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1.
Aim: To investigate the nature and cause of a progressive ataxia in three 20-month-old Huntaway dogs that were litter mates.

Methods: Affected dogs were examined before they were humanely killed and submitted to necropsy. Selected formalin-fixed tissues were examined by light and electron microscopy.

Results: The lesions were those of axon and myelin degeneration within sensory, proprioceptive and motor tracts of the spinal cord and to a lesser degree some peripheral nerves.

Conclusion: A progressive myelopathy and neuropathy, tentatively described as a central-peripheral distal axonopathy, was present in all 3 dogs.The cause was not determined but was likely to be either genetic or nutritional.

Clinical relevance: In the early stages of this disease, careful examination maybe necessary to distinguish the signs of ataxia from orthopaedic disease such as hip dysplasia. Affected animals are unlikely to be of use as working dogs.  相似文献   

2.
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3.
AIM: To determine the cause and nature of a disease in newborn New Zealand Romney lambs characterised by progressive weakness and premature death. METHODS: Affected lambs were examined clinically, humanely killed and submitted to necropsy. Selected fonmalin-fixed tissues were examined histologically. Data on the parentage of the lambs were collected. RESULTS: The principle lesions found were degeneration and loss of neurons in ventral horns of the spinal cord and brain stem and Wallerian degeneration of motor nerves and denervation atrophy of skeletal muscles fibres. CONCLUSION: The lesions are those of a lower motor neuron disease which appeared to have a genetic cause.  相似文献   

4.
Three closely related, Siberian Husky dogs had chronic progressive paresis and ataxia with muscle atrophy in the hindlimbs. Radiologic and myelographic examination of the spine revealed no abnormalities. On histologic examination, disseminated degeneration of the white matter, particularly in the thoracic segments, was seen. The clinical and pathological findings were similar to those described in aging large dogs with so-called degenerative myelopathy. The cause of this disease is unknown but the fact that these 3 Huskies were closely related suggest that hereditary factors may play a role.  相似文献   

5.
Progressive ataxia due to central demyelination in Rottweiler dogs   总被引：1，自引：0，他引：1  
A clinicopathological study of a neurologic disease in Rottweiler dogs was conducted. Clinical data were available on 16 dogs, 11 of which were examined pathologically. All dogs had a history of progressive gait abnormalities, which had commenced insidiously at an age varying from 1.5 to 3.5 years. In most dogs the fore limbs were affected prior to the hind limbs. At neurologic examination ataxia of all 4 limbs was seen, in some instances accompanied by an apparent paresis. Proprioceptive positioning was delayed whereas spinal reflexes were often hyperactive. Plain and contrast radiographs of the spine did not reveal any compressive lesions in 5 dogs examined. Cerebrospinal fluid analysis in 4 dogs was normal. Electrodiagnostic testing in 3 dogs revealed no abnormalities. At pathologic examination demyelinating lesions were found in the central nervous system. These were largely confined to the cervical spinal cord and brain stem and had a rather characteristic more or less symmetric distribution. Pedigree data suggested that the disease is transmitted genetically.  相似文献   

6.
OBJECTIVE: To estimate the prevalence of laryngeal paresis within a selected population of dogs and identify some of the distinguishing characteristics of affected dogs. DESIGN: A prospective study involving laryngoscopic examination of 250 dogs. PROCEDURE: The laryngeal movements of 250 dogs undergoing general anaesthesia were observed. The severity of laryngeal paresis in these dogs was graded (0 = normal laryngeal movements, 4 = bilateral laryngeal paralysis). The following information was also recorded for each dog: age, sex, weight, breed, condition score, anaesthetic protocol, clinical suspicion of disease and observer. RESULTS: Twenty five percent of the dogs examined had some degree of laryngeal paresis. Affected dogs were significantly older than unaffected dogs (P < 0.001). There was a trend for the severity of laryngeal paresis to increase with age. There was no difference between the sexes. Dogs with laryngeal paresis were significantly heavier than normal animals (P < 0.02). Overweight animals had a significantly higher laryngeal grade than those with a normal condition score (P < 0.05). Labrador Retrievers and Rottweilers had a significantly higher risk of having laryngeal paresis (P < 0.05). Clinical suspicion was found to have high diagnostic value. An intra-class correlation coefficient for inter-rater reliability between the two observers was 0.95. CONCLUSIONS: Laryngeal paresis had a high prevalence in the animals surveyed and was strongly associated with age and breed. The results of this study are consistent with the concept of a progressive degenerative disease with a breed susceptibility. Clinical suspicion for the presence of the disease was a reliable indicator. The grading system used had a high degree of inter-observer agreement.  相似文献   

