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1.
Cantile C Salvadori C Modenato M Arispici M Fatzer R 《Journal of veterinary medicine. A, Physiology, pathology, clinical medicine》2002,49(10):523-525
A severe atrophy of the cerebellum was observed in a 7-month-old male Italian hound with a history of progressive ataxia and head tremor from the age of 3 months. On clinical examination, signs included severe hypermetric gait, head tremors and proprioception deficits in all limbs. At necropsy, a pronounced symmetrical reduction in size of the cerebellum was the only gross lesion observed. Histological examination of the cerebellum revealed marked thinning of the granular and molecular layers with almost complete loss of granule cells. Purkinje cells had normal morphology and distribution. These findings differ from those of previous reports of cerebellar cortical abiotrophy in dogs, which were mainly characterized by prominent Purkinje cell degeneration and loss. 相似文献
2.
Nibe K Kita C Morozumi M Awamura Y Tamura S Okuno S Kobayashi T Uchida K 《The Journal of veterinary medical science / the Japanese Society of Veterinary Science》2007,69(10):1047-1052
Neuroaxonal dystrophy (NAD) was examined in two Papillon dogs and a mix breed dog between Papillon and Chihuahua. In addition, cerebellar cortical abiotrophy (CCA) in a Papillon dog, which had similar clinical and magnetic resonance imaging (MRI) features to those of NAD, was also investigated. The common clinical symptoms of all dogs affected with NAD and CCA, were pelvic limb ataxia and cerebellar ataxia including intention tremor, head tremor, and hypermetria in the early onset. These clinical signs were progressed rapidly, and two dogs with NAD were euthanized by owner's request and the other two died by aspiration pneumonia. MRI examinations and gross observations at necropsy revealed moderate to severe cerebellar atrophy in all cases of NAD and CCA. The most typical histological change of NAD was severe axonal degeneration with marked spheroid-formation in the dorsal horn of the spinal cords, the nuclei gracilis, cuneatus, olivalis and its circumference in the medulla oblongata. The spheroids were characterized as large eosinophilic or granular globes within the enlarged myelin sheaths, sometimes accompanied by moderate accumulation of microglias and/or macrophages. In contrast, such spheroid formation was minimal in the brain of CCA. In the cerebellum, mild to moderate loss of the Purkinje and granular cells were recognized in three dogs with NAD, whereas these changes were more prominent in a dog with CCA. Although the clinical signs and MRI findings relatively resembled between NAD and CCA, the histopathological features considered to be quite differ, suggesting distinct pathogenesis and etiology. Since both NAD and CCA are proposed as the autosomal recessive hereditary disorders, careful considerations might be needed for the breeding of Papillon and Chihuahua dogs. 相似文献
3.
There have been anecdotal reports since 1962 of 'staggers' in sheep grazing Romulea rosea infested pastures, but this is the first detailed account. In September 2005, a locomotor disorder developed in 12 of 120 Merino wethers that had grazed R. rosea infested pasture at Albury, New South Wales, over several months. Affected sheep displayed signs that included limb paresis, knuckling over in the fetlocks, fine head tremor, incoordination, and an equilibrium disturbance characterised by frequent falling. The microscopic examination of brain and spinal cord tissues from two affected sheep revealed mild vacuolation, occasional lymphocytic cuffing around blood vessels, mild Wallerian degeneration, and occasional glial cells that contained honey-brown cytoplasmic pigments. The most significant changes were found in the cerebellum, where there were decreased numbers of Purkinje cells, increased numbers of glial cells, scattered vacuoles and occasional swollen axons. Previous reports of cerebellar toxicoses in ruminants have involved goats and cattle and have been associated with the ingestion of six Solanum spp. The Purkinje cell loss in this type of disorder is ultimately extensive and consequently affected animals may survive, but will remain permanently disabled. Aust Vet J 2008;86:354 -356. 相似文献
4.
Nineteen cats, aged three to 16 months, developed neurological signs including hindleg paralysis, head shaking, nystagmus, defective vision and reduced proprioception. Most of the animals were in cat colonies in research centres and were derived from specific pathogen-free stock. One was referred from veterinary practice. Over 40 per cent of litters could be affected constituting a serious commercial loss. Wallerian degeneration affected long tracts in the spinal cord and variously in the brain stem and cerebral white matter. In seven animals there was loss of Purkinje cells in the cerebellum and in eight there was neuronal loss in the spinal cord. Gliosis accompanied all changes. Although no viral agent was isolated the clinical pattern of the disease and evidence from other cases reported in the literature suggest an infectious cause. 相似文献
5.
