Alejandra Mondino

Objectives: To describe current clinical practices in the management of cervical Hansen type I intervertebral disc herniation among American College of Veterinary Internal Medicine/European College of Veterinary Neurology neurologists. Materials and Methods: An anonymous web‐based survey was distributed via professional listservs between October and November 2025. Survey items addressed diagnostic imaging, indications and urgency for surgery, surgical technique and fenestration, foraminal injections, analgesia, medical management, activity restriction and perceived prognostic factors. Responses were summarised descriptively and compared between North American and European veterinary neurologists. Results: Of 233 responses, 198 met inclusion criteria. Magnetic resonance imaging was the most commonly used diagnostic modality. Surgery was infrequently recommended for first‐presentation cervical pain without neurological deficits, but was commonly recommended for recurrent or refractory pain, ambulatory tetraparesis and non‐ambulatory tetraparesis or tetraplegia, with increasing urgency reported for more severe neurological dysfunction and the presence of hypoventilation. Ventral slot decompression was the predominant surgical approach. Fenestration practices varied, with prophylactic fenestration reported more frequently by American College of Veterinary Internal Medicine neurologists. Compared with European College of Veterinary Neurology neurologists, American College of Veterinary Internal Medicine neurologists reported more frequent use of corticosteroids and strict crate confinement, whereas European College of Veterinary Neurology neurologists more commonly reported use of non‐steroidal anti‐inflammatory drugs and opioid‐based local or bolus analgesic techniques. Additionally, European College of Veterinary Neurology neurologists reported more frequent use of foraminal injections. Clinical Significance: Management of cervical Hansen type I intervertebral disc herniation shows strong agreement regarding diagnostic imaging and surgical decompression, but notable variation in analgesic strategies, medical management and activity restriction. These findings identify areas where further evidence and consensus guidelines may help standardise clinical decision‐making.

Canine degenerative myelopathy (DM) is a hereditary disease of the spinal cord, characterized by a progressive clinical course, and the death of affected animals. This study aimed to investigate the population distribution of the SODc.118:G˃A mutation responsible for the disease. For this purpose, 131 dogs from both breeds (Pit Bull Terrier, n=64, and Boxer, n=67) were studied. Genomic DNA was extracted from peripheral blood, and the mutation was identified using the PCR-RFLP technique. For each population, the mutant allele frequency, genotypic frequency, and Hardy–Weinberg equilibrium were calculated. The frequency of the DM-related A allele was 0.16 in the Pit Bull Terrier and 0.52 in the Boxer breed. Both populations were in Hardy–Weinberg equilibrium (p > 0.05). The genotypic distribution differed between the two breeds analyzed and also between different populations within each breed (p < 0.05). Simulation of the evolution of the mutant allele frequency under different genetic drift models showed that the variance of the allele frequency increased as the effective population size (Ne) decreased. The frequency detected in the Boxer breed was high, and although it was lower in the Pit Bull Terrier, the allele was still present. These findings support the potential use of genotyping tests for degenerative myelopathy management and provide descriptive population data from dogs of both breeds in Uruguay. A mielopatia degenerativa canina (MD) é uma doença hereditária da medula espinhal, caracterizada por um curso clínico progressivo e pela morte dos animais afetados. Este estudo teve como objetivo investigar a distribuição populacional da mutação SODc.118:G˃A responsável pela doença. Para isso, foram estudados 131 cães de ambas as raças (Pit Bull Terrier, n=64, e Boxer, n=67). O DNA genômico foi extraído do sangue periférico e a mutação foi identificada usando a técnica PCR-RFLP. Para cada população, foram calculadas a frequência do alelo mutante, a frequência genotípica e o equilíbrio de Hardy-Weinberg. A frequência do alelo A relacionado à DM foi de 0,16 na raça Pit Bull Terrier e de 0,52 na raça Boxer. Ambas as populações estavam em equilíbrio de Hardy-Weinberg (p > 0,05). A distribuição genotípica diferiu entre as duas raças analisadas e também entre diferentes populações dentro de cada raça (p < 0,05). A simulação da evolução da frequência do alelo mutante sob diferentes modelos de deriva genética mostrou que a variância da frequência do alelo aumentou à medida que o tamanho efetivo da população (Ne) diminuiu. A frequência detectada na raça Boxer foi alta e, embora fosse menor no Pit Bull Terrier, o alelo ainda estava presente. Esses achados apoiam o uso potencial de testes de genotipagem para o manejo da mielopatia degenerativa e fornecem dados descritivos da população de cães de ambas as raças no Uruguai

Acute non‐compressive nucleus pulposus extrusion (ANNPE) is a recognised cause of peracute spinal cord injury in dogs, involving sudden extrusion of non‐degenerated nucleus pulposus with minimal compression. While often linked to vigorous activity, its triggers remain unclear. This case describes an 8‐year‐old neutered male poodle cross dog who developed peracute non‐ambulatory paraparesis while running to retrieve a ball. Neurological examination was consistent with a T3–L3 myelopathy. Magnetic resonance imaging (MRI) revealed disc space narrowing with intramedullary T2W hyperintensity at T13–L1 consistent with ANNPE and a T13 vertebral body lesion that was hyperintense in T1W/STIR and contrast‐enhancing, later confirmed as T‐cell lymphoma by surgical biopsy. The dog demonstrated rapid clinical improvement, with motor function recovery by day 6 and becoming ambulatory with mild ataxia by week 3. This case highlights the importance of considering underlying vertebral pathology in dogs with presumed ANNPE and emphasises that vertebral lesions detected on MRI may have clinical relevance and should not be overlooked.

