Comparison between noncontrast computed tomography and magnetic resonance imaging for detection and characterization of thoracolumbar myelopathy caused by intervertebral disk herniation in dogs.

Magnetic resonance imaging (MRI) and computed tomography (CT) are commonly used to evaluate dogs with thoracolumbar myelopathy; however, relative diagnostic sensitivities for these two modalities have not been previously reported. The purpose of this prospective study was to compare diagnostic sensitivity and observer agreement for MRI and CT in a group of dogs with thoracolumbar myelopathy due to surgically confirmed intervertebral disk herniation (IVDH). All included dogs had magnetic resonance (MR) imaging followed by noncontrast CT using standardized protocols. Three experienced observers interpreted each imaging study independently without knowledge of clinical or surgical findings. The operating surgeon was aware of MR findings but not CT findings at the time surgical findings were recorded. Forty-four dogs met the inclusion criteria. The sensitivity of CT was 88.6% (79.5%-94.2%) and of MR was 98.5% (95% confidence interval, 94.1%-99.7%) for diagnosis of intervertebral disk herniation. Specificity was not calculated, as all dogs had IVDH at surgery. Magnetic resonance imaging was more accurate than CT for identifying the site of intervertebral disk herniation-associated spinal cord compression and differentiating disk extrusion vs. protrusion. Computed tomography was less accurate for lesion localization in per acute cases, as well as for chondrodystrophic, female, older and smaller (<7 kg) dogs. Inter-rater agreement was good for lesion lateralization for both MR and CT (κ = 0.687, 95% CI = 0.552, 0.822, P = 0.002, and κ = 0.692, 95% CI = 0.542, 0.842, P = 0.003). Findings from the current study indicated that MR imaging was more sensitive and accurate than noncontrast CT for diagnosis and characterization of thoracolumbar myelopathy due to IVDH in dogs.

Hypereosinophilic syndrome presenting as coagulopathy.

BACKGROUND: Hypereosinophilic syndrome (HES) is an extremely uncommon group of disorders. It rarely presents with coagulopathy without cardiac involvement. CASE PRESENTATION: A 33-year-old previously healthy male with no history of atopic disease presented with abdominal pain, hematochezia, peripheral eosinophilia as high as 10,000 eos/µL, right and left portal vein, mesenteric, and splenic vein thrombi with ischemic colitis resulting in hemicolectomy and small bowel resection. Despite an extensive workup for primary and secondary etiologies of hypereosinophilia by hematology/oncology, infectious disease, rheumatology and allergy/immunology, no other clear causes were identified, and the patient was diagnosed with idiopathic HES. His eosinophilia was successfully treated with high-dose oral corticosteroids (OCS) and subsequently transitioned to anti-IL-5-receptor therapy with benralizumab. He has continued this treatment for over a year with no recurrence of eosinophilia or thrombosis while on benralizumab. CONCLUSION: In patients with an unexplained coagulopathy and eosinophilia, eosinophilic disorders such as HES should be considered. Corticosteroid-sparing agents, such as benralizumab show promise for successfully treating these patients.

Pregabalin as an adjunct to phenobarbital, potassium bromide, or a combination of phenobarbital and potassium bromide for treatment of dogs with suspected idiopathic epilepsy.

OBJECTIVE: To assess tolerability and short-term efficacy of oral administration of pregabalin as an adjunct to phenobarbital, potassium bromide, or a combination of phenobarbital and potassium bromide for treatment of dogs with poorly controlled suspected idiopathic epilepsy. DESIGN: Open-label, noncomparative clinical trial. ANIMALS: 11 client-owned dogs suspected of having idiopathic epilepsy that was inadequately controlled with phenobarbital, potassium bromide, or a combination of these 2 drugs. PROCEDURES: Dogs were treated with pregabalin (3 to 4 mg/kg [1.4 to 1.8 mg/lb], PO, q 8 h) for 3 months. Number of generalized seizures in the 3 months before and after initiation of pregabalin treatment was recorded. Number of responders (>or= 50% reduction in seizure frequency) was recorded, and seizure frequency before and after initiation of pregabalin treatment was compared by use of a nonparametric Wilcoxon signed rank test. RESULTS: Seizures were significantly reduced (mean, 57%; median, 50%) after pregabalin administration in the 9 dogs that completed the study; 7 were considered responders with mean and median seizure reductions of 64% and 58%, respectively. Adverse effects for pregabalin were reported in 10 dogs. Mean and median plasma pregabalin concentrations for all dogs were 6.4 and 7.3 microg/mL, respectively. CONCLUSIONS AND CLINICAL RELEVANCE: Pregabalin may hold promise as a safe and effective adjunct anticonvulsant drug for epileptic dogs poorly controlled with the standard drugs phenobarbital or potassium bromide. Adverse effects of pregabalin appeared to be mild. Additional studies with larger numbers of dogs and longer follow-up intervals are warranted.