C. L. Chrisman 《The Journal of small animal practice》1992,33(10):500-504
Neuroaxonal dystrophy (NAD) and leukoencephalomalacia (LEM) are two neurological disorders of the rottweiler that initially present as ataxia of all four limbs. Disorders to be included in the differential diagnosis are caudal cervical spondylomyelopathy, canine distemper virus meningoencephalomyelitis, other nervous system infections or inflammations and spinal cord neoplasia. All diagnostic tests including myelography, cerebrospinal fluid analysis, electrodiagnos-tic testing and serum and cerebrospinal fluid titres for canine distemper virus are normal in NAD and LEM. There is no treatment for either disease and neurological signs progressively deteriorate. Eventually neurological deficits develop besides ataxia and these help differentiate NAD from LEM. Dogs with NAD develop head tremors and nystagmus while dogs with LEM develop conscious proprioceptive deficits and quadriparesis; the short term prognosis for NAD is better than LEM. Most dogs with LEM are euthanased because of non-ambulatory tetraparesis within one year. The histopathological lesions associated with NAD include axonal spheroids in many spinal cord and caudal brainstem nuclei and reduced numbers of Purkinje cells in the cerebellum, while in LEM, multifocal areas of demyelination and malacia of the spinal cord and brainstem are the primary histopathological lesions. Both NAD and LEM are suspected to have an autosomal recessive genetic transmission. 相似文献
6.
Sasaki N Yamada M Morita Y Furuoka H Itoh M Satoh M Yamada H 《The Journal of veterinary medical science / the Japanese Society of Veterinary Science》2006,68(12):1367-1369
We report a case of EMND in a heavy horse that was bred and trained in Hokkaido, Japan. Clinical symptoms included severe ataxia of all four limbs, tilted head, lethargy, and flaccid lips. Numerous axonal degenerations and swellings were observed in nuclei, mostly in the cerebellar dentate nucleus and the nucleus of the hypoglossal nerve, and in the ventral horn of the spinal cord. In the ventral horn of the spinal cord, neuronal degeneration, swelling, and/or necrosis were observed sporadically. The case was diagnosed as EMND from the clinical symptoms and pathological findings. 相似文献
7.
AIM: To investigate the nature of a neurological disease in Wiltshire sheep. METHODS: Three affected lambs were examined, humanely killed and necropsied. Selected neurological tissues were examined by light and electron microscopy. RESULTS: Primary neurological lesions were confined to the cerebellum and were characterised by loss of Purkinje cells and the presence of large hypertrophied dendrites of surviving Purkinje cells. These contained stacks of smooth endoplasmic reticulum. There was hyperplasia and cell swelling of Bergmann glia. Mild Wallerian-type degeneration affected white matter in the cerebellum and spinal cord. CONCLUSION: The cerebellar lesions were of a degenerative and reactive rather than hypoplastic nature. These, and the history, suggest a genetic cause with putative inheritance as an autosomal recessive trait. Accordingly, the disorder is described as a cerebellar abiotrophy. 相似文献
8.
AIM: To investigate the nature of a neurological disease in Wiltshire sheep. METHODS: Three affected lambs were examined, humanely killed and necropsied. Selected neurological tissues were examined by light and electron microscopy. RESULTS: Primary neurological lesions were confined to the cerebellum and were characterised by loss of Purkinje cells and the presence of large hypertrophied dendrites of surviving Purkinje cells. These contained stacks of smooth endoplasmic reticulum. There was hyperplasia and cell swelling of Bergmann glia. Mild Wallerian-type degeneration affected white matter in the cerebellum and spinal cord. CONCLUSION: The cerebellar lesions were of a degenerative and reactive rather than hypoplastic nature. These, and the history, suggest a genetic cause with putative inheritance as an autosomal recessive trait. Accordingly, the disorder is described as a cerebellar abiotrophy. 相似文献
9.