The placebo effect, or the positive effects observed after an inert treatment which result from patients’ expectations for the therapy, is well documented in human medicine. However, in veterinary medicine, where owner’s expectations serve as a proxy for their pets, it remains underexplored, particularly for elderly dogs with cognitive decline. To address this gap, we examined 21 dogs (mean age: 12.85 years, SD: 1.46) from a placebo group in a randomized controlled trial (RCT) and compared their results to 17 dogs (mean age: 13.24 years, SD:1.56) from an observational, longitudinal study to distinguish placebo effect from trial participation effect. Both populations had statistically comparable baseline data. Cognitive changes were evaluated with two remotely administered owner questionnaires (Canine Cognitive Dysfunction Scale (CCDR) and Canine Dementia Scale (CADES)) and three in-house cognitive assessments (Cylinder Task, Detour and Sustained Gaze). We hypothesized that placebo effect would be greater than trial participation effect, particularly in owner-reported measures. Matched pairs T -tests and effect size calculations (Hedge’s g ) were used to calculate changes across 6 months. A strong ( g = 0.76), significant ( p = 0.021) improvement in CADES was observed in the placebo cohort after 6 months, while no changes were detected with CCDR. Conversely, the observational cohort showed a small ( g = 0.35) and significant ( p = 0.03) deterioration on CCDR, and no change in CADES. No significant changes were noted on the in-house cognitive assessments in either cohort. We conclude that study context influences remotely delivered owner assessments and CCDR is more robust against caregiver placebo effect in RCTs than CADES.

Phenobarbital (PB) is an antiseizure medication widely used in dogs that is metabolized by hepatic cytochrome P450 (CYP) enzymes. Fluconazole, a commonly prescribed antifungal medication, inhibits several CYP isoenzymes and can impair PB metabolism. Genetic polymorphisms such as the CYP2C41 gene deletion can alter CYP activity and influence drug interactions, although not well characterized in dogs. We describe two epileptic dogs on chronic PB treatment that developed marked sedation and ataxia, and increased serum PB concentrations after receiving fluconazole. Both dogs were homozygous for the CYP2C41 deletion. Discontinuation of fluconazole resulted in decreased PB concentrations and resolution of clinical signs. These findings suggest fluconazole can inhibit PB metabolism, leading to clinically relevant toxicity, and this interaction does not require CYP2C41 enzyme expression. Monitoring PB concentrations during fluconazole co-administration is advised. Further characterization of the role of CYP enzymes in PB metabolism in dogs is needed to better predict drug interactions.

Abundant clinical and preclinical evidence demonstrates that sleep and pain have bidirectional interactions. Sleep loss enhances pain perception and pain disrupts sleep. However, the exact neurobiological mechanisms through which sleep loss alters pain remain poorly understood. The preoptic area of the hypothalamus is crucial for the regulation of sleep onset and sleep homeostasis, and it innervates downstream regions that regulate arousal states and pain. Adenosine neurotransmission in the preoptic region plays a key role in the sleep homeostatic response following prolonged wakefulness or sleep deprivation. Previous studies showed that pharmacologically blocking adenosine A _2A receptors within the median preoptic nucleus of sleep‐deprived rats prevented the increase in pain caused by sleep deprivation. These data suggest that preoptic adenosine levels, presumably elevated during sleep deprivation, increase pain sensitivity. Thus, here we investigated whether adenosine administration into the median preoptic nucleus of non‐sleep‐deprived, pain‐naïve rats increased pain. Adenosine microinjection into the preoptic (and septal) regions significantly increased thermal hyperalgesia and extended the duration of pain‐like behaviours after subcutaneous capsaicin injection, but did not affect mechanical hyperalgesia or the affective/motivational response in a mechanical conflict avoidance paradigm. Additionally, adenosine administration significantly reduced cFos expression in the ventrolateral periaqueductal grey, a key node in the descending pain modulation pathway. These data demonstrate that preoptic adenosine may act as a link between sleep disruption and pain.

