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1.
Christian Walzer Angelika Url Nadia Robert Anna Kübber-Heiss Norbert Nowotny Peter Schmidt 《Journal of zoo and wildlife medicine》2003,34(1):36-46
Numerous cases of ataxia, hind limb paresis, and paralysis have occurred in cheetah (Acinonyx jubatus) cubs over the past 10 yr within the European Endangered Species Program population, including 12 in mainland Europe, two in the British Isles, one in Namibia, and one in Dubai. The condition is the most important medical factor limiting European cheetah population growth. Eight cubs at the Salzburg Zoo, Austria, were affected. They demonstrated upper motor neuron lesions when alive and bilateral, symmetrical myelin degeneration of the spinal cord on necropsy. Ballooning of myelin sheaths surrounded mostly preserved axons, and no spheroids, characteristic of acute axonal degeneration, were found. Myelin loss markedly exceeded axonal degeneration. The syndrome's etiology is unclear, although viral, bacterial, parasitic, genetic, nutritional-metabolic, toxic, and physical causes have been considered. 相似文献
2.
Thiamine deficiency encephalopathy with concurrent myocardial degeneration and polyradiculoneuropathy in a cat 总被引：1，自引：0，他引：1
Hyaline degeneration, myofiber fragmentation, and mineralization were present in the left ventricle of an aged, female Siamese cat with both clinical and histopathological evidence suggestive of a thiamine deficiency encephalopathy. Both a thiamine related biochemical lesion and neurogenic myocardial degeneration ("Brain-Heart" Syndrome) may have contributed to the development of the heart lesions. A concurrent lumbar polyradiculoneuropathy, characterized by ballooning myelin sheaths with axonal degeneration, was considered an incidental, age-related finding. 相似文献
3.
Harkin KR Cash WC Shelton GD 《Journal of the American Veterinary Medical Association》2005,227(8):1263-5, 1250
A 5-month-old female Border Collie was evaluated because of progressive hind limb ataxia. The predominant clinical findings suggested a sensory neuropathy. Sensory nerve conduction velocity was absent in the tibial, common peroneal, and radial nerves and was decreased in the ulnar nerve; motor nerve conduction velocity was decreased in the tibial, common peroneal, and ulnar nerves. Histologic examination of nerve biopsy specimens revealed considerable nerve fiber depletion; some tissue sections had myelin ovoids, foamy macrophages, and axonal degeneration in remaining fibers. Marked depletion of most myelinated fibers within the peroneal nerve (a mixed sensory and motor nerve) supported the electrodiagnostic findings indicative of sensorimotor neuropathy. Progressive deterioration in motor function occurred over the following 19 months until the dog was euthanatized. A hereditary link was not established, but a littermate was similarly affected. The hereditary characteristic of this disease requires further investigation. 相似文献
4.
Lesions in bovine progressive degenerative myeloencephalopathy ("Weaver") of Brown Swiss cattle 总被引：3，自引：0，他引：3
Gross changes and other necropsy findings in 36 purebred Brown Swiss cattle affected with bovine progressive degenerative myeloencephalopathy were nonspecific. Primary microscopic lesions were confined to the central nervous system, specifically the white matter of the spinal cord, axons in some brainstem nuclei, and Purkinje cells of the cerebellar cortex. Spinal cord lesions involved only the white matter and consisted of axonal degeneration, loss of axons and myelin, and status spongiosus. Axonal degeneration was characterized by swelling and fragmentation of the axoplasm or formation of large, discontinuous swellings referred to as spheroids. Lesions were qualitatively similar at all levels, but quantitatively dissimilar in the same funiculi at different levels. Both ascending and descending fibers were involved but correlation to specific fasciculi was not evident. Lesions always were most severe in thoracic spinal cord segments. Little or no astroglial response, no inflammatory response, and no involvement of gray matter were observed in the spinal cord. Cerebellar lesions were limited to selective degeneration and loss of Purkinje cells and occasional swelling of Purkinje cell axons (torpedos) in the granular layer of the cerebellar cortex. Brainstem lesions were inconsistent and limited to occasional axonal swelling in brainstem nuclei. The pathogenesis of bovine progressive degenerative myeloencephalopathy is unknown and possible mechanisms were discussed. The disease exhibits a familial pattern in Brown Swiss cattle and may be hereditary. Extraneural lesions were considered secondary to central nervous system lesions. 相似文献
5.