A 12-month-old American Miniature horse colt was presented to the Virginia Tech Veterinary Teaching Hospital with a 7-month history of progressive ataxia. Physical examination revealed a head intention tremor, base-wide stance, and ataxia. Necropsy findings were confined to the brain. There were bilateral areas of liquefactive necrosis and cavitation corresponding to the dorsal accessory olivary and lateral (accessory) cuneate nuclei. Cerebellar folia of the dorsal vermis were thin. Microscopically, the cerebellar cortex was characterized by patchy areas of Purkinje cell loss with associated variable thinning of the molecular and granule cell layers and astrogliosis. Dorsal accessory olivary and lateral cuneate nuclei were cavitated and had mild glial response around their periphery. Additionally, a focus of necrosis and neuropil vacuolization was found in the right putamen. These findings indicate the presence of a neurodegenerative disorder centered, but not confined to, the cerebellum and its connections in this American Miniature horse colt. 相似文献
10.
Two domestic shorthair littermate kittens had signs of cerebellar dysfunction, first observed between seven and eight weeks of age; a third littermate was unaffected. The signs were progressive and the more severely affected kitten was euthanased after six days. A postmortem examination revealed no gross lesions but the kitten had cerebellar cortical degeneration with extensive loss of Purkinje cells. The second kitten was euthanased at 10 months of age with similar, though more pronounced, changes. One of the two kittens in the next litter of the same parents had similar clinical signs and histopathological findings. The lesions in the cerebellum are interpreted as probably due to genetically determined abiotrophy. In addition, the two older kittens had medullary neuronal changes interpreted as probable neuraxonal dystrophy, and focal vacuolation of the neuropil in the medulla and cervical spinal cord. 相似文献
11.
A 3.5-month-old papillon puppy was brought to our clinic with chief complaints of progressive quadriparesis, ataxia and head tremor. Lesions in the cerebellum, brainstem and spinal cord were suspected on the basis of a neurological examination. No abnormality was found in a clinicopathological examination or on magnetic resonance imaging. On the basis of these results differential diagnoses including an inflammatory disease, a degenerative condition or a storage disorder were considered. Subsequently, the signs progressed and glossoplegia and dysphagia developed at six months of age. At a second magnetic resonance imaging, severe atrophy of the entire brain was found. After these examinations, the puppy was euthanased and histopathologically diagnosed with neuroaxonal dystrophy. Because magnetic resonance imaging detected abnormal features that were characteristic of neuroaxonal dystrophy in this case, we speculate that magnetic resonance imaging can assist in the pre-mortem diagnosis of this disease. 相似文献
12.
A late onset of cerebellar degeneration was diagnosed in a one-and-a-half-year-old Siamese cat. The animal had been presented with mild ataxia involving all four limbs. Over the following two years, the signs gradually progressed to severe incoordination, a frequent tendency to fall and a head tremor. The neurological signs were consistent with a diffuse cerebellar lesion and the cat was euthanased. Profound and diffuse Purkinje cell loss was found on histopathological examination, but no aetiological agent was detected. 相似文献
13.
A captive adult puma developed ataxia, a hypermetric gait and whole body tremor. The signs progressed over a period of six weeks. Histopathological examination following euthanasia demonstrated spongiform encephalopathy, gliosis and mild non-suppurative meningoencephalitis. Immunostaining with a polyclonal antiserum revealed prion protein (PrP) associated with these changes in sections of cervical spinal cord and medulla. This is the first confirmed case of a scrapie-like spongiform encephalopathy described in a non-domestic cat in the United Kingdom. 相似文献
14.
Gandini G Botteron C Brini E Fatzer R Diana A Jaggy A 《The Journal of small animal practice》2005,46(6):291-294
This case report describes the clinical and neuropathological findings in three young English bulldogs affected by cerebellar cortical degeneration. The dogs, born from the same parents, were presented with clinical signs indicating progressive cerebellar dysfunction: a wide-based stance, severe cerebellar ataxia characterised by marked hypermetria, spasticity, and intention tremors of the head and trunk with loss of balance. On histopathological examination, lesions were confined to the cerebellum and consisted of diffuse degenerative cortical lesions, and there was a loss of Purkinje and granule cells. The history, clinical signs and neuropathological findings confirmed the diagnosis of cerebellar cortical degeneration. To the authors' knowledge, this is the first report of cerebellar cortical degeneration in the English bulldog. 相似文献
15.