Levetiracetam (LEV) is a commonly used antiseizure medication in dogs, available in immediate‐release (LEV‐IR) and extended‐release (LEV‐XR) formulations. LEV‐XR improves owner compliance with less frequent dosing, but its lowest concentration tablet (500 mg) often exceeds recommended doses for small dogs. This study evaluated how modifying LEV‐XR tablets affects dissolution rates, comparing intact, split, and crushed LEV‐XR tablets with intact LEV‐IR tablets. Dissolution testing followed United States Pharmacopeia (USP) guidelines for LEV‐XR tablets. Tablets were placed in a buffer solution (pH 6.0) and agitated at 100 rpm. Samples were collected at 0, 0.5, 2, 4, 6, and 8 h, then analyzed by high‐pressure liquid chromatography (HPLC) using a USP reference standard. Results indicated that splitting LEV‐XR tablets slightly increased drug release compared to intact tablets, while crushing eliminated extended‐release properties, mimicking LEV‐IR dissolution. These findings suggest that splitting LEV‐XR tablets may be a viable strategy for dosing small dogs without compromising sustained release. Conversely, crushing LEV‐XR tablets may be useful for rapid drug release in cluster seizure protocols. Future pharmacokinetic studies are needed to confirm if these in vitro results correlate with in vivo performance for both maintenance and emergency seizure management in dogs.

Background: Familial narcolepsy in dogs has been associated with mutations in the HCRTR2 gene in Labrador retrievers, dachshunds, and Doberman pinschers, with the causal mutation differing between breeds. Objective: To characterize the genetic mutation responsible for familial narcolepsy in Dogo Argentino dogs. Animals: Ten Dogo Argentino dogs, three narcoleptic and seven clinically normal, of which four were related and three were unrelated to the narcoleptic dogs. Methods: Case control prospective study. DNA was extracted from blood samples of all dogs. Whole-genome sequencing was performed on two affected dogs, and variants were identified using bioinformatic pipelines, with comparisons made to a database of 2766 dogs. Structural variants were validated through PCR and Sanger sequencing. Results: A novel tandem duplication in the HCRTR2 gene was identified. All three affected dogs and the clinically normal parents of one affected dog had this duplication, suggesting an autosomal recessive pattern of inheritance. This duplication was absent in the 2766 dogs in the database, emphasizing its potential relevance in the Dogo Argentino breed. Conclusions and Clinical Importance: This discovery emphasizes the critical role of the HCRTR2 gene in narcolepsy in dogs, and the diversity of mutations that can lead to this condition. Further genetic testing in this breed is warranted to identify carriers and prevent the further spread of this condition.

Background: The bidirectional relationship between epilepsy and sleep is well characterized in humans but has not been thoroughly explored in dogs. Objective: Evaluate sleep differences between dogs with idiopathic epilepsy and healthy controls and determine associations among epilepsy characteristics, antiseizure medications (ASMs), and sleep. Animals: Sixty-four dogs with idiopathic epilepsy and 64 non-epileptic control dogs matched by age, breed, and sex. Methods: Owners of all dogs completed an online survey that included questions regarding signalment, epilepsy history if applicable, and sleep. Owners of epileptic dogs were asked whether their dogs experienced changes in sleep after a seizure. Sleep scores were calculated using the Sleep and Nighttime Restlessness Evaluation (SNoRE) questionnaire, consisting of two factors: “sleep quality” and “sleep interruptions caused by dreaming.” Data were analyzed for differences in sleep scores between epileptic and control dogs and any effects of seizure frequency, cluster seizures, and ASMs. Results: Significant differences in sleep scores were identified between epileptic dogs and controls (median, 12 vs. 8, respectively; p < 0.001), driven by poorer sleep quality in the epileptic group. No significant associations were found between sleep scores and seizure frequency, clusters, or ASM use. Fifty-nine percent of dog owners noticed changes in sleep patterns after a seizure, most often increased sleep duration. Conclusions and Clinical Importance: Dogs with idiopathic epilepsy experience negative changes in sleep, emphasizing the importance of monitoring and managing sleep disturbances in this cohort. Larger, multicenter studies controlling for confounding factors are needed to better understand the impact of epilepsy on sleep.

Myasthenia gravis is a disorder of neuromuscular transmission characterized by muscle weakness and exercise intolerance that is rarely diagnosed in dogs younger than 6 months. We report a case of juvenile‐onset myasthenia gravis in a 5‐month‐old, intact male Australian Shepherd with onset of clinical signs at 4 months of age. The dog presented with a 4‐week history of progressive weakness and regurgitation. Diagnosis was confirmed by an elevated serum acetylcholine receptor antibody concentration. Treatment with pyridostigmine provided only partial improvement. Leflunomide was added to achieve immunosuppression while avoiding the side effects of corticosteroids, such as muscle weakness. This treatment combination was well‐tolerated; the dog went into clinical remission, including resolution of megaesophagus, and progressive reduction in acetylcholine receptor antibody concentration was noted. This report highlights the importance of considering myasthenia gravis in juvenile dogs and emphasizes the utility of measuring acetylcholine receptor antibodies in suspected cases regardless of age. The safe and possibly efficacious use of leflunomide in a dog with this disease is also demonstrated. Further studies are needed to characterize the juvenile presentation of this disease and to evaluate the efficacy of treatment with leflunomide as the sole immunosuppressant medication in a larger canine population.