common spinal disorder in dogs, especially within chondrodystrophic breeds. Loss of deep pain perception is a well-documented negative prognostic indicator in dogs with TL-IVDE. The objectives of this study were to report the rate of return of deep pain perception and independent ambulation in surgically treated, paraplegic, deep pain perception negative French bulldogs with TL-IVDEs. Methods: A retrospective case series of deep pain perception negative dogs with TL-IVDE presenting to two referral centres between 2015 and 2020 was conducted. Medical and MRI records were reviewed, including the following quantitative MRI changes: lesion length, extent of spinal cord swelling and severity of spinal cord compression. Results: Thirty-seven French bulldogs met the inclusion criteria, with 14 of 37 (38%) regaining deep pain perception by the time of discharge (median hospitalisation 10.0 days [interquartile range 7.0-15.5 days]) with two dogs independently ambulatory (6%). Ten of the 37 dogs were euthanased during hospitalisation. Significantly fewer dogs (3/16, 19%) with L4-S3 lesions regained deep pain perception compared to 11 of 21 (52%) of dogs with T3-L3 lesions (p = 0.048). Quantitative MRI changes were not associated with the return of deep pain perception. After discharge, with a median 1-month follow-up period, an additional three dogs regained deep pain perception and five dogs became independently ambulatory (17/37 [46%] and 7/37 [19%], respectively). Conclusions and clinical importance: This study adds support to the contention that the recovery of French bulldogs with TL-IVDE from surgery is poor compared with other breeds; further prospective, breed-controlled studies are indicated.

Risk factors associated with short-term mortality and recurrence of status epilepticus in dogs.

BACKGROUND: Status epilepticus (SE) is an emergency associated with serious consequences for both patient and owner. Data regarding risk factors for short-term mortality or recurrence in dogs with SE is limited. OBJECTIVE: Identify risk factors associated with short-term mortality (euthanasia or spontaneous death) and recurrence of SE in dogs. ANIMALS: One hundred twenty-four client-owned dogs that sustained an episode of SE. METHODS: Retrospective multicenter study using data collected from medical records of dogs presented in SE to the contributing institutions. Multivariable logistic regression analysis was performed using a manual backwards stepwise approach to identify risk factors associated with short-term mortality and recurrence of SE after discharge. RESULTS: Short-term mortality for affected dogs was 29.8%. Factors significantly associated with short-term mortality included increased patient age, shorter duration of hospitalization, development of SE before arrival, and SE caused by a potentially fatal etiology. Status epilepticus recurred in 27% of dogs that survived to discharge. Factors significantly associated with recurrence of SE included prior history of pharmacoresistant epilepsy and predominance of a focal seizure phenotype. CONCLUSIONS AND CLINICAL IMPORTANCE: Our results may be used to inform clinicians and dog owners regarding risk factors for both short-term mortality and recurrence in dogs with SE.

Linear magnetic resonance imaging measurements of the hippocampal formation differ in young versus old dogs.

Age-related hippocampal formation (HF) atrophy has been documented on MRI studies using volumetric analysis and visual rating scales.This retrospective cross-sectional study aimed to compare linear MRI measurements of the HF between young (1-3 years) and old (>10 years) non-brachycephalic dogs, with normal brain anatomy and cerebrospinal fluid (CSF) analysis. Right and left hippocampal formation height (HFH), height of the brain (HB) and mean HFH/HB ratio were measured by two observers on a transverse T2 fluid-attenuated inversion recovery sequence containing rostral colliculi and mesencephalic aqueduct.119 MRI studies were enrolled: 75 young and 44 old dogs. Left and right HFH were greater (p<0.0001) in young, while HB was greater in old dogs (p=0.024). Mean HFH/HB ratio was 15.66 per cent and 18.30 per cent in old and young dogs (p<0.0001). No differences were found comparing measurements between epileptic and non-epileptic dogs.Old dogs have a greater HB; this may represent the different study populations or a statistical phenomenon. Ageing affects HF linear measurements. A reduction of mean HFH/HB ratio between 18.30 per cent and 15.66 per cent should be considered a physiological age-related process of the canine lifespan. The use of mean HFH/HB ratio could be considered for quantifying brain atrophy in elderly dogs.

Hereditary ataxia in four related Norwegian Buhunds.

