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The authors have observed a vertebral anomaly in French and English Bulldogs and termed this anomaly "vertebral vascular canal dysplasia (VVCD)." No previously published descriptions of this anomaly were found. The aims of this retrospective, multi-institutional, observational study were to (1) describe the clinical, CT, and MRI characteristics of VVCD, and (2) estimate the prevalence and describe the characteristics of VVCD in a group of French and English Bulldogs. For descriptions of the anomaly, medical records and imaging studies of nine clinical cases with VVCD from several countries were reviewed. For estimation of prevalence, imaging studies of French and English Bulldogs from the United Kingdom (UK) and Italy were reviewed. All clinical case dogs had ≥5 thoracic vertebrae with VVCD affecting >50% of vertebral body height (VBH). The prevalence of VVCD involving ≥1 thoracic vertebra in the UK population (CT identified) of English Bulldogs and French Bulldogs was, respectively, 83.3% (30/36) and 68.3% (28/41). English Bulldogs had significantly more thoracic vertebrae with VVCD than French Bulldogs (P = < 0.01). The prevalence of VVCD in ≥1 thoracic vertebra in the Italian population (MRI identified) of English Bulldogs and French Bulldogs was, respectively, 21.7% (5/23) and 6.6% (7/106). Vertebral vascular canal dysplasia was observed in normal as well as in malformed vertebrae (e.g., hemivertebrae). Findings from the current study introduced descriptions of VVCD that can be used as background for future studies.
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Doenças do Cão , Doenças da Coluna Vertebral , Animais , Doenças do Cão/diagnóstico por imagem , Doenças do Cão/epidemiologia , Cães , Imageamento por Ressonância Magnética/veterinária , Prevalência , Estudos Retrospectivos , Doenças da Coluna Vertebral/veterinária , Vértebras Torácicas/anormalidades , Vértebras Torácicas/diagnóstico por imagem , Tomografia Computadorizada por Raios X/veterináriaRESUMO
Introduction: Chiari-like malformation (CM) and syringomyelia (SM) are disorders that, in dogs, affect mainly small and toy breeds, including the Pomeranian. These disorders are linked to a great number of (owner-reported) clinical signs (ORCS) suggestive of pain. Aging was associated with an increased risk of having SM in several studies. However, there are only a few longitudinal studies that assess the presence and severity of CM/SM over time in CKCS dogs and progression of SM was linked to progression of clinical signs. The aim of this study was to investigate ORCS, CM/SM classification, and quantitative syrinx parameters in relation to progression of time (age) within individual Pomeranians. Materials and methods: Pomeranians with or without ORCS and with or without diagnoses of CM/SM were included that had undergone two (or more) MRI studies of the craniocervicothoracic region between January 2020 and June 2023. Classification of CM/SM and quantitative syrinx measurements were performed. Absolute values as well as ratios for syrinx height, width, and cross-sectional area were included for analysis. Results: A total of 19 Pomeranians were included in the study, of which 11 were male (58%) and 8 were female (42%). The median age at the time of MRI1 was 26 months (range 7-44 months). The median scan interval was 26 months (range 11-49 months). Eleven dogs (58%) were presented with ORCS at the time of MRI1, whereas the other 8 dogs (42%) had no ORCS at that time. At the time of MRI2, there were 17/19 dogs (89%) with ORCS and 2/19 dogs without ORCS (11%). Dogs were significantly more likely to have ORCS at MRI2 than MRI1 (p = 0. 0411). There was no significant difference between CM/SM classification at the time of MRI1 and MRI2. Significant differences were found between MRI1 and MRI2 for syrinx height (based on transverse images) (absolute value and ratio P = 0.0059), syrinx width (absolute value P = 0.1055, ratio P = 0.0039), and syrinx cross sectional area (absolute value P = 0.0195, ratio P = 0.0217). Discussion: There are differences in the presence or absence of ORCS as well as quantitative syrinx measurements in Pomeranians at different ages. This finding supports that longitudinal changes occur in the SM status of Pomeranians.
