Two unrelated 8‐month‐old male mixed breed dogs were presented for evaluation of progressive ataxia, knuckling, and lack of pain perception in the distal limbs. Because of the similarity in age of onset, progression, and clinical findings with previously described sensory neuropathy in Border Collies, the affected dogs were screened for an FAM134B mutation and were determined to be homozygous for the mutation. Despite few phenotypic similarities with other breeds, genetic testing for specific diseases should be considered in mixed breed dogs with compatible clinical signs, especially if ancestry is unknown.
Background: Traumatic skull fractures (TSF) are relatively frequent in dogs and cats, but little information is available regarding their clinical and imaging features. Hypothesis/Objectives: To describe the neurological and computed tomographic (CT) features of a large cohort of dogs and cats with TSF. Animals: Ninety-one dogs and 95 cats with TSF identified on CT. Methods: Multicenter retrospective comparative study. Signalment, cause of trauma, fracture locations and characteristics, presence of neurological deficits, and 1-week survival were recorded. Fractures were classified according to the extent of fragmentation and displacement. Results: The cranial vault was affected more frequently in dogs (P = .003), whereas the face and base of the cranium more often was affected in cats (P < .001). Cats presented with multiple fractures more frequently (P < .001). All animals with TSF in the cranial vault were more likely to develop neurological signs (P = .02), especially when depressed fractures were present (95% confidence interval [CI], 1.7-8.2; P = .001). Animals with TSF located only in the facial region were less likely to have neurological signs (odds ratio with Mantel-Haenszel's method [OR MH ], 0.2; 95% CI, 0.1-0.6; P = .004). Most affected animals (84.9%) survived the first week post-trauma.
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.
Background Little is known about the spectrum of underlying disorders in dogs with unilateral masticatory muscle (MM) atrophy. Objectives To evaluate the clinical presentation, magnetic resonance imaging (MRI) findings, and outcome of dogs with unilateral MM atrophy. Animals Sixty‐three client‐owned dogs. Methods The medical database was retrospectively reviewed for dogs that underwent MRI for evaluation of unilateral MM atrophy. Imaging studies were reviewed and follow‐up information was obtained from telephone interviews. Results Presumptive trigeminal nerve sheath tumor (pTNST) was diagnosed in 30 dogs (47.6%); survival time varied from 1 day to 21 months (median, 5 months). Other extra‐axial mass lesions were observed in 13 dogs (20.6%); survival time varied from 6 days to 25 months (median, 2.5 months). In 18 dogs (28.6%), no abnormalities were observed on MRI; neurological signs only progressed in 1 dog. Diagnosis had a significant influence on the type of neurological abnormalities, with additional neurological deficits observed in most dogs with pTNST and in all dogs with other extra‐axial mass lesions. Diagnosis had a significant effect on euthanasia at the time of diagnosis and likelihood of neurological deterioration. Dogs with mass lesions were more likely to be euthanized or experience neurological deterioration, whereas these outcomes occurred less often in dogs in which no causative lesion could be identified. Conclusions and Clinical Importance Trigeminal nerve sheath tumors should not be considered the only cause of unilateral MM atrophy. Our results illustrate the importance of performing a neurological examination and MRI when evaluating dogs with unilateral MM atrophy.
In this pilot study we investigated the expression of 14 microRNAs in the cerebrospinal fluid (CSF) of dogs with neoplastic, inflammatory and degenerative disorders affecting the central nervous system (CNS). CSF microRNA (miRNA) expression profiles were compared to those from dogs with neurological signs but no evidence of structural or inflammatory CNS disease. Seven miRNAs were easily detected in all samples: miR-10b-5p, miR-19b, miR-21-5p, miR-30b-5p, miR-103a-3p, miR-124, and miR-128-3p. Expression of miR-10b-5p was significantly higher in the neoplastic group compared to other groups. There was no relation between miRNA expression and either CSF nucleated cell count or CSF protein content. Higher expression of miR-10b-5p in the neoplastic group is consistent with previous reports in human medicine where aberrant expression of miR-10b is associated with various neoplastic diseases of the CNS.
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