CASE DESCRIPTION Two 12-week-old Norwegian Buhunds from a litter of 5 were evaluated because of slowly progressive cerebellar ataxia and fine head tremors. Two other females from the same pedigree had been previously evaluated for similar signs. CLINICAL FINDINGS Findings of general physical examination, CBC, and serum biochemical analysis were unremarkable for all affected puppies. Brain MRI and CSF analysis, including PCR assays for detection of Toxoplasma gondii, Neospora caninum, and canine distemper virus, were performed for 3 dogs, yielding unremarkable results. Urinary organic acid screening, enzyme analysis of fibroblasts cultured from skin biopsy specimens, and brainstem auditory-evoked response testing were performed for 2 puppies, and results were also unremarkable. TREATMENT AND OUTCOME The affected puppies were euthanized at the breeder's request, and their brains and spinal cords were submitted for histologic examination. Histopathologic findings included a markedly reduced expression of calbindin D28K and inositol triphosphate receptor 1 by Purkinje cells, with only mild signs of neuronal degeneration. Results of pedigree analysis suggested an autosomal recessive mode of inheritance. Candidate-gene analysis via mRNA sequencing for 2 of the affected puppies revealed no genetic variants that could be causally associated with the observed abnormalities. CLINICAL RELEVANCE Findings for the dogs of this report suggested the existence of a hereditary form of ataxia in Norwegian Buhunds with histologic characteristics suggestive of Purkinje cell dysfunction. The presence of hereditary ataxia in this breed must be considered both in clinical settings and for breeding strategies.

Clinical and genetic characterisation of dystrophin-deficient muscular dystrophy in a family of Miniature Poodle dogs.

Four full-sibling intact male Miniature Poodles were evaluated at 4-19 months of age. One was clinically normal and three were affected. All affected dogs were reluctant to exercise and had generalised muscle atrophy, a stiff gait and a markedly elevated serum creatine kinase activity. Two affected dogs also showed poor development, learning difficulties and episodes of abnormal behaviour. In these two dogs, investigations into forebrain structural and metabolic diseases were unremarkable; electromyography demonstrated fibrillation potentials and complex repetitive discharges in the infraspinatus, supraspinatus and epaxial muscles. Histopathological, immunohistochemical and immunoblotting analyses of muscle biopsies were consistent with dystrophin-deficient muscular dystrophy. DNA samples were obtained from all four full-sibling male Poodles, a healthy female littermate and the dam, which was clinically normal. Whole genome sequencing of one affected dog revealed a >5 Mb deletion on the X chromosome, encompassing the entire DMD gene. The exact deletion breakpoints could not be experimentally ascertained, but we confirmed that this region was deleted in all affected males, but not in the unaffected dogs. Quantitative polymerase chain reaction confirmed all three affected males were hemizygous for the mutant X chromosome, while the wildtype chromosome was observed in the unaffected male littermate. The female littermate and the dam were both heterozygous for the mutant chromosome. Forty-four Miniature Poodles from the general population were screened for the mutation and were homozygous for the wildtype chromosome. The finding represents a naturally-occurring mutation causing dystrophin-deficient muscular dystrophy in the dog.

Magnetic resonance imaging features of leukoaraiosis in elderly dogs.

Leukoaraiosis is a descriptive term used to designate bilateral, symmetrical, white matter lesions identified in brains of elderly human patients. These lesions are isointense to normal in magnetic resonance imaging (MRI) T1-weighted pulse sequences, non-contrast enhancing, and hyperintense in T2-weighted and FLAIR pulse sequences. Pathophysiologic mechanisms for leukoaraiosis remain incompletely understood; however, an ischemic origin is currently being favored. Age-related changes, such as brain atrophy, ventricular enlargement, and well-demarcated sulci, have also been previously described in dogs over 9 years of age. Objectives of this retrospective case series study were to describe MRI features of leukoaraiosis and brain atrophy in a group of elderly dogs. The Dick White Referrals MRI database between October 2009 and April 2016 was reviewed. Dogs with bilaterally symmetrical periventricular areas of T2 and FLAIR hyperintensity compatible with leukoaraiosis, and older than 9 years, were included. Fourteen dogs met the inclusion criteria, with a total of 18 MRI studies available for review. Median age for sampled dogs was 13 years. Ten dogs had MRI signs of concurrent brain atrophy; one of them had signs of brain atrophy before leukoaraiotic changes could be identified. In those cases where serial MRIs were available, progressive reduction of interthalamic adhesion thickness was observed. The current study introduces leukoaraiosis as a descriptive term for the MRI sign of bilaterally symmetrical, periventricular T2, and FLAIR hyperintensities in brains of elderly dogs. Future studies are needed to determine pathophysiologic mechanisms for this MRI sign.

Slowly progressive lymphohistiocytic meningoencephalomyelitis in 21 adult cats presenting with peculiar neurological signs.

