Preliminary investigation of serum cardiac troponin I in dogs with acute ischaemic stroke.

OBJECTIVES: To describe the incidence of elevated serum cardiac troponin I in dogs with acute ischaemic strokes, to evaluate its prognostic value in these patients and characterise a possible relationship between cardiac troponin I elevation in dogs with ischaemic strokes and underlying cardiac dysfunction. MATERIALS AND METHODS: Prospective study of 18 dogs with acute ischaemic stroke diagnosed by MRI of the brain. Serum cardiac troponin I concentration, trans-thoracic echocardiography and six-lead electrocardiography were performed and findings were compared between dogs with good and poor outcome. RESULTS: Serum cardiac troponin I was increased in 17 dogs (median 0.95 ng/mL; range 0.146 to 153). Focal hyperechoic regions of myocardium were visible in two dogs using trans-thoracic echocardiography and presumed to represent acute infarcts. A significant association was found between cardiac troponin I and creatinine concentrations. No difference in cardiac troponin I concentrations was detected between dogs that experienced good and poor outcomes. Clinically important cardiac dysfunction was identified in two dogs. CLINICAL SIGNIFICANCE: Cardiac troponin I is commonly elevated in patients diagnosed with acute ischaemic stroke but, in this small study population, did not have prognostic value. Larger studies (recruiting a study population of 98 dogs for a power of 0.8 and a 0.05 alpha/critical value) would aid in further investigation of these preliminary results.

Clinicopathologic Features and Magnetic Resonance Imaging Findings in 24 Cats With Histopathologically Confirmed Neurologic Feline Infectious Peritonitis.

BACKGROUND: Feline infectious peritonitis (FIP) is the most common infectious central nervous system (CNS) disease in the cat and is invariably fatal. Improved means of antemortem diagnosis is required to facilitate clinical decision making. Information regarding the magnetic resonance imaging (MRI) findings of neurologic FIP currently is limited, resulting in the need for better descriptions to optimize its use as a diagnostic tool. OBJECTIVE: To describe the clinicopathologic features and MRI findings in cases of confirmed neurologic FIP. ANIMALS: Twenty-four client-owned cats with histopathologic confirmation of neurologic FIP. METHODS: Archived records from 5 institutions were retrospectively reviewed to identify cases with confirmed neurologic FIP that had undergone antemortem MRI of the CNS. Signalment, clinicopathologic, MRI, and histopathologic findings were evaluated. RESULTS: Three distinct clinical syndromes were identified: T3-L3 myelopathy (3), central vestibular syndrome (7), and multifocal CNS disease (14). Magnetic resonance imaging abnormalities were detected in all cases, including meningeal contrast enhancement (22), ependymal contrast enhancement (20), ventriculomegaly (20), syringomyelia (17), and foramen magnum herniation (14). Cerebrospinal fluid was analysed in 11 cases; all demonstrated a marked increase in total protein concentration and total nucleated cell count. All 24 cats were euthanized with a median survival time of 14 days (range, 2-115) from onset of clinical signs. Histopathologic analysis identified perivascular pyogranulomatous infiltrates, lymphoplasmacytic infiltrates, or both affecting the leptomeninges (16), choroid plexuses (16), and periventricular parenchyma (13). CONCLUSIONS AND CLINICAL IMPORTANCE: Magnetic resonance imaging is a sensitive means of detecting neurologic FIP, particularly in combination with a compatible signalment, clinical presentation, and CSF analysis.

Magnetic resonance imaging findings in epileptic cats with a normal interictal neurological examination: 188 cases.

Epilepsy is a common neurological condition in dogs and cats. Although an increased likelihood of significant brain lesions with age has been identified in neurologically normal dogs with epileptic seizures, the underlying aetiology of epileptic seizures in cats that present with normal physical and neurological examinations remains unknown. In this cross-sectional study, the authors examined MRI findings in a large population of cats with a normal interictal physical and neurological examination. They hypothesised that age would have an impact on the prevalence of detectable lesions. First, following the guidelines for dogs and in accordance with previous studies, the authors divided the cats into three age groups (aged one year or younger, between one and six, and older than six) and calculated the proportion of cats with a detectable lesion on MRI in these groups. In the first group, 3/32 cats (9.4 per cent) had significant MRI abnormalities that were all consistent with congenital malformation; in the second group, only 5/92 (5.4 per cent) MRI scans were abnormal and in the third group, 15/ 65 (23.1 per cent) cats showed abnormal findings that were predominantly lesions of neoplastic origin. Second, to investigate the impact of age further, data were investigated as a continuous variable using receiver operating characteristic analysis. This indicated an optimal cut-off age of five years, above which MRI abnormalities were more likely, with an increase in the odds of a significant structural lesion increasing by 14 per cent per year.