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Paroxysmal dyskinesias (PDs) are a group of involuntary, hyperkinetic movement disorders that recur episodically and may last seconds to hours. An important feature of PD is that there is no loss of consciousness during the episode. Using a clinical classification, three main types of PDs have been distinguished in canine PD: (1) paroxysmal kinesigenic dyskinesia (PKD) that commences after (sudden) movements, (2) paroxysmal non-kinesigenic dyskinesia (PNKD) not associated with exercise and can occur at rest, and (3) paroxysmal exertion-induced dyskinesia (PED) associated with fatigue. Canine PDs are diagnosed based on the clinical presentation, history, and phenomenology. For the latter, a video recording of the paroxysmal event is extremely useful. An etiological classification of canine PDs includes genetic (proven and suspected), reactive (drug-induced, toxic, metabolic, and dietary), structural (neoplasia, inflammatory, and other structural causes), and unknown causes. In this review, an overview of all reported canine PDs is provided with emphasis on phenotype, genotype, and, where possible, pathophysiology and treatment for each reported canine PD.
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A 2.5-year-old female entire Pomeranian dog was presented for acute paraparesis progressing within 2 days to paraplegia. General physical examination was unremarkable. Neurological examination showed paraplegia without nociception, a mass reflex upon testing perineal reflexes and withdrawal reflexes in the pelvic limbs and patellar hyperreflexia. Cutaneous trunci reflexes were absent caudal to the level of the 6th thoracic vertebra. Spinal hyperesthesia was present. Neuroanatomical localization was consistent with a T3-L3 myelopathy. Hematological and biochemical blood tests [including C-reactive protein (CRP)] were within reference ranges. MRI of the spinal cord from the level of the 1st thoracic vertebra to the sacrum revealed a patchy, ill-defined, moderate to marked T2W hyperintense, contrast enhancing intramedullary lesion extending from T1 to L4. Medical treatment based on a working diagnosis of meningomyelitis of unknown cause was initiated with corticosteroids and methadone based on pain scores. Prognosis was grave and after 3 days without return of nociception, the dog was euthanized according to the owners' wishes. Post-mortem histopathological examination of the brain and spinal cord yielded a morphological diagnosis of severe, segmental, bilateral and fairly symmetrical, necrotizing lymphohistiocytic leukomyelitis, with a non-suppurative angiocentric leptomeningitis. Some minor, focal, lymphocytic perivascular cuffing was found in the medulla oblongata as well, but otherwise there were no signs of brain involvement. No infectious causes were identified with ancillary tests. This case report underlines the importance of including meningomyelitis in the differential diagnosis list of dogs presented for acute progressive neurological signs referable to a myelopathy.
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A 10-year-old male Shar-Pei was referred for lethargy and proprioceptive deficits of the left thoracic limb. An magnetic resonance imaging (MRI) examination of the cervical spinal column and the brain was performed. The MRI examination of the brain was normal. A left-sided C3-C4 intervertebral disc extrusion with spinal cord compression was diagnosed. Medical treatment was elected. Within a week after the MRI examination, the dog presented with deep partial-thickness skin burn wounds in both axillae. Since the specific absorption rate had not exceeded the safety limits during any of the scans and no other procedures or circumstances were identified that could possibly have resulted in burn injuries, the thermal burn injuries were diagnosed as radiofrequency (RF) burns. The wounds healed by secondary intent over the next month. RF burns are the most reported complication in humans undergoing MRI but have not been reported in veterinary patients. Clinicians and technicians should consider the potential risk for RF burns in veterinary patients and take precautions regarding positioning of the patient and take notice of any signs of burn injury when performing follow-up examinations.