A diagnosis of fibrocartilaginous embolism was made in a mature mixed-breed sow with a history of an acute onset of pelvic limb paralysis. Within a single section of lumbar spinal cord, there was severe focally-extensive infarction of the right ventral gray horn. Within affected white matter, there was dilatation of multiple myelin sheaths with concurrent axonal swelling. A smaller focus of infarction was present on the contralateral side. Arteries at the periphery of both lesions contained a blue-gray material with staining characteristics similar to that evidenced by the nucleus pulposus present within intervertebral discs. Grossly, no abnormalities were present within the vertebral column. 相似文献
6.
Salvadori C Cantile C De Ambrogi G Arispici M 《Journal of veterinary medicine. A, Physiology, pathology, clinical medicine》2003,50(6):292-296
A severe myelopathy was observed in a 9-year-old neutered male cat with a clinical history of chronic pancreatitis associated with deficiency of serum cobalamin and folates concentrations, and progressive spinal ataxia. The spinal cord lesions mainly involved the dorsal columns of the caudal cervical and cervico-thoracic segments, and were characterized by diffuse vacuolated myelin sheaths and axonal degeneration, marked gliosis, fibrosis and presence of gitter cells. The pancreas showed severe atrophy of the exocrine tissue, periductular fibrosis and infiltration of inflammatory cells, consistent with chronic interstitial pancreatitis. This condition can be accountable for cobalamin deficiency, as the pancreas is the only source of intrinsic factor in cats. The spinal cord lesions in the cat of this report resembled the subacute combined degeneration of the spinal cord described in human beings with cobalamin deficiency and hence a similar pathogenetic mechanism is hypothesized. 相似文献
7.
The recurrent laryngeal nerves were examined by electron microscopy in five control, four subclinical and four clinical laryngeal hemiplegic horses. In addition, the peroneal nerve was examined in two horses in the latter group. The distally distributed loss of large myelinated fibres in the left recurrent laryngeal nerve seen by light microscopy was confirmed. In addition, active axonal pathology was found to be more evident than indicated by light microscopic investigations. The onion bulb formations observed indicated the repetitive nature of the damaging influence to nerve fibres. Although the pathological changes were most obvious in the distal left recurrent laryngeal nerve, alterations similar in type and distribution were present in other areas of the left and right nerves, and in the distal hindlimb nerves. The observation of fibres with inappropriately thick myelin sheaths relative to their axonal calibre, was confirmed statistically by determining the regressions of axis cylinder perimeter against the number of myelin lamellae. In conclusion, the peripheral nerve pathology of equine laryngeal hemiplegia was demonstrated to be a distally distributed loss of myelinated fibres, with considerable active axonal damage, in conjunction with axonal atrophy. These features suggest that this disease may be classified as a distal axonopathy. 相似文献
8.
The spinal nerve roots and dorsal ganglia of 104- to 135-week-old rats with spontaneous radiculoneuropathy were examined by light and electron microscopy. Demyelination was common in myelinated fibers of various diameters of both ventral and dorsal roots. The most striking alteration was wide distention of myelin sheaths, which extended throughout the entire internode. The spaces formed between separated lamellae frequently were invaded by macrophages. Subsequent vesicular degeneration of myelin seemed to be mediated by invading macrophages. These processes caused complete myelin destruction, but most axons showed no degenerative changes except for obvious reduction in diameter. Occasionally, there were clumping and partial degradation of neurofilaments and ruptured axolemma in the severely demyelinated axons. A few fibers also were undergoing wallerian-type degeneration, perhaps secondary to the severe demyelinative changes. Remyelinating fibers in various phases of repair were coexistent with markedly demyelinated ones. Demyelinative changes described above also developed within some of these remyelinated internodes. There were no remarkable changes in neurons of the dorsal root ganglia, though accumulation of lipofuscin was common. Our findings suggest that the changes in the nerve roots are essentially a primary segmental demyelination in aging rats with radiculoneuropathy. 相似文献
9.