Dystrophin-deficient muscular dystrophy in a Norfolk terrier.

A six-month-old male entire Norfolk terrier was presented with a 3-month history of poor development, reluctance to exercise and progressive and diffuse muscle atrophy. Serum creatine kinase concentration was markedly elevated. Magnetic resonance imaging of the epaxial muscles revealed asymmetrical streaky signal changes aligned within the muscle fibres (hyperintense on T2-weighted images and short-tau inversion recovery with moderate contrast enhancement on T1-weighted images). Electromyography revealed pseudomyotonic discharges and fibrillation potentials localised at the level of the supraspinatus, epaxial muscles and tibial cranialis muscles. Muscle biopsy results were consistent with dystrophin-deficient muscular dystrophy. The dog remained stable 7 months after diagnosis with coenzyme Q10 and l-carnitine; however after that time, there was a marked deterioration and the owners elected euthanasia. This case report describes the clinical presentation, magnetic resonance imaging, electrodiagnostic and histopathological findings with immunohistochemical analysis in a Norfolk terrier with confirmed dystrophin-deficient muscular dystrophy, which has not been previously described in this breed.

Dorsal stabilization of atlantoaxial subluxation using non-absorbable sutures in toy breed dogs.

OBJECTIVE: To describe a novel dorsal technique for stabilization of atlantoaxial subluxation in toy breed dogs using 3-metric nylon suture. STUDY: Retrospective study. ANIMALS: Fifteen toy breed dogs with a body weight of 2 kg or less with atlantoaxial subluxation. MATERIALS AND METHODS: The atlantoaxial joint of each dog was surgically stabilized through a dorsal approach by placing a double strand of non-absorbable, 3-metric, nylon suture material between the dorsal muscles of the atlanto-occipital and the atlantoaxial joint muscles. Pre- and postoperative neurological status, diagnostic imaging, and complications were reviewed. Clinical follow-up examination was performed at six months. For long-term assessment, a telephone follow-up was performed. RESULTS: No intra-operative complications were observed. Functional improvement occurred in 12 dogs. One dog did not improve and four dogs required revision surgery. In two of those four cases, suture material breakage was proven and it was suspected in the other two. Two cases underwent a second dorsal approach with the same suture material and two cases underwent a ventral approach (transarticular fixation and multiple implants embedded with polymethylmethacrylate). CONCLUSIONS: Dorsal stabilization using 3-metric nylon may be adequate as a safe, effective, and simple alternative technique for atlantoaxial stabilization in toy breed dogs of ≤1.5 kg of weight, in which the use of ventral screws and pins is challenging.

Hypomyelination in three Weimaraner dogs.

Hypomyelination syndrome of the Weimaraner dog is a disease characterised by a reduction or absence of myelin in the axons of the central nervous system (CNS) exclusively. The objective of this study was to analyse the cause of this deficiency of myelin. Tissue samples of the CNS of three Weimaraner dogs with neurological signs were fixed in 10% formalin and embedded in paraffin wax, and histochemical, immunohistochemical and ultrastructural studies were performed. Histochemical staining with haematoxylin and eosin and Kluver-Barrera techniques showed generalised pallor in the peripheral areas of the ventral and lateral funiculi of the spinal cord. Immunohistochemical analysis showed a weak expression of both proteolipid protein (PLP) and myelin basic protein (MBP) and a marked decrease of Olig2(+) cells in the demyelinated areas. The immunohistochemical findings suggested a myelination or remyelination failure because of the smaller population of oligodendrocytes. However, PLP gene mutations may also be the cause of the decrease of PLP expression as described in other species.