7.
A lysosomal storage disease was diagnosed in 2 Australian Cattle Dog siblings, using light and electron microscopic evaluation. Both dogs developed clinical signs of disease at about 1 year of age. Vision and motor function deteriorated over several months; by 2 years of age, the dogs were blind and had progressive ataxia. Cytoplasmic inclusions with ultrastructural patterns characteristic of ceroid lipofuscin were observed in most neurons examined and in the cells of several other parenchymatous tissues. Biochemical studies, including determination of lysosomal enzyme activities, excluded several other lysosomal storage diseases. In these dogs, the clinical and pathologic features of the disease were similar to those of the juvenile subtype of ceroid lipofuscinosis (Batten disease) in human beings.  相似文献   

8.
Background: Familial juvenile glomerulonephropathy (JGN) is reported in several breeds of dogs. The mode of inheritance and spectrum of pathological lesions vary among breeds. A progressive JGN was detected in a pedigree of French Mastiff (FM) dogs. Objectives: To describe clinical, laboratory, and histopathologic findings in related FM dogs suffering from progressive JGN and to determine the mode of inheritance of this condition. Animals: Sixteen affected and 35 healthy related FM dogs Methods: FM dogs <24 months of age and diagnosed with chronic kidney disease with evidence of proteinuria entered the study. Clinical, laboratory, histopathologic findings, and pedigree data were recorded. Results: Clinical signs were typical of progressive glomerulopathy with resultant renal failure. Increased blood urea nitrogen, creatinine and total cholesterol concentrations, and proteinuria were found in all patients. Affected dogs had abnormal kidney structure on abdominal ultrasound examination. Histopathologic examination revealed extensive cystic glomerular atrophy, glomerular hypercellularity, and capillary wall thickening without immune complex deposition when tested with immunohistochemistry or immunofluorescence. Electron microscopy did not disclose specific primary glomerular lesions. Mean age at death was 20 months and mean length of survival after diagnosis was 6 months. Both males and females from healthy parents were affected. An autosomal recessive mode of transmission is suspected, but a more complex mode of inheritance cannot be excluded. Conclusions and Clinical Importance: Progressive familial JGN occurs in FM dogs. Characterization of the pathogenesis and mode of inheritance of this disease warrants additional study.  相似文献   

9.
BACKGROUND: A sensory ataxic neuropathy has been observed in Swedish Golden Retrievers recently. ANIMALS: Twenty-one affected Golden Retrievers. METHODS: Clinical and neurologic status, electrophysiologic, and pathologic status as well as pedigree analyses were evaluated. RESULTS: Clinical signs had an insidious onset between 2 and 8 months of age and a slowly progressive course. Affected dogs were ataxic and dysmetric. They had abnormal postural reactions and decreased spinal reflexes but no apparent muscle atrophy. Clinical pathology, radiography, and electrophysiology of motor systems were all within reference values. Sensory nerve conduction results of affected dogs were significantly different from those of a group of control dogs. Necropsy revealed a chronic progressive central and peripheral sensorimotor axonopathy; the proprioceptive pathways were most severely affected. CONCLUSIONS AND CLINICAL IMPORTANCE: This disease in these Golden Retrievers is distinct from other canine breed-related neurodegenerative diseases or hereditary neurodegenerative diseases described in humans. Pedigree analyses indicated a hereditary background, but the mode of inheritance could not be established.  相似文献   

