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Abstract Background Myoclonus has been described in aging Cavalier King Charles Spaniels (CKCS), but the natural course of the disease and response to treatment have not been described. Objectives Report the clinical features and course of myoclonus in CKCS. Animals Twenty‐seven caregivers provided questionnaire responses at a median of 24 months after the onset of myoclonus in their CKCS. Fifteen caregivers completed a second follow‐up questionnaire at a median of 17 months after submission of the first questionnaire. Methods The caregivers of affected CKCS were invited to provide video footage for review. Owners of CKCS with videos demonstrating myoclonus then completed the online questionnaire for further evaluation. A second shortened questionnaire was sent to participants at least 6 months after completion of the first. Results Most CKCS displayed spontaneous myoclonus affecting predominantly the head (25/27). Overall, the majority had episodes that increased in frequency (20/27) and severity (17/27). Eighteen dogs had developed changes in behavior since the onset of myoclonus. These dogs were typically older and had experienced myoclonic episodes for longer than dogs without behavioral changes. Generalized epileptic seizures were reported in 4/27 dogs. Ten dogs received medical treatment. Eight were prescribed levetiracetam; all had an initial decrease in episode frequency, but a subsequent increase in both frequency and severity of episodes was common. Conclusions and Clinical Importance Myoclonus in CKCS tends to progress in frequency and severity regardless of treatment. Progressive behavioral changes suggestive of cognitive decline are common. These findings support the possibility of an underlying neurodegenerative process.

Abstract Hereditary ataxias are a large group of neurodegenerative diseases that have cerebellar or spinocerebellar dysfunction as core feature, occurring as an isolated sign or as part of a syndrome. Based on neuropathology, this group of diseases has so far been classified into cerebellar cortical degenerations, spinocerebellar degenerations, cerebellar ataxias without substantial neurodegeneration, canine multiple system degeneration, and episodic ataxia. Several new hereditary ataxia syndromes are described, but most of these diseases have similar clinical signs and unspecific diagnostic findings, wherefore achieving a definitive diagnosis in these dogs is challenging. Eighteen new genetic variants associated with these diseases have been discovered in the last decade, allowing clinicians to reach a definitive diagnosis for most of these conditions, and allowing breeding schemes to adapt to prevent breeding of affected puppies. This review summarizes the current knowledge about hereditary ataxias in dogs, and proposes to add a “multifocal degenerations with predominant (spino)cerebellar component” category regrouping canine multiple system degeneration, new hereditary ataxia syndromes that do not fit in 1 of the previous categories, as well as specific neuroaxonal dystrophies and lysosomal storage diseases that cause major (spino)cerebellar dysfunction.

Abstract Background Computed tomography (CT) findings of dogs with discospondylitis have not been widely described despite increased availability of this imaging modality. Objectives Describe the CT features of discospondylitis in a population of clinically affected dogs with discospondylitis diagnosed by magnetic resonance imaging (MRI). Animals Forty‐one dogs (63 affected discs) with MRI‐identified discospondylitis presented to a single referral hospital between 2012 and 2022. Methods Retrospective, single center, descriptive case series with analysis of MRI‐identified discospondylitis sites and concomitant CT imaging. Computed tomographic features of MRI‐affected sites including intervertebral disc space (IVDS), endplates, vertebral body, epidural space and paraspinal tissues were described. Results The most frequently found changes were: (1) endplate involvement (87.3%) most frequently bilateral (94.5%), with erosion (61.9%) and multifocal osteolysis (67.3%); (2) periosteal proliferation adjacent to the IVDS (73%) and spondylosis (66.7%); and (3) vertebral body involvement (66.7%) involving one‐third of the vertebra (85.7%) with multifocal osteolysis (73.5%). Other less prevalent features included an abnormal IVDS (narrowed or collapsed), sclerosis of the adjacent vertebral body or endplates, presence of disseminated idiopathic skeletal hyperostosis or vacuum artifact. Conclusions and Clinical Importance We determined that bilateral endplate erosion and periosteal proliferation were very common in dogs with discospondylitis. Careful evaluation of CT in all 3 planes (dorsal, sagittal, transverse) is necessary to identify an affected IVDS. These described CT features can aid in the diagnosis of discospondylitis in dogs but equivocal cases might still require MRI.