L M Miller S M Reed A M Gallina G H Palmer 《Journal of the American Veterinary Medical Association》1985,186(6):601-603
Two adult horses with progressive neurologic signs were examined clinically and at necropsy. Both horses had signs of progressive ataxia and weakness, clinically diagnosed as spinal cord in origin. Differential diagnoses for cervical spinal ataxia in horses included cervical vertebral malformation, equine degenerative myeloencephalopathy, equine herpes-virus-I myeloencephalopathy, and equine protozoal myeloencephalopathy. Necropsy findings in both horses were similar and consisted of a large hematoma in the fourth ventricle, with upward compression of the cerebellum and downward compression of the pons and rostral portion of the medulla. 相似文献
16.
The clinical signs and neuropathological changes of a nervous disease of pedigree cairn terriers are described. Three animals, of both sexes, between five and seven months of age showed hind leg weakness, quadriparesis, ataxia, loss of superficial and deep reflexes and tremor of the head. Pathologically there was chromatolysis of neurons in the spinal cord and brain stem. Although Wallerian-type degeneration was present in the spinal cord and peripheral nerves, its severity did not correlate with the intensity of the neuronal changes. This suggests that the chromatolysis observed may reflect a primary neuronal abnormality rather than represent a secondary change resulting from a primary degeneration of peripheral axons. Although the age of onset and some of the clinical signs are similar to those seen with globoid cell leucodystrophy (an inherited disease which also affects cairn terriers), the presence of lower motor neuron paralysis and the absence of signs of severe brain involvement in progressive neuronopathy should enable the conditions to be distinguished clinically. 相似文献
17.
Neuroaxonal dystrophy in a rottweiler pup 总被引：1，自引：0，他引：1
M G Evans T P Mullaney C T Lowrie 《Journal of the American Veterinary Medical Association》1988,192(11):1560-1562
An 8-month-old Rottweiler pup was evaluated for neurologic disorder. Clinical signs included ataxia, hypermetria of all 4 limbs, intention tremors of the head, lack of a menace reflex bilaterally, and mild proprioceptive deficits. The pup was euthanatized because of the progressive nature of the disease. Histopathologic findings consisted of decreased numbers of Purkinje cells in the cerebellum and moderate numbers of axonal spheroids in the nucleus cuneatus. This latter finding confirmed the diagnosis of neuroaxonal dystrophy. 相似文献
18.
A progressive neurological disease affecting twenty-two young adult dogs of smaller breeds is reported. The disease was most often acute in onset and the neurological signs included cervical pain, seizures, behavioural changes, ataxia, head tilt, muscle tremor and paresis. The lesions were those of a disseminated granulomatous meningoencephalomyelitis in which perivascular cuffs of macrophages and lymphoid cells were the predominant finding. Severe lesions were most often seen in the cerebral white matter although the brain stem, mid-brain and spinal cord were also commonly affected. 相似文献
19.
20.
Coates JR O'Brien DP Kline KL Storts RW Johnson GC Shelton GD Patterson EE Abbott LC 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》2002,16(6):680-689
A neonatal ataxia syndrome was observed in Coton de Tulear dogs. Seven affected pups (32%; 7/22) of both genders came from 5 different litters with phenotypically normal parents. Neurologic examination revealed normal mental status, head titubation, intention tremors, and severe gait, stance, and ocular ataxia beginning at 2 weeks of age. One of the pups was able to walk with assistance, but most of the affected pups were unable to stand and used propulsive movements ("swimming") for goal-oriented activities. They frequently would fall to lateral recumbency with subsequent decerebellate posturing and paddling. Ocular motor abnormalities included fine vertical tremors at rest and saccadic dysmetria. The condition was nonprogressive at least until 4 months of age. No specific abnormalities were identified in routine laboratory screening of blood and urine. Cerebrospinal fluid (CSF) analysis was normal in 1 dog, and a mild increase in protein concentration was observed in a second dog. CSF organic and amino acid concentrations were within normal limits. Magnetic resonance imaging and computed tomography of the brain, electromyography, motor nerve conduction studies, and brain stem auditory-evoked potentials were within normal limits. Postmortem examinations were performed on 5 affected dogs between 2 and 4 months of age. Routine light microscopic and immunocytochemical examination of brain, spinal cord, peripheral nerve, and muscle did not disclose any gross or histologic lesions. Compared with the cerebellum from an age-matched normal dog, the cerebellum from an affected dog showed synaptic abnormalities, including loss of presynaptic terminals and organelles associated with parallel fiber varicosities within the molecular layer and increased numbers of lamellar bodies in Purkinje cells. An autosomal recessive trait affecting development of the cerebellum is suspected. 相似文献