10.
OBJECTIVE: To evaluate use of transcranial magnetic motor evoked potentials for assessment of the functional integrity of the cervical spinal cord in large-breed dogs with cervical spinal cord disease. DESIGN: Randomized, controlled, masked study. ANIMALS: 10 healthy large-breed control dogs and 25 large-breed dogs with cervical spinal cord diseases. PROCEDURE: Affected dogs were allocated to 3 groups on the basis of neurologic status: signs of neck pain alone, ambulatory with ataxia in all limbs, or nonambulatory. Transcranial magnetic stimulation was performed on each dog with the same standard technique. Motor evoked potentials (MEP) were recorded from electrodes inserted in the tibialis cranialis muscle. Following the procedure, each dog was anesthetized and cervical radiography, CSF analysis, and cervical myelography were performed. The MEP latencies and amplitudes were correlated with neurologic status of the dogs after correction for neuronal path length. RESULTS: Mean MEP latencies and amplitudes were significantly different between control dogs and dogs in each of the 3 neurologic categories, but were not significantly different among dogs in the 3 neurologic categories. A linear association was evident between MEP latencies and amplitudes and severity of neurologic deficits; the more severe the neurologic deficits, the more prolonged the latencies and the more decreased the amplitudes. CONCLUSIONS AND CLINICAL RELEVANCE: Transcranial magnetic MEP are useful to assess severity of cervical spinal cord disease in large-breed dogs. Impairment of the functional integrity of the cervical spinal cord was found even in dogs with neck pain alone.  相似文献   

11.
Acral mutilation and analgesia (AMA) is reported in 13 French spaniels in Canada. This newly recognized disorder shares striking similarities in clinical features and biopsy findings to the other acral mutilation syndromes or hereditary sensory neuropathies reported in German short-haired pointer dogs, English pointer dogs and English springer spaniels. Clinical signs are first noted between 3.5 and 12 months of age. Affected dogs lick, bite and severely self-mutilate their distal extremities resulting in ulcers with secondary bacterial infection. Auto-amputation of claws, digits and footpads occurs in severe cases. Single or multiple feet can be affected. Affected dogs walked on their severely mutilated feet without evidence of pain, lameness, or ataxia. The majority of the dogs were euthanized within days to months of diagnosis.  相似文献   

12.
OBJECTIVE: To determine clinical features, diagnostic imaging abnormalities, underlying disease, disease progression, and outcome in dogs with bilateral cavernous sinus syndrome. DESIGN: Retrospective study. ANIMALS: 6 dogs. PROCEDURE: Dogs were included if clinical signs consistent with bilateral cavernous sinus syndrome (i.e., deficits of the third, fourth, and sixth cranial nerves and at least 1 of the first 2 branches of the fifth cranial nerve) were present and a lesion of the cavernous sinus was identified by means of diagnostic imaging or postmortem examination. RESULTS: 5 dogs were evaluated because of problems referable to abnormal ocular motility or pupillomotor dysfunction, and 1 dog was evaluated because of partial motor seizures involving the face and bilateral mydriasis. Four dogs had neurologic signs referable to an extrasinusoidal lesion at the time of initial examination, and the remaining 2 dogs eventually developed extrasinusoidal signs. Besides neuroanatomic location, the only consistent neuroimaging feature was variably intense, heterogeneous enhancement of cavernous sinus lesions. Neoplasia was histologically confirmed as the underlying cause in 5 of the dogs and was suspected in the remaining dog. Median survival time for the 4 dogs that were treated was 199 days (range, 16 to 392 days). CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that bilateral cavernous sinus syndrome is rare in dogs but should be suspected in dogs with compatible clinical signs. Affected dogs have a poor prognosis, and dogs with clinical signs of bilateral cavernous sinus syndrome should be systematically evaluated for neoplastic disease.  相似文献   