Abstract Movement disorders are a heterogeneous group of clinical syndromes in humans and animals characterized by involuntary movements without changes in consciousness. Canine movement disorders broadly include tremors, peripheral nerve hyperexcitability disorders, paroxysmal dyskinesia, and dystonia. Of these, canine paroxysmal dyskinesias remain one of the more difficult to identify and characterize in dogs. Canine paroxysmal dyskinesias include an array of movement disorders in which there is a recurrent episode of abnormal, involuntary, movement. In this consensus statement, we recommend standard terminology for describing the various movement disorders with an emphasis on paroxysmal dyskinesia, as well as a preliminary classification and clinical approach to reporting cases. In the clinical approach to movement disorders, we recommend categorizing movements into hyperkinetic vs hypokinetic, paroxysmal vs persistent, exercise‐induced vs not related to exercise, using a detailed description of movements using the recommended terminology presented here, differentiating movement disorders vs other differential diagnoses, and then finally, determining whether the paroxysmal dyskinesia is due to either inherited or acquired etiologies. This consensus statement represents a starting point for consistent reporting of clinical descriptions and terminology associated with canine movement disorders, with additional focus on paroxysmal dyskinesia. With consistent reporting and identification of additional genetic mutations responsible for these disorders, our understanding of the phenotype, genotype, and pathophysiology will continue to develop and inform further modification of these recommendations.

Abstract Myasthenia, a syndrome of impaired neuromuscular transmission, occurs as either an acquired or congenital condition. Myasthenia gravis (MG) is an acquired autoimmune disorder with autoantibodies against the neuromuscular junction (NMJ) of skeletal muscle whereas congenital myasthenic syndromes (CMSs) are a clinically heterogeneous group of genetic disorders affecting the NMJ with a young age of onset. Both conditions are diseases for which recognition is important with regard to treatment and outcome. We review the published literature on MG and CMSs in dogs and cats, and by comparison with published classification used in humans, propose a classification system for MG and CMSs in dogs and cats. Myasthenia gravis is first classified based on focal, generalized, or acute fulminating presentation. It then is subclassified according to the autoimmune disease mechanism or seronegativity. Autoimmune disease mechanism relates to the presence or absence of a thymoma, or administration of thiourylene medication in cats. Congenital myasthenic syndromes are classified according to the affected NMJ component, the mechanism of the defect of neuromuscular transmission, the affected protein, and ultimately the mutated gene responsible. In proposing this categorization of MG and CMSs, we hope to aid recognition of the disease groups for both conditions, as well as guide treatment, refine prognosis, and provide a framework for additional studies of these conditions.

Abstract Background Seizures triggered by eating (STE) behavior are very rare in humans and have not been documented previously in dogs. Objectives To document the occurrence of STE in dogs and describe their clinical features. Animals Ten client‐owned dogs with STE diagnosed at 5 European referral centers. Methods A call for suspected cases of STE was made online. This call was followed by a retrospective review of medical records, combined with a questionnaire to be completed by both the owner and the board‐certified neurologist who made the diagnosis. Cases were included if >50% of the seizures that occurred were related to eating and if a minimum diagnostic evaluation for seizures had been performed. Results Four cases only had STE and 6 cases had both STE and spontaneous seizures. Four of the dogs were retrievers. The most common seizure type was focal epileptic seizures evolving to become generalized. Nine dogs were diagnosed with idiopathic epilepsy. One dog had a presumptive diagnosis of glioma involving the margins of the parietal, temporal, and frontal cortex (the perisylvian region), an area known to have a key role in eating‐associated epilepsy in people. Treatment strategies included a combination of pharmacological management and eating habit changes. Conclusions and Clinical Importance We have identified a form of reflex epilepsy in dogs, with STE behavior. Further studies are warranted to improve the characterization and management of STE.

Abstract Traditionally, immune memory is regarded as an exclusive hallmark of adaptive immunity. However, a growing body of evidence suggesting that innate immune cells show adaptive characteristics has challenged this dogma. In the past decade, trained immunity, a de facto innate immune memory, has been defined as a long‐term functional reprogramming of cells of the innate immune system: the reprogramming is evoked by endogenous or exogenous insults, the cells return to a nonactivated state and subsequently show altered inflammatory responses against a second challenge. Trained immunity became regarded as a mechanism selected in evolution to protect against infection; however, a maladaptive effect might result in hyperinflammation. This dual effect is consistent with the Yin‐Yang theory in traditional Chinese philosophy, in which Yang represents active, positive, and aggressive factors, whereas Yin represents passive, negative, and inhibitory factors. In this review, we give a brief overview of history and latest progress about trained immunity, including experimental models, inductors, molecular mechanisms, clinical application and so on. Moreover, this is the first time to put forward the theory of Yin‐Yang balance to understand trained immunity. We envision that more efforts will be focused on developing novel immunotherapies targeting trained immunity in the coming years.