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Metabolic/neurodegenerative encephalopathies encompass a wide list of conditions that share similar clinical and magnetic resonance imaging (MRI) characteristics, challenging the diagnostic process and resulting in numerous tests performed in order to reach a definitive diagnosis. The aims of this multicentric, retrospective and descriptive study are: (I) to describe the MRI features of dogs and cats with metabolic/neurodegenerative encephalopathies; (II) to attempt an MRI recognition pattern classifying these conditions according to the involvement of grey matter, white matter or both; and (III) to correlate the MRI findings with previous literature. A total of 100 cases were recruited, comprising 81 dogs and 19 cats. These included hepatic encephalopathy (20 dogs and three cats), myelinolysis (five dogs), intoxications (seven dogs and one cat), thiamine deficiency (two dogs and seven cats), hypertensive encephalopathy (three dogs and two cats), neuronal ceroid lipofuscinosis (11 dogs and one cat), gangliosidosis (three dogs and two cats), fucosidosis (one dog), L-2-hydroxyglutaric aciduria (13 dogs and one cat), Lafora disease (11 dogs), spongiform leukoencephalomyelopathy (one dog) and cerebellar cortical degeneration (four dogs and two cats). None of the hepatic encephalopathies showed the previously described T1-weighted hyperintensity of the lentiform nuclei. Instead, there was involvement of the cerebellar nuclei (8/23), which is a feature not previously described. Dogs with myelinolysis showed novel involvement of a specific white matter structure, the superior longitudinal fasciculus (5/5). Thiamine deficiency affected numerous deep grey nuclei with novel involvement of the oculomotor nuclei (3/9), thalamic nuclei, subthalamus and cerebellar nuclei (1/9). Cats with hypertensive encephalopathy had a more extensive distribution of the white matter changes when compared to dogs, extending from the parietal and occipital lobes into the frontal lobes with associated mass effect and increased brain volume. Lysosomal storage disease showed white matter involvement only, with neuronal ceroid lipofuscinosis characterised by severe brain atrophy when compared to gangliosidosis and fucosidosis. All patients with L-2-hydroxyglutaric aciduria had a characteristic T2-weighted hyperintense swelling of the cerebral and cerebellar cortical grey matter, resulting in increased brain volume. Lafora disease cases showed either normal brain morphology (5/11) or mild brain atrophy (6/11). Dogs with cerebellar cortical degeneration had more marked cerebellar atrophy when compared to cats. This study shows the important role of MRI in distinguishing different metabolic/neurodegenerative encephalopathies according to specific imaging characteristics.
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In human medical neurology, the clinical neurological examination is variably augmented by specific tests that may be either unsuitable for veterinary patients or not included in the clinical evaluation of veterinary neurological patients due to clinicians presumably being unfamiliar with these tests. An example of the latter can be found in testing for the Stewart and Holmes' rebound phenomenon ("rebound test"). In this article, a veterinary case example is presented in which a modified version of this test was performed ("head rebound test"). The interpretation of the results of this test is discussed, and the literature on the Stewart and Holmes' rebound phenomenon and testing thereof is reviewed.
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A 5.5 years-old male Dachshund was presented for evaluation because of undesirable behavior including barking, biting, sucking and licking the right-side flank, ventrally and slightly caudally to the level of the surgical incision 7 days after hemilaminectomy for a right-sided L1-2 intervertebral disc extrusion. The dog was being treated with oral gabapentin 10 mg/kg q8h. Repeat clinical examination on three occasions after post-operative discharge did not reveal any signs of hyperesthesia or neurological deficits and the behavior was not observed in the clinic during consultations. During a separate day of hospital admittance with the aim of evaluating for the presence or absence of the behavior, the dog also did not exhibit the behavior. Oral paracetamol 12 mg/kg q8h was added to medical treatment. When the dog was discharged and returned home, the behavior was immediately seen again. When the owners implemented verbal punishment, the behavior immediately ceased. The owner verbally corrected the dogs' behavior for two excitative days. Upon telephone consultation 3 days later, the owner reported that they only had observed three recurrences of the behavior that immediately ceased following verbal correction and did not recur thereafter. Oral analgesic medication was tapered and discontinued. No recurrence of the behavior was noticed during the next 2 months. The authors postulated the dog possibly expressed signs of neuropathic pain in the post-operative period, or that the behavior was of a "compulsive disorder-like" nature as it only occurred when the dog was at home and in the presence of the owner. The eventual outcome and result of verbal corrections implemented by the owner seem to support the latter. In conclusion, compulsive-like undesirable behavior should be considered a differential diagnosis in dogs in the post-operative period of procedures possibly associated with the development or expression of signs of neuropathic pain.
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Epilepsy is one of the most common chronic neurological syndromes in dogs and has serious implications for the quality of life of both the dogs and owners. Seizure-precipitating factors (SPFs) (also termed "triggers" or "provocative factors") have been studied and reported in both humans and dogs with idiopathic epilepsy. In dogs stress, hormones, sleep deprivation, and the weather have been reported as SPFs. The Border Collie (BC) is a breed of dog that is predisposed to idiopathic epilepsy, and the outcome is often poor. BC is described as a very sensitive dog with a strong focus on their owners, and this may have an influence on their and their owners' stress level. In this article, we described six unrelated BCs with idiopathic epilepsy in which several remarkable SPFs were identified, and avoiding them improved the outcome of these dogs. The possible SPFs were different for each dog. The SPFs were, among others, the other dog in the family, the lack of intellectual challenge, the presence of an autistic child, a busy street, the relation with the owner, and throwing a ball at the beach. These cases illustrate that recognizing the SPF(s) and taking measures with regard to management can lead to a reduction in epileptic seizure frequency or even achieving seizure freedom.