13.
OBJECTIVE: To determine the clinical usefulness of cardiac event recording in evaluating dogs and cats with unexplained syncope, episodic collapse, or intermittent weakness. DESIGN: Retrospective study. ANIMALS: 58 dogs and 2 cats. PROCEDURE: Medical records and electrocardiographic rhythm strips obtained by cardiac event recordings were reviewed. Cardiac rhythm data from the event recordings were classified as diagnostic or nondiagnostic. Diagnostic yield was calculated by dividing the number of animals for which cardiac event recording was diagnostic by the total number of animals undergoing cardiac event recording. RESULTS: For 51 animals, cardiac event recording was classified as diagnostic; therefore, overall diagnostic yield was 85%. Diagnostic yield was lower for animals without underlying structural heart disease (75.5%) than for animals with structural heart disease (95.6%). A specific arrhythmia was identified as the cause of clinical signs in 18 of the 51 (35%) animals for which cardiac event recording was diagnostic. Cardiac arrhythmia was definitively excluded as the cause of clinical signs in the remaining 33 (65%) animals in which cardiac event recording was diagnostic. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicate that cardiac event recording had a high diagnostic yield in dogs and cats examined because of unexplained syncope, episodic collapse, or transient weakness and ataxia, regardless of whether animals did or did not have an underlying structural heart disease. Diagnostic yield of cardiac event recording was higher than that reported previously for Holter monitoring.  相似文献   

14.
Hereditary ataxia in the Jack Russell Terrier (JRT) is characterized by a gait disturbance with symmetric generalized ataxia and hypermetric and spastic movements. Histopathology shows a disease of the entire central nervous system, predominantly an axonopathy. In the present study, 35 clinically affected dogs were examined. Gait abnormalities began at 2-9 months of age. Generalized seizures occurred in 13 dogs in addition to the ataxia, and 7 dogs developed respiratory distress. Brain stem auditory-evoked potentials (BAEPs) were abnormal in 4 of 8 examined dogs, in which only waves I and II were detected. Abnormal BAEPs suggest the possibility of hereditary ataxia in the JRT. Investigations regarding the mode of inheritance were performed by complex segregation analyses on 3 pedigrees with a total of 115 JRTs (27 clinically affected dogs and 88 unaffected littermates and ancestors). Different modes of inheritance were tested, including monogenic, mixed, and polygenic models, as well as a model with environmental effects only. Models with genetic effects explained the data significantly better than the environmental model. The monogenic model had to be rejected in this study because of an insufficient match of data when compared to that of the most general model. The polygenic and mixed major gene models explained the pedigree data best and therefore have to be regarded as possible hypotheses for the mode of inheritance of hereditary ataxia in the JRT. The polygenic model proved best suited to explain the segregation pattern in the JRT, because it had the fewest number of parameters.  相似文献   

15.
Baylisascaris spp larvae were determined to cause CNS disease in 3 prairie dogs maintained at a research facility. Clinical signs consisted of ataxia, stumbling, and head tilt, which progressed to severe torticollis, paddling in lateral recumbency, and loss of the righting reflex. Gross lesions were not found at necropsy. Microscopically, the cerebellar white matter and medulla oblongata were most severely affected and had numerous sections of large ascarid larvae. Our findings indicated that natural infections of Baylisacaris spp larvae can cause CNS disease in prairie dogs. Also, Baylisascaris spp larval infection should be considered in differential diagnoses of CNS disease in prairie dogs.  相似文献   

16.
The autonomic nervous system can be affected as part of a more diffuse peripheral nerve disease such as inflammatory polyneuropathy or diabetes, or as a primary disease, such as dysautonomia. Dysautonomia is being diagnosed with increasing frequency in dogs and other species in the Midwest. Affected animals present with absence of parasympathetic and autonomic ganglia and brainstem nuclei degenerate with minimal inflammation. The cause is unknown and treatment symptomatic.  相似文献   