Twenty-one cats presented with a history of slowly progressive neurological signs characterised by a stiff extended tail, behavioural changes, and spastic and ataxic gait. All cats had outdoor access and lived in the same geographical rural area in north-east Scotland. Histological findings were consistent with lymphohistiocytic meningoencephalomyelitis. Immunohistochemistry ruled out 15 pathogens and showed a significant expression of the interferon-inducible Mx protein, suggesting an as yet unidentified infective or environmental immunogenic trigger as the possible causative agent. The late age at onset (mean 9 years), the very slow progression of clinical signs (mean 11 months) and the peculiar clinical presentation (particularly the posture of the tail) have not been reported previously in cats with lymphohistiocytic meningoencephalomyelitis.

Surgical technique, postoperative complications and outcome in 14 dogs treated for hydrocephalus by ventriculoperitoneal shunting.

OBJECTIVE: To report frequency and type of complications, and outcome in dogs with severe neurologic signs secondary to internal, suspected obstructive hydrocephalus treated by ventriculoperitoneal (VP) shunting. STUDY DESIGN: Case series. ANIMALS: Dogs (n=14). METHODS: Medical records (2001-2006) was reviewed for dogs that had VP shunting. Inclusion criteria were complete medical record, progressive forebrain signs unresponsive to medical treatment, normal metabolic profile, negative antibody titers and/or cerebrospinal PCR for Toxoplasma gondii, Neospora caninum, and canine distemper virus, magnetic resonance images of the brain, confirmed diagnosis of VP shunting, and follow-up information. RESULTS: Hydrocephalus was idiopathic in 5 dogs and acquired (interventricular tumors, intraventricular hemorrhage, inflammatory disease) in 9 dogs. Four dogs developed complications 1 week to 18 months postoperatively, including ventricular catheter migration, infection, shunt under-drainage, kinking of the peritoneal catheter, valve fracture, and abdominal skin necrosis. Three of these dogs had 1 or more successful revision surgeries and 1 dog was successfully treated with antibiotics. All, but 1 dog, were discharged within 1 week of surgery, and had substantial neurologic improvement. Median survival time for all dogs was 320 days (1-2340 days), for dogs with idiopathic hydrocephalus, 274 (60-420) days and for dogs with secondary hydrocephalus, 365 (1-2340) days. CONCLUSIONS: VP shunting was successful in relieving neurologic signs in most dogs and postoperative complications occurred in 29%, but were resolved medically or surgically.

Prevalence, heritability and genetic correlations of congenital sensorineural deafness and pigmentation phenotypes in the Border Collie.

The objectives of this study were to estimate prevalence, heritability and genetic correlations of congenital sensorineural deafness (CSD) and pigmentation phenotypes in the Border Collie. Entire litters of Border Collies that presented to the Animal Health Trust (1994-2008) for assessment of hearing status by brain stem auditory evoked response (BAER) at 4-10 weeks of age were included. Heritability and genetic correlations were estimated using residual maximum likelihood (REML). Of 4143 puppies that met the inclusion criteria, 97.6% had normal hearing status, 2.0% were unilaterally deaf and 0.4% were bilaterally deaf. Heritability of deafness as a trichotomous trait (normal/unilaterally deaf/bilaterally deaf) was estimated at 0.42 using multivariate analysis. Genetic correlations of deafness with iris colour and merle coat colour were 0.58 and 0.26, respectively. These results indicate that there is a significant genetic effect on CSD in Border Collies and that some of the genes determining deafness also influence pigmentation phenotypes.

Disseminated mast cell tumor infiltrating the sphenoid bone and causing blindness in a dog.

Mast cell tumors are found in most organs and tissues with variable biologic behavior in dogs. This case illustrates the clinical and magnetic resonance imaging (MRI) findings in a dog with disseminated mast cell tumor infiltrating the sphenoid bones. A 6-year-old male neutered Greyhound presented with a 3-day history of acute onset of blindness. General physical examination was normal. Neurological examination revealed mildly disorientated mental status, absent menace response in both eyes, bilaterally decreased vestibulo-oculocephalic reflexes and absent direct and consensual pupillary light reflex in both eyes. An electroretinogram indicated normal retinal function in both eyes. A lesion involving the middle and rostral cranial fossa was suspected. Hematology and serum biochemistry were normal except decreased urea (1.2 mmol/L). MRI of the head revealed heterogeneous signal intensity of the sphenoid bones on T2-weighted images and loss of their normal internal architecture. Cerebrospinal fluid analysis was normal. Abdominal ultrasound revealed hepatosplenomegaly and mesenteric lymphadenopathy. Fine needle aspirates were taken from the jejunal lymph nodes and the spleen. Results were consistent with disseminated mast cell tumor. The owner declined any treatment and the dog was euthanatized. Postmortem examination confirmed disseminated mast cell tumor affecting multiple organs, including the sphenoid bones. To our knowledge, this is the first case describing MRI features of disseminated mast cell tumor affecting the sphenoid bones and causing acute onset of blindness in a dog.