Retinal pathology in a canine model of late infantile neuronal ceroid lipofuscinosis.

PURPOSE: Late infantile neuronal ceroid lipofuscinosis (NCL) is an inherited disorder characterized by progressive vision loss. The disease results from mutations in the TPP1 (CLN2) gene. Studies were undertaken to characterize the effects of a TPP1 frameshift mutation on the retina in Dachshunds. METHODS: A litter of four puppies consisting of one homozygous affected dog, two heterozygotes, and one homozygous normal dog were monitored for neurologic and retinal changes through 10 months of age. The affected and homozygous normal dogs, as well as one of the heterozygotes, were then euthanatized, and the retinas were examined morphologically. RESULTS: The affected dog exhibited normal visual behavior and retinal function at 3 months of age, but vision was clearly impaired by 7 months, with markedly reduced ERG b-wave amplitudes. Beyond 7 months of age, the affected dog was functionally blind, and pupillary light reflexes and ERG response amplitudes continued to decline through 10 months of age. Both rod and cone system functions were severely impaired. The retina exhibited accumulation of autofluorescent storage bodies with distinctive curvilinear contents. Substantial cell loss occurred in the inner nuclear layer, with a smaller reduction in photoreceptor cell density. CONCLUSIONS: The canine TPP1 mutation results in progressive vision loss and retinal degeneration similar to that which occurs in human late infantile NCL. With the canine model, the natural history of disease progression in the retina provides a better understanding of the pathologic course of the disease and provides objective markers that can be used to assess the efficacy of therapeutic interventions.

Human rhinovirus infection causes different DNA methylation changes in nasal epithelial cells from healthy and asthmatic subjects.

BACKGROUND: Mechanisms underlying the development of virus-induced asthma exacerbations remain unclear. To investigate if epigenetic mechanisms could be involved in virus-induced asthma exacerbations, we undertook DNA methylation profiling in asthmatic and healthy nasal epithelial cells (NECs) during Human Rhinovirus (HRV) infection in vitro. METHODS: Global and loci-specific methylation profiles were determined via Alu element and Infinium Human Methylation 450 K microarray, respectively. Principal components analysis identified the genomic loci influenced the most by disease-status and infection. Real-time PCR and pyrosequencing were used to confirm gene expression and DNA methylation, respectively. RESULTS: HRV infection significantly increased global DNA methylation in cells from asthmatic subjects only (43.6% to 44.1%, p = 0.04). Microarray analysis revealed 389 differentially methylated loci either based on disease status, or caused by virus infection. There were disease-associated DNA methylation patterns that were not affected by HRV infection as well as HRV-induced DNA methylation changes that were unique to each group. A common methylation locus stood out in response to HRV infection in both groups, where the small nucleolar RNA, H/ACA box 12 (SNORA12) is located. Further analysis indicated that a relationship existed between SNORA12 DNA methylation and gene expression in response to HRV infection. CONCLUSIONS: We describe for the first time that Human rhinovirus infection causes DNA methylation changes in airway epithelial cells that differ between asthmatic and healthy subjects. These epigenetic differences may possibly explain the mechanism by which respiratory viruses cause asthma exacerbations.

Imaging diagnosis--magnetic resonance imaging pseudolesion associated with the petrous temporal bone.

Normal anatomic variation in the amount of fat within the petrous temporal bone of dogs can result in a magnetic resonance (MR) imaging pseudolesion. Focal hyperintense areas in the region of the hippocampus on T1-weighted, T1-weighted, and fluid-attenuated inversion recovery imaging sequences were noted in a dog being imaged for seizure activity. Further investigation of this region, aided by the use of cadaveric specimens, led to the identification of normal anatomic variability in the amount of fat in the substantia spongiosa of the petrous temporal bone. The presence of normal adipose tissue was confirmed histopathologically. Fat suppression MR imaging sequences can be used to differentiate whether hyperintensity ventral to the hippocampus is a result of a pathologic process, or fat in the substantia spongiosa of the petrous temporal bone.

Intracranial magnetic resonance imaging artifacts and pseudolesions in dogs and cats.

Normal anatomic variation, study design, external factors, and tissue characteristics can all influence the manifestation of structures on magnetic resonance images (MRI). For the purpose of this review, imaging artifacts are considered to be nonpathologic abnormalities resulting from study design, intrinsic tissue characteristics, or external factors, while MRI pseudolesions are due to normal anatomic variation. Awareness of imaging artifacts and pseudolesions, as well as normal anatomic structures, is important when determining pathologic vs. normal or clinically insignificant abnormalities. The purpose of this report is to examine the literature to compile a review of selected artifacts and pseudolesions that are commonly encountered when imaging the canine and feline brain.