Abstract Background Acquired myasthenia gravis (AMG) is increasingly recognized in cats, yet information regarding the natural history of the disease, treatment, and outcome including occurrence of immune and spontaneous remission remains limited. Objective To determine the long‐term outcome of cats with AMG without evidence of a cranial mediastinal mass (CMM). Animals Eight cats diagnosed with AMG without evidence of a CMM. Methods Retrospective case series. The medical records of cats diagnosed with AMG between 2005 and 2018 from 2 veterinary referral hospitals were reviewed for inclusion. Inclusion criteria consisted of a diagnosis of AMG, thoracic imaging, serum biochemistry including measurement of creatine kinase, and a CBC. Exclusion criteria were the presence of an identifiable CMM, or administration of methimazole or carbimazole. Results All cats had an excellent long‐term outcome, achieving immune remission within 6 months of diagnosis, including 4 cats that did not receive any treatment and whose natural course of disease involved spontaneous remission. Clinical presentation was heterogeneous, and skeletal muscle weakness and fatigability induced or exacerbated by the wheelbarrow exercise stress test were the most consistent abnormalities associated with AMG. Conclusion and Clinical Importance Cats diagnosed with AMG without evidence a CMM have a favorable outcome and frequently achieve immune remission. Moreover, the natural history of AMG in cats includes spontaneous remission when there is no evidence of a CMM. Attempting to rule out the presence of a CMM therefore refines prognosis, and treatment is not always necessary in this disease population.

Abstract Background Paramyotonia congenita and Brody disease are well‐described conditions in humans, characterized by exercise‐induced myotonic‐like muscle stiffness. A syndrome similar to Brody disease has been reported in cattle. Reports of a similar syndrome in dogs are scarce. Objectives To define and describe the clinical, diagnostic, and genetic features and disease course of paradoxical pseudomyotonia in Spaniel dogs. Animals Seven client‐owned dogs (4 English Springer Spaniels and 3 English Cocker Spaniels) with clinically confirmed episodes of exercise‐induced generalized myotonic‐like muscle stiffness. Methods Sequential case study. Results All dogs were

Abstract Background Although thoracic hemivertebra can cause neurological signs, they occur commonly in neurologically normal dogs. Objectives To evaluate whether computed tomography (CT) findings and factors associated with signalment can be used to differentiate between dogs with and without neurological signs associated with hemivertebra. Animals One hundred sixty dogs with ≥1 hemivertebrae were retrospectively studied. This group consisted of 40 dogs with clinical signs caused by hemivertebra and 40 French Bulldogs, 40 Pugs, and 40 English Bulldogs that underwent CT for reasons unrelated to neurological disease. Methods All dogs underwent CT and affected dogs also underwent magnetic resonance imaging. All CT studies were randomly evaluated by an observer blinded to signalment and clinical status. The following variables were evaluated: presence, number, location, and subtype of hemivertebra; presence of vertebral subluxation; severity of vertebral canal stenosis; presence, location, and severity of kyphosis, and number of vertebrae involved in the kyphotic segment. Statistical modeling was performed to identify factors associated with clinical status. Results Pug breed (odds ration [OR], 10.8; P = .01), more severe kyphosis (OR, 1.1 per grade increase; P

Background Paroxysmal gluten‐sensitive dyskinesia (PGSD) in border terriers (BTs) results from an immunologic response directed against transglutaminase (TG)2 and gliadin. Recent evidence suggests that PGSD is only one aspect of a range of possible manifestations of gluten sensitivity in the breed. Hypothesis/Objectives Gluten sensitivity in BTs is a heterogeneous disease process with a diverse clinical spectrum; to characterize the phenotype of PGSD using TG2 and gliadin autoantibodies as diagnostic markers. Animals One hundred twenty‐eight client‐owned BTs with various disorders. Methods Prospective study. BTs with paroxysmal episodes and a normal interictal examination were phenotyped using footage of a representative episode and assigned to 3 groups: idiopathic epilepsy (IE), paroxysmal dyskinesia (PD), or other. Owners of each dog completed a questionnaire to obtain information regarding clinical signs. Healthy BTs formed a control group. Serum antibodies against TG2 and AGA were measured in all dogs. Results One hundred twenty‐eight BTs were enrolled; 45 with PD, 28 with IE, 35 with other conditions, and 20 controls. Three overlapping phenotypes were identified; PD, signs suggestive of gastrointestinal disease, and dermatopathy. AGA‐IgG concentrations were increased in PD, compared with IE (P = 0.012), controls (P