Clinical and magnetic resonance imaging findings in 92 cats with clinical signs of spinal cord disease.

Medical records of 92 cats presented with clinical signs of spinal cord disease, which had undergone magnetic resonance imaging (MRI), were reviewed. The cats were grouped into seven categories based upon the diagnosis suggested by results of MRI, cerebrospinal fluid analysis and other diagnostic procedures: neoplastic (n=25), inflammatory or infectious (n=13), traumatic (n=8), vascular (n=6), degenerative (n=5), anomalous (n=3) and those with an unremarkable MRI (n=32). There were two independent predictors of abnormal MRI findings: severity of clinical signs and presence of spinal pain. Abnormal MRI findings and speed of onset of disease were significantly associated with survival. For the 32 cats with unremarkable MRI findings, only nine died due to spinal disease and, therefore, the median survival time (MST) was not reached (lower 95% confidence interval (CI)=970 days). For the 60 cats with abnormal MRI findings, 37 died due to their disease and the MST was 138 days (95% CI: 7-807).

Magnetic resonance imaging features of spinal epidural empyema in five dogs.

Spinal epidural empyema is defined an accumulation of purulent material in the epidural space of the vertebral canal. Spinal epidural empyema should be considered as a differential diagnosis in dogs with pyrexia, spinal pain, and rapidly progressing myelopathy. Magnetic resonance (MR) imaging is the imaging test of choice in humans. Here, we describe the MR imaging features of five dogs with confirmed spinal epidural empyema. The epidural lesions appeared as high or mixed signal masses in T2-weighted (T2W) images. Increased signal within the spinal cord gray matter at the site of the lesion was detected in T2W images in all dogs. Two patterns of enhancement were detected on postcontrast T1-weighted (T1W) images. Mild to moderate peripheral enhancement was seen in three dogs and a diffuse pattern of enhancement was seen in one. Discospondylitis was identified in three dogs on T1W postcontrast images. Decompressive spinal surgery was performed in all dogs. Bacteria isolated from the abnormal epidural tissue were Enterobacter cloacae, coagulase-positive Staphylococci, Pasteurella multocida, and Escherichia coli. In one dog bacteria were not isolated. These MR imaging features, along with appropriate clinical signs, can allow prompt diagnosis and appropriate treatment planning.

Spinal cord injury resulting from incorrect microchip placement in a cat.

A 2-year-old, male neutered domestic shorthair cat was presented for investigation of an acute onset of tetraparesis immediately following the implantation of a pet identification microchip. A left-sided C6-T2 spinal segment localisation was suspected from the neurological examination, with spinal cord trauma being the primary differential diagnosis. Myelography demonstrated obliteration of the contrast columns by the microchip at the C5-C6 intervertebral disc space. A dorsal laminectomy was undertaken and the microchip was successfully removed. Eleven months after the surgery, the cat was able to weight bear in all limbs but with mild residual paresis in the left thoracic limb.

Magnetic resonance imaging in the diagnosis of canine inflammatory myopathies in three dogs.

In humans affected with inflammatory myopathies, regions of altered signal intensity are found on magnetic resonance (MR) images of affected muscles. Although electromyography (EMG) is more practical for muscle disease evaluation, and a muscle biopsy is the only manner in which a definitive diagnosis can be made, MR imaging has proven useful if a specific anatomic localization is difficult to achieve. Three dogs with focal inflammatory myopathy diagnosed with the assistance of MR imaging are discussed and the findings are compared with those found in humans. MR images of the affected muscles in each dog were characterized by diffuse and poorly marginated abnormal signal on T1- and T2-weighted images. Marked enhancement was noted in these muscles after contrast medium administration. An inflammatory myopathy was confirmed histologically in all three dogs. A good association existed between the MR images and muscle inflammation identified histopathologically. MR imaging may be a useful adjunctive procedure for canine inflammatory myopathies.

Hematomyelia secondary to lumbar cerebrospinal fluid acquisition in a dog.

A 2-year-old male (Hungarian Vizsla) was evaluated for progressive discomfort of possible spinal origin. A minimum data base, thoracolumbar magnetic resonance (MR) imaging examination and electrophysiologic investigation were all normal. Cerebellomedullary and lumbar cerebrospinal fluid (CSF) was collected. The fluid was unremarkable except for elevated total protein. Shortly, thereafter, the dog had progressive neurologic deterioration referable to a caudal lumbar spinal cord lesion. In a repeated MR examination there was a well-circumscribed intramedullary lesion at the site where lumbar CSF was collected. The signal characteristics of the lesion were compatible with subacute hemorrhage, which was confirmed to be hematomyelia at the time of successful decompressive surgery.