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A 1.5-year-old female entire French bulldog was referred for neurological evaluation, further diagnostic tests, and treatment 24 h after a road traffic accident. Initial emergency treatment, diagnostic tests, and stabilization had been performed by the referring veterinarian. Neurological examination revealed severe spastic non-ambulatory tetraparesis and was consistent with a C1-5 myelopathy. A magnetic resonance imaging (MRI) study revealed an irregular to elongated ovoid intramedullary lesion centered over the body of C2. The lesion showed marked signal heterogeneity with a central T2W and T2* hyperintense region, surrounded by a hypointense rim on both sequences. The lesion appeared heterogeneously T1W hypointense. The lesion was asymmetric (right-sided), affecting both white and gray matter. The C2-3 intervertebral disk appeared moderately degenerate with a Pfirrmann grade of 3. No evidence of vertebral fracture or luxation was found on radiographs or MRI of the vertebral column. Additional soft tissue abnormalities in the area of the right brachial plexus were suggestive of brachial plexus and muscle injury. A diagnosis of traumatic hemorrhagic myelopathy at the level of C2 and concurrent brachial plexus injury was formed. Conservative treatment was elected and consisted of physiotherapy, bladder care with an indwelling urinary catheter, repeated IV methadone based on pain scoring (0.2 mg/kg), oral meloxicam 0.1 mg/kg q24h, and oral gabapentin 10 mg/kg q8h. The dog was discharged after 4 days, with an indwelling urinary catheter and oral medication as described. The catheter was replaced two times by the referring veterinarian and finally removed after 10 days. Thereafter, voluntary urination was seen. During the 2 months after the road traffic accident, slow recovery of motor function was seen. The right thoracic limb recovery progressed more slowly than the left limb, also showing some lower motor neuron signs during follow-up. This was judged to be consistent with a right-sided brachial plexus injury. The dog was reported ambulatory with mild residual ataxia and residual monoparesis of the right thoracic limb at the last follow-up 3 months post-injury. This case report highlights the MRI-based diagnosis of traumatic hemorrhagic myelopathy in a dog. A fair short-term outcome was achieved with conservative treatment in this case.
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Introduction: Trigeminal ganglion contrast enhancement (TGCE) is reported to be a normal and a common finding on magnetic resonance imaging studies of dogs, cats and humans. The intent of the present study was to describe the anatomical characteristics of the trigeminal ganglion, its surrounding structures, and histological features that are relevant to explain or hypothesize on the reason for TGCE on T1-weighted post-contrast MRI studies of the brain in dogs. Methods: Eight dog cadavers were dissected to study the anatomy of the trigeminal ganglion. The presence and anatomy of vessels was studied by dissection and by histological techniques. Two trigeminal ganglia were isolated and stained with hematoxylin-eosin (HE). Two other trigeminal ganglia included in the trigeminal canal and trigeminal cavity were decalcified with formic acid/formalin for 12 weeks and stained with HE to study the related vessels. Additionally, a corrosion cast was obtained from a separate canine specimen. Results: Leptomeninges and a subarachnoid space were identified at the level of the trigeminal nerve roots and the trigeminal ganglion. No subarachnoid space was identified and leptomeninges were no longer present at the level of the three trigeminal nerve branches. Small arterial vessels ran to and supplied the trigeminal ganglion, passing through the dura mater. No venous plexus was visualized at the level of the trigeminal ganglion in the dissections. A complex arterial vascular network was identified within the leptomeningeal covering of the trigeminal ganglion and was best appreciated in the corrosion cast. Histological examination revealed small-to moderate-sized blood vessels located in the epineurium around the ganglion; from there a multitude of arterioles penetrated into the perineurium. Small endoneurial branches and capillaries penetrated the ganglion and the trigeminal nerve branches. Discussion: Limitations to this study include the limited number of canine specimens included and the lack of electron microscopy to further support current hypotheses included in our discussion. In conclusion, this study provides further support to the theory that TGCE in dogs may be due an incomplete blood-nerve barrier or blood-ganglion barrier at the interface between the central nervous system and the peripheral nervous system.
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A 1-year-old male intact Staffordshire terrier, born and raised in the Netherlands, was presented with a 3-week history of progressive lethargy and spinal, predominantly cervical, hyperesthesia. Other than hyperthermia and cervical hyperesthesia, general and neurological examination did not reveal any abnormalities. Comprehensive hematological and biochemical tests were considered normal. Magnetic resonance imaging of the craniocervical region revealed heterogeneity of the subarachnoid space, characterized by pre-contrast T1W hyperintensity, corresponding to a T2* signal void. Extending from the caudal cranial fossa to the level of the third thoracic vertebra, there were uneven patchy extra-parenchymal lesions that caused mild spinal cord compression, most marked at the level of C2. At this level, the spinal cord showed an ill-defined hyperintense T2W intramedullary lesion. Mild intracranial and spinal meningeal contrast enhancement was evident on post-contrast T1W images. Subarachnoid hemorrhage was suspected, and further diagnostic tests including Baermann coprology resulted in a diagnosis of hemorrhagic diathesis caused by an Angiostrongylus vasorum infection. The dog rapidly responded to treatment with corticosteroids, analgesic medication, and antiparasitic treatment. Follow-up over 6 months yielded complete clinical remission and repeatedly negative Baermann tests. This case report details clinical and magnetic resonance imaging findings in a dog with subarachnoid hemorrhage associated with an Angiostrongylus vasorum infection.
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A 15-year-old spayed female domestic shorthaired cat was evaluated for chronic progressive paraparesis and proprioceptive ataxia. Neurological examination was consistent with a T3-L3 myelopathy. Plain thoracolumbar vertebral column radiographs and CT without intravenous contrast or myelography performed at another facility did not highlight any abnormalities. MRI of the thoracolumbar spinal cord identified an intraparenchymal space-occupying lesion extending from T10-T12. Surgery was performed to remove as much of the mass as possible, and to submit samples for histopathology. A dorsal laminectomy was performed over T9-T13. A midline myelotomy provided access to the mass, which was debrided with an intraoperative estimate of 80% removal. Histopathologic examination was consistent with a diagnosis of an astrocytoma. Post-operative treatment consisted of amoxicillin clavulanic acid, prednisolone, gabapentin, and additional analgesic medications in the direct post-operative period. Over the following 4 months, slow recovery of motor function was seen with continued physiotherapy. During the following 2 months, renal and cardiopulmonary disease were diagnosed and treated by other veterinarians. The cat was also reported to have lost voluntary movement in the pelvic limbs during this period, suggesting regression to paraplegia. Finally, 6 months post-surgery, the owner elected humane euthanasia. This is the second documentation of surgical treatment and outcome of an astrocytoma in the spinal cord of a cat.
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Introduction: Chiari-like malformation (CM) and syringomyelia (SM) are frequently diagnosed conditions in small and toy dog breeds, such as the Cavalier King Charles Spaniel and Griffon Bruxellois. CM/SM is only rarely reported in Pomeranians in literature to date. The aims of this study are to 1/describe the phenotype of Pomeranians with or without CM/SM and 2/evaluate for differences and associations between CM/SM and owner-reported clinical signs (ORCS) or signalment factors. Materials and methods: From February 2015 to June 2023, historical data and signalment (including country of origin, pedigree, sex and neuter status, age, and body weight) and ORCS of Pomeranians were recorded at multiple institutions. MRI studies of all dogs were evaluated for classification of CM/SM. Additionally, quantitative measurements were performed for SM. Results: A total of 796 dogs from 22 different countries were included. Total prevalence of CM was 54.9% (437/796) and the prevalence of SM was 23.9% (190/796). The top 5 ORCS included 1/scratching with skin contact, rubbing head or ears, or both (57.6% of dogs with ORCS), 2/air licking (30.7% of dogs with ORCS), 3/spontaneous signs of pain (26.0% of dogs with ORCS), 4/persistent licking front and/or hind paws (22.6% of dogs with ORCS), 5/phantom scratching (22.6% of dogs with ORCS). Phantom scratching, vocalization, head shaking, spontaneous signs of pain, and air licking were associated with having SM. There were no statistically significant associations between quantitative syrinx measurements and ORCS. There were statistically significant associations between CM classification and 1/country of origin, 2/having a pedigree, and 3/age. There were statistically significant associations between SM classification and 1/age and 2/body weight. Discussion: This is the first large study evaluating CM/SM in the Pomeranian dog breed. Veterinary clinicians can use these findings to increase the likelihood of correctly determining the presence or absence of CM/SM in Pomeranians. Breeders may consider using the information regarding signalment factors as well as ORCS associated with CM/SM classifications to select dogs for screening procedures. But an MRI-based diagnosis is needed to properly ascertain the exact CM/SM status of their breeding stock until a fool-proof characteristic or genetic marker is found.
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A 3.5-year-old male intact Staffordshire terrier crossbreed dog was presented with a one-week history of progressive paraparesis with fecal and urinary incontinence. Neurological examination was consistent with a T3-L3 myelopathy. A magnetic resonance imaging study revealed the presence of a well-circumscribed hemorrhagic space-occupying lesion at the level of T12, suspected to be a vascular malformation, such as cavernoma or arteriovenous fistula, primary hematoma or hamartoma; less likely considerations included hemorrhagic inflammation or hemorrhagic primary or secondary neoplasia. A dorsal laminectomy, durotomy, and midline dorsal myelotomy were performed with a surgical microscope, and the vascular lesion was identified and removed. Histological examination of surgical samples yielded fibrin, hemorrhage, hematoidin pigment, and some neural tissue. Although a lining wall was visualized during surgery consistent with a vascular malformation, there was no histological confirmation of such a structure, hampering definitive classification of the lesion. There was no gross or histopathological evidence that would support a diagnosis of a hamartoma or benign neoplasia. The dog was paraplegic with intact nociception the day following surgery. Ambulation was recovered within 2 weeks. Progressive and complete recovery of neurological function was seen over the next 12 weeks. No recurrence of neurological dysfunction was seen over a 12-month follow-up period. Surgical treatment should be considered in dogs with spinal intramedullary vascular lesions which can have a successful long-term outcome.
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[This corrects the article DOI: 10.3389/fvets.2022.1066094.].
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Dystonia is a clinical sign and main feature of many movement disorders in humans as well as veterinary species. It is characterized by sustained or intermittent involuntary muscle contractions causing abnormal (often repetitive) movements, postures, or both. This review discusses the terminology and definition of dystonia, its phenomenology, and its pathophysiology, and provides considerations regarding the diagnosis and treatment of dystonia in dogs and cats. In addition, currently recognized or reported disorders in dogs and cats in which dystonia is a particular or main feature are discussed and comparisons are made between disorders featuring dystonia in humans and animals. We suggest that when describing the phenomenology of dogs and cats with dystonia, if possible the following should be included: activity being performed at onset (e.g., resting or running or exercise-induced), body distribution, duration, responsiveness (subjective), severity, temporal pattern (i.e., paroxysmal or persistent, severity at onset and at later stages), presence or absence of autonomic signs (e.g., salivation), presence or absence of preceding signs (e.g., restlessness), presence or absence of signs after dystonia subsides (e.g., sleepiness), coexistence of other movement disorders, any other neurological manifestations, and possible links to administered medications, intoxications or other associated factors. We also suggest that dystonia be classified based on its etiology as either structural genetic, suspected genetic, reactive, or unknown.
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Doenças do Gato , Doenças do Cão , Distonia , Transtornos dos Movimentos , Neurologia , Humanos , Gatos , Cães , Animais , Distonia/diagnóstico , Distonia/terapia , Distonia/veterinária , Doenças do Gato/diagnóstico , Doenças do Gato/terapia , Doenças do Cão/diagnóstico , Doenças do Cão/terapia , Transtornos dos Movimentos/complicações , Transtornos dos Movimentos/veterináriaRESUMO
Canine epileptic seizures are common neurological symptom presenting to veterinary practice. Idiopathic epilepsy (IE) with a suspected genetic background has been reported in several dog breeds. Although it has been reported in the Irish Setter (IS), the phenotypic characteristics have not yet been described. The aim of this study was to characterize the phenotype of IE in this breed and to trace its mode of inheritance. Owners of IS were requested to fill in a questionnaire via the Dutch Irish Setter Club concerning the epileptic seizures in their dogs. The data was assessed retrospectively using descriptive statistics. Forty-eight privately owned IS dogs fulfilling tier I criteria for IE according to the International Veterinary Epilepsy Task Force of both sexes were included in the study. The mean age of seizure onset was 41 months. Five of the dogs included in the study had an onset of seizures >6 years of age. These dogs were classified with epilepsy of unknown cause (EUC). Primary generalized tonic-clonic seizures were the most common type of seizure and were seen in almost all dogs. Cluster seizures were reported in 54% of the studied population. Most owners reported pre- (56%) and post-ictal (97%) signs in their dogs. A pedigree analysis of one subpopulation was performed and traced the lineage of 13 affected IS. A segregation analysis of this population rejected a simple autosomal recessive inheritance pattern. The present study supports the occurrence of IE and EUC in the IS. The results provide clinical insight into epileptic seizures in this breed and may be a starting point for further, including genetic, analysis.
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Epilepsy in dogs is a common chronic and serious disorder and may have an impact on the quality of life of the owners as well as the dogs themselves. The aim of this pilot study was to investigate the QoL score of dogs suffering from idiopathic epilepsy and their owners and if possible, investigate whether a breed specific difference exists. Owners, either Dutch or Belgium, were asked to participate in a web based SurveyMonkey questionnaire. A total of 402 questionnaires representing 402 dogs with epilepsy were suitable for further analysis. Of the 402 dogs, 253 were males and 149 were females. Ninety-nine different breeds were represented. Fourteen breeds (177 dogs in total) were used to calculate breed specific scores; Australian Shepherd (n = 8), Beagle (n = 7), Belgian Tervuren dog (n = 9), Belgian Groenendaeler dog (n = 8), Border Collie (n = 38), Chihuahua (n = 9), Dachshund (n = 13), Drentsche Patrijshond (a Dutch partridge dog) (n = 14), French Bulldog (n = 12), Golden Retriever (n = 17), Labrador Retriever (n = 18), and Rottweiler (n = 12). For the Border Collie, there was a statistically significant correlation between "epilepsy related death," the severity of the seizures (p < 0.001) and cluster seizures (p < 0.001). The quality of life of the Border Collie was scored lower compared to all other dogs (p = 0.02). There were three breeds that had a minimal decrease in the overall quality of life score compared to all other dogs: the Chihuahua (p = 0.03), Dachshund (p = 0.001), and Golden retriever (p = 0.01). The score for "caring for my epileptic dog decreases my own QoL" was high for the Border Collie, Boxer, French Bulldog, and Rottweiler, but was only found to be statistically significantly higher in the Border Collie (p = 0.01). Scores for the Golden Retriever (p = 0.04) and Labrador (p = 0.006) were lower. In conclusion, this study reports breed specific quality of life scores of dogs with epilepsy and their owners, and underlines that breed by itself, is also an important factor when managing epilepsy in dogs.
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The prevalence of idiopathic epilepsy (IE) within the Border Collie (BC) dog breed is high. The aim of this retrospective study was to describe the phenotype of BCs with IE and assess correlations between phenotypic variables and owner-provided quality-of-life (QoL) scores. Data of BCs diagnosed with IE during the period of five consecutive years were retrospectively analyzed. All the dogs were presented at least once to a veterinary neurology specialist at one of three veterinary referral hospitals and most were under the continued medical care of that specialist. Owners were requested to complete a standardized online questionnaire including quality-of-life (QoL) scoring questions. Data of a total of 116 BC dogs were included for analysis. The median age at onset of the first epileptic seizure (ES) was 33.5 months (6-188). A total of 34/86 (40%) of medically treated dogs received 1 antiseizure medication (ASM) and 52/86 (60%) received ≥2 ASMs. Phenobarbital was the most commonly employed ASM, used in 70/86 of treated dogs (81%). Four or more side effects were observed in 20/86 (23%) of treated dogs. Age at onset of first ES was significantly lower for dogs having experienced cluster seizures (CSs), status epilepticus (SE), or both (median 27 months) vs. dogs that had not experienced CS or SE (median 43 months). The QoL of BC with IE was scored with a median score of 7 out of 10. Owners scored their dog's QoL to have declined by a median of 30% during the course of life with IE with 39% (37/95) of owners scoring their dog's QoL to have declined by ≥50%. This study confirms the association of age at onset of first ES with the severity of epilepsy (e.g., presence of CS and/or SE) and further characterizes the phenotype of IE in BC dogs. QoL of BC can be heavily impacted by IE.