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
10.
K G Braund J R Mehta M Toivio-Kinnucan K A Amling L G Shell M E Matz 《Veterinary pathology》1989,26(3):202-208
Serial peripheral nerve biopsies from two golden retriever littermates with chronic neurologic disease were taken for morphologic and morphometric evaluation. Teased nerve preparations were difficult to interpret due to the lightness of myelin staining. Light and electron microscopic findings were characterized by the following: reduced number of myelinated axons, presence of myelinated sheaths inappropriately thin for the caliber of the fiber, poor myelin compaction, increased numbers of Schwann cell nuclei, increased concentration of neurofilaments in myelinated axons, many Schwann cells with voluminous cytoplasm, and increased perineurial collagen. Onion bulb formation was not seen. In contrast to control data, a poor correlation was seen between numbers of myelin lamellae (ML) and axonal circumference (AC). The frequency distribution of ML ranged from 5 to 55 lamellae in affected animals (mean, 28 lamellae) compared to 20 to 140 lamellae in controls (mean, 66 lamellae). The ML/AC ratio was significantly reduced (P less than 0.001) in nerves of affected dogs. Morphometric results indicated that fibers of all calibers were hypomyelinated. 相似文献
11.
W I Anderson J F Cummings H Steinberg A de Lahunta J M King 《The Cornell veterinarian》1989,79(4):339-344
Lumbar polyradiculopathy, characterized by ballooning myelin sheaths and axonal distortion, was documented in multiple, aged, domestic, laboratory, and exotic mammalian species. Animals studied that exhibited this nerve rootlet change included the goat, sheep, pig, white-tailed deer, gerbil, vole, ferret, beaver, hedgehog, chinchilla, North Chinese leopard, lion, cheetah, mountain lion, llama, East African eland, Uganda giraffe, polar bear, and drill. Ultrastructurally, lumbar nerve rootlets from the North Chinese leopard revealed prominent and often multiple lamellar separations in the area of myelin bubbling. Clefts in myelin sheaths contained macrophages with engulfed fragments of myelin. Axons were sometimes variously attenuated, and the axoplasm contained densely packed neurofilaments. In all species, the lesion was subclinical and considered an incidental age-related finding. 相似文献
12.
The long-term effect of betamethasone on the myelination of commissural and associational fibres was investigated in fetal sheep. We studied the corpus callosum and subcortical white matter by electron microscopy. Axons were subdivided into classes according to their axonal diameter: class I: < or =0.65 microm; class II: 0.66-0.84 microm; class III: > or =0.85 microm. Under control conditions, the different functions of the white matter tracts examined were reflected by three morphological criteria: (1) there was a diverse percentage of axonal classes in the investigated areas. In corpus callosum the axons of class II predominate (47.1%). In the subcortical white matter, class I axons with small diameter are in majority (40.8%). (2) In the subcortical white matter more axons are present, with especially large diameter and hence of axonal class III. (3) The axons of subcortical white matter have thicker myelin sheaths than those of the corpus callosum. Betamethasone administration caused a significant decrease of class II axons in the corpus callosum (36.9%). In corpus callosum, axons of all classes present thicker myelin sheaths. Betamethasone administration resulted in a change in the formation of the myelin sheath in the commissural fibres of the corpus callosum but not in the associational fibres of the subcortical white matter. This could be the morphological correlate to behavioral and cognitive changes known to occur in humans