17.
BACKGROUND: Adult dogs with degenerative myelopathy (DM) have progressive ataxia and paresis of the pelvic limbs, leading to paraplegia and euthanasia. Although most commonly reported in German Shepherd dogs, high disease prevalence exists in other breeds. OBJECTIVE: Our aim was the clinical and histopathologic characterization of familial degenerative myelopathy (FDM) in Pembroke Welsh Corgi (PWC) dogs. ANIMALS: Twenty-one PWCs were prospectively studied from initial diagnosis until euthanasia. METHODS: Neurologic examination, blood tests, cerebrospinal fluid (CSF) analysis, electrodiagnostic testing, and spinal imaging were performed. Concentrations of 8-iso-prostaglandin F2alpha (8-isoprostane) were measured in CSF. Routine histochemistry was used for neuropathology. Deoxyribonucleic acid and pedigrees were collected from 110 dogs. RESULTS: Median duration of clinical signs before euthanasia was 19 months. Median age at euthanasia was 13 years. All dogs were nonambulatory paraparetic or paraplegic, and 15 dogs had thoracic limb weakness at euthanasia. Electrodiagnostic testing and spinal imaging were consistent with noncompressive myelopathy. No significant difference was detected in 8-isoprostane concentrations between normal and FDM-affected dogs. Axonal and myelin degeneration of the spinal cord was most severe in the dorsal portion of the lateral funiculus. Pedigree analysis suggested a familial disease. CONCLUSIONS AND CLINICAL IMPORTANCE: Clinical progression of FDM in PWC dogs was similar to that observed in other breeds but characterized by a longer duration. Spinal cord pathology predominates as noninflammatory axonal degeneration. Oxidative stress injury associated with 8-isoprostane production is not involved in the pathogenesis of FDM-affected PWC dogs. A familial disease is suspected.  相似文献   

18.
AIM: To investigate the nature of a progressive ataxia in a New Zealand Huntaway dog. METHODS: The affected dog was examined clinically before being humanely killed and necropsied. Selected tissues were submitted to light and electron microscopy and to biochemical analyses. RESULTS: The histological lesions were interpreted as indicative of one of the forms of mucopolysaccharidosis type-III (MPS-III), a lysosomal storage disease. Biochemically there was a deficiency of heparan sulphamidase. All the heparan sulphate chains had non-reducing-end glucosamine-N-sulphate residues. CONCLUSION: The disease is MPS-IIIA (Sanfilippo syndrome). An autosomal recessive mode of inheritance can be provisionally assumed from the nature of this disease in other species.  相似文献   

19.
The roles of the calcium sensing receptor gene (CaSR) and the multiple endocrine neoplasia gene (MEN1) were investigated in Keeshond dogs with familial hyperparathyroidism. Mutations in these genes have been shown to cause familial isolated hyperparathyroidism (FIH) in humans. Affected dogs were identified through measurement of blood calcium and parathyroid hormone levels. Parathyroid tissue and whole blood was used to clone the cDNAs and individual exonic sequences of both candidate genes. No sequence abnormalities were identified when comparing normal and affected dogs, suggesting that a mapping strategy may be the most appropriate approach for identifying the genetic basis of this valuable comparative canine disease model.  相似文献   

20.
Background: Nephrotic syndrome (NS) develops most commonly in people with glomerular diseases associated with marked albuminuria. Hypernatremia, hypertension, and progressive renal failure are more prevalent in nephrotic than nonnephrotic human patients. Hypothesis/Objectives: Dogs with NS have higher serum cholesterol, triglyceride, and sodium concentrations, higher urine protein:creatinine ratios (UPC) and systolic blood pressure, and lower serum albumin concentrations than dogs with nonnephrotic glomerular disease (NNGD). NS is associated with membranous glomerulopathy and amyloidosis. Affected dogs are more likely to be azotemic and have shorter survival times. Animals: Two hundred and thirty‐four pet dogs (78 NS dogs, 156 NNGD dogs). Methods: Multicenter retrospective case‐control study comparing time‐matched NS and NNGD dogs. NS was defined as the concurrent presence of hypoalbuminemia, hypercholesterolemia, proteinuria, and extravascular fluid accumulation. Signalment, clinicopathologic variables, histopathologic diagnoses, and survival time were compared between groups. Results: Age, serum albumin, chloride, calcium, phosphate, creatinine, and cholesterol concentrations, and UPC differed significantly between NS and NNGD dogs. Both groups were equally likely to be azotemic at time of diagnosis, and NS was not associated with histologic diagnosis. Median survival was significantly shorter for NS (12.5 days) versus NNGD dogs (104.5 days). When subgrouped based on serum creatinine (< or ≥1.5 mg/dL), survival of NS versus NNGD dogs was only significantly different in nonazotemic dogs (51 versus 605 days, respectively). Conclusions and Clinical Importance: Presence of NS is associated with poorer prognosis in dogs with nonazotemic glomerular disease. Preventing development of NS is warranted; however, specific interventions were not evaluated in this study.  相似文献   

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