Transthoracic Vertebral Distraction and Stabilization in 10 Dogs with Congenital Thoracic Vertebral Malformations.

OBJECTIVE: The aim of this study was to describe the surgical technique and outcomes of dogs with congenital thoracic vertebral body malformations (CTVBM) treated with unilateral vertebral distraction and stabilization with monocortical screws and polymethylmethacrylate (PMMA). STUDY DESIGN: Medical records of 10 client-owned dogs with CTVBM were retrospectively searched for signalment, history, neurological examination, neurological grade based on the modified Frankel scale (MFS), diagnostic method, CTVBM location, Cobb's angle, and vertebral canal angle (VCA), surgical procedure, complications and long-term follow-up. RESULTS: One dog suffered cardiac arrest 24 hours post-surgery and died. Median follow-up in nine dogs was 26.5 months (12-50 months). Cobb's angle improved from 33-83 to 10-46 degrees and the VCA ratio from 97-138 to 122-164 degrees. The MFS improved from 3 (n = 3)-4 (n = 7) to 4 (n = 2)-6 (n = 7). Seven dogs recovered full function. Nine dogs improved after surgery compared with preoperative status, recovering ambulation when lost or achieving normal neurological examination in seven cases. No complications were reported during the follow-up period (12-50 months). CONCLUSION: Unilateral transthoracic vertebral distraction and stabilization with monocortical screws and PMMA for treatment of compressive myelopathy due to CTVBM achieved long-term neurological improvement in 9 of 10 dogs.

Clinical features, diagnosis, and survival analysis of dogs with glioma.

BACKGROUND: Gliomas in dogs remain poorly understood. OBJECTIVES: To characterize the clinicopathologic findings, diagnostic imaging features and survival of a large sample of dogs with glioma using the Comparative Brain Tumor Consortium diagnostic classification. ANIMALS: Ninety-one dogs with histopathological diagnosis of glioma. METHODS: Multicentric retrospective case series. Signalment, clinicopathologic findings, diagnostic imaging characteristics, treatment, and outcome were used. Tumors were reclassified according to the new canine glioma diagnostic scheme. RESULTS: No associations were found between clinicopathologic findings or survival and tumor type or grade. However, definitive treatments provided significantly (P = .03) improved median survival time (84 days; 95% confidence interval [CI], 45-190) compared to palliative treatment (26 days; 95% CI, 11-54). On magnetic resonance imaging (MRI), oligodendrogliomas were associated with smooth margins and T1-weighted hypointensity compared to astrocytomas (odds ratio [OR], 42.5; 95% CI, 2.42-744.97; P = .04; OR, 45.5; 95% CI, 5.78-333.33; P < .001, respectively) and undefined gliomas (OR, 84; 95% CI, 3.43-999.99; P = .02; OR, 32.3; 95% CI, 2.51-500.00; P = .008, respectively) and were more commonly in contact with the ventricles than astrocytomas (OR, 7.47; 95% CI, 1.03-53.95; P = .049). Tumor spread to neighboring brain structures was associated with high-grade glioma (OR, 6.02; 95% CI, 1.06-34.48; P = .04). CONCLUSIONS AND CLINICAL IMPORTANCE: Dogs with gliomas have poor outcomes, but risk factors identified in survival analysis inform prognosis and the newly identified MRI characteristics could refine diagnosis of tumor type and grade.

Traumatic L7 articular processes fracture and spondylolisthesis following dorsal lumbosacral laminectomy in a cat.

CASE SUMMARY: A 12-year-old neutered male domestic shorthair cat was presented to our referral hospital with a chronic history of tenesmus and lumbosacral pain. A diagnosis of degenerative lumbosacral stenosis (DLSS) was made and a standard dorsal L7-S1 laminectomy was performed uneventfully, with complete recovery within 1 month. The cat was brought back 4 months later for investigation of lumbosacral pain after having suffered a minor traumatic event. Neurological examination identified a low tail carriage, weakness, exercise intolerance, left pelvic limb lameness and diminished withdrawal reflexes in both pelvic limbs with severe sacrocaudal pain. A traumatic facet fracture of the L7 articular processes and subsequent spondylolisthesis was diagnosed. A second surgery was performed to stabilise the region. The cat was normal on neurological examination 1 month later and no further clinical signs were noted. RELEVANCE AND NOVEL INFORMATION: This is the first description of a fracture and spondylolisthesis as a possible postoperative complication after L7-S1 dorsal laminectomy in a cat. The case highlights the importance of postoperative changes in the supportive structures of the lumbosacral spine in cats after surgical treatment of DLSS.

Long-term follow-up of surgical resection alone for primary intracranial rostrotentorial tumors in dogs: 29 cases (2002-2013).

Intracranial neoplasia is frequently encountered in dogs. After a presumptive diagnosis of intracranial neoplasia is established based on history, clinical signs and advanced imaging characteristics, the decision to treat and which treatment to choose must be considered. The objective of this study is to report survival times (ST) for dogs with intracranial meningiomas and gliomas treated with surgical resection alone (SRA), to identify potential prognostic factors affecting survival, and to compare the results with the available literature. Medical records of 29 dogs with histopathologic confirmation of intracranial meningiomas and gliomas treated with SRA were retrospectively reviewed. For each dog, signalment, clinical signs, imaging findings, type of surgery, treatment, histological evaluation, and ST were obtained. Twenty-nine dogs with a histological diagnosis who survived >7 days after surgery were included. There were 15 (52%) meningiomas and 14 (48%) gliomas. All tumors had a rostrotentorial location. At the time of the statistical analysis, only two dogs were alive. Median ST for meningiomas was 422 days (mean, 731 days; range, 10-2735 days). Median ST for gliomas was 66 days (mean, 117 days; range, 10-730 days). Kaplan-Meier analysis indicated that ST was significantly longer for meningiomas than for gliomas (P<0.05). A negative correlation between the presence of a midline shift and ST (P=0.037) and ventricular compression and ST (P=0.038) was observed for meningiomas. For gliomas, there were no significant associations between ST and any of the variables evaluated. In conclusion, the results of this study suggest that, for dogs that survived >7 days postoperatively, SRA might be an appropriate treatment, particularly for meningiomas, when radiation therapy is not readily available. Also, the presence of midline shift and ventricular compression might be negative prognostic factors for dogs with meningiomas.

L-2-hydroxyglutaric aciduria in two female Yorkshire terriers.

Two female Yorkshire terrier puppies were presented with generalized tonic-clonic seizures and ataxia. MRI revealed bilaterally symmetrical, diffuse regions of gray matter hyperintensity on T2-weighted and fluid-attenuated inversion recovery sequences. Urinary organic acids were quantified by gas chromatography-mass spectroscopy and were consistent with a diagnosis of L-2-hydroxyglutaric aciduria (L2HGA). The L2HGDH gene encodes for the enzyme L-2-hydroxyglutarate dehydrogenase, which helps break down L-2-hydroxyglutaric acid. In both puppies described in this report, a homozygous mutation at the translation initiation codon of the homolog canine L2HGDH gene was detected (c.1A>G; p.Met1?), confirming the diagnosis of L2HGA at the DNA level. Canine L2HGA is caused by more than one mutation of L2HGDH, as reported in humans.

Magnetic resonance imaging of cerebral involutional changes in dogs as markers of aging: an innovative tool adapted from a human visual rating scale.

The dog is increasingly considered as a natural animal model for the study of normal and pathological human brain aging, because it exhibits anatomical, biochemical and cognitive changes that parallel those seen in humans. This study presents a novel visual semi-quantitative rating scale of canine cerebral magnetic resonance imaging (MRI). Ninety-eight dogs of both sexes from 27 pure breeds, aged 2-15 years, were used. The results suggest that (like in humans) both hippocampal and progressive global atrophy are characteristic features that correlate with aging. When classified according to head shape, cerebral atrophy was highest in mesaticephalic and brachycephalic dogs. This is the first MRI study to characterise a simple, rapid tool for studying age-related canine brain changes that can even be applied by non-experienced observers. The results confirm the possibility of transferring innovative tools developed for human diagnosis to the veterinary field.

Canine cognitive dysfunction and the cerebellum: acetylcholinesterase reduction, neuronal and glial changes.

The specific functional and pathological alterations observed in Alzheimer's disease are less severe in the cerebellum than in other brain areas, particularly the entorhinal cortex and hippocampus. Since dense core amyloid-beta plaque formation has been associated with an acetylcholinesterase heterogeneous nucleator action, we examined if an acetylcholinesterase imbalance was involved in cerebellum plaque deposition. By using the canine counterpart of senile dementia of the Alzheimer's type, a promising model of human brain aging and early phases of Alzheimer's disease, we investigated how cerebellar pathology and acetylcholinesterase density could be related with cognitive dysfunction. As in Alzheimer's disease, the late affectation of the cerebellum was evidenced by its lack of amyloid-beta plaque and the presence of diffuse deposition throughout all cortical grey matter layers. The highest acetylcholinesterase optic density corresponded to cerebellar islands of the granular layer and was predominantly associated with synaptic glomeruli and the somata of Golgi cells. Its reduction correlated with aging and loss of granule cells, whereas cognitive deficit only correlated with loss of Purkinje cells. The observed Bergmann glia alterations may correspond to a reactive response to the loss and damage of the Purkinje cells, their specific neuronal partner. Regarding the role of acetylcholinesterase mediation in amyloid-beta deposition, our data argue against an interaction between these two proteins because acetylcholinesterase reduction correlates with aging but not with cognitive deficit. Finally, our data support the use of companion dogs of all breeds to study aging and early phases of Alzheimer's disease.

Treatment with oral cyclosporin A of a case of vesicular cutaneous lupus erythematosus in a rough collie.

Cyclosporin A (CsA) is an immunosuppressive agent that can be used as alternative treatment to glucocorticoid therapy. This case report describes a case of vesicular cutaneous lupus erythematosus in a rough collie successfully controlled with oral CsA for more than 18 months.

Intervertebral disk prolapse in a ferret.

This case report describes the diagnosis and resolution of an inter-vertebral disk prolapse in a 6-year-old ferret. No predisposing causes were found in the patient's history. A right hemilaminectomy, performed 1 week after presentation, was chosen to treat the patient surgically, and complete remission of clinical signs was achieved 2 months after presentation.

Diffuse beta-amyloid plaques and hyperphosphorylated tau are unrelated processes in aged dogs with behavioral deficits.

Single and double-labeling immunocytochemistry has been used to learn about the localization, distribution, and possible relationship between beta-amyloid protein (Abeta) deposition and tau hyperphosphorylation in the canine cerebral cortex with age. Behavioral impairment, as reported by the owners and tested in all dogs, correlated with increased Abeta burden in old dogs. Abeta plaques were diffuse and they were not accompanied by modifications in synaptic protein expression. Plaques were not associated with increased active mitogen activated protein kinase (MAPK/ERK-P) and p38 kinase (p38-P) expression, and tau hyperphosphorylation in neighboring cell processes. Yet tau hyperphosphorylation, as revealed with phospho-specific antibodies to tauThr181 and tauSer396, increased with age in individual neurons. Moreover, the subcellular pattern shifted from perinuclear localization to granular cytoplasmic and nuclear distribution with age. Our results in dog suggest that Abeta diffuse plaque formation and tau hyperphosphorylation are independent events, both occurring during the process of aging. Although increased cognitive dysfunction is associated with increased tau hyperphosphorylation, further investigation is needed to understand whether tau hyperphosphorylation is causative of cognitive impairment or an independent process related to aging.

Canine cognitive deficit correlates with diffuse plaque maturation and S100beta (-) astrocytosis but not with insulin cerebrospinal fluid level.

Like humans, canines develop with aging beta-amyloid (Abeta) plaques and a progressive cognitive deficit on tasks similar to those used in diagnosis and follow-up of Alzheimer's disease. Owing to that, dogs are quite unique to investigate the early events taking place in the diffuse Abeta plaque maturation and its relationship with cognitive deficit. The aim of the present investigation was to study the link between the diffuse Abeta plaque maturation and the astro- and microglial reactivity. The involvement of insulin and beta-subunit of S100 protein (S100beta) overexpression in the process was also investigated. Abeta plaques were measured and counted in prefrontal cortex of 16 pet dogs of different breeds, weight and sex, classified as control and with a light or severe cognitive deficit. A correlation between canine graded cognitive deficit, diffuse plaque maturation, and S100beta (-) astrocytosis, but not with cerebrospinal fluid insulin level, was found that may reflect the very early events of Abeta deposition in Alzheimer's disease.

Severe cognitive impairment correlates with higher cerebrospinal fluid levels of lactate and pyruvate in a canine model of senile dementia.

Diagnosis of dementia of the Alzheimer's type depends on clinical criteria and exclusion of other disorders because, at this time, a validated biological marker, aside from histological brain examination, remains to be established. The canine counterpart of senile dementia of the Alzheimer type (ccSDAT) is considered a promising model for examining behavioral, cellular and molecular processes involved in early phases of human brain aging and Alzheimer disease (AD). In order to investigate the first events taking place in canine cognitive dysfunction, in this paper we established a new and rapid behavioral test that finely discriminates the degrees of cognitive impairment. Cerebrospinal fluid (CSF) analysis was performed to determine the relationship between each disease stage and modification of cerebral energy metabolism. Our results demonstrate a parallel increase of lactate, pyruvate and potassium concentrations in the severe cognitive deficit. These differences are discussed in view of the neuroprotective role presently given to lactate.

Calcium precipitation in acute and chronic brain diseases.

In rat brain, calcification associated with excitotoxicity has been proposed to play a protective role, whereas in human brain, nonartherosclerotic calcification is present in several pathological conditions without any clear significance. To determine if calcification can be viewed as a protective step of calcium homeostasis during chronic and acute neuronal suffering, cerebral cortex and hippocampus of patients with Alzheimer's disease, vascular dementia and neonatal hypoxia-ischemia were investigated. To investigate the human specificity, these two areas were also studied in dogs with established cognitive deficits. In all groups, calcium precipitates were observed in the cerebral parenchyma associated with neuronal damage. The cerebral cortex presented a higher degree of calcification than the hippocampus. The neonatal hypoxia-ischemia group was characterised by a higher degree of calcification, whereas the groups with lowest calcification were the Alzheimer's patients and dogs. As shown by X-ray microanalysis, in the precipitates, calcium is mainly associated with phosphorus in a form that resembles hydroxyapatites. Thus, intracellular calcium concentration associated with neuronal suffering may reduce the energy extrusion. We propose that, to help overcome excitotoxicity, calcium precipitation acts in CNS of vertebrates as a new compartment of the calcium homeostasis in which free cytoplasmic calcium ions are inactivated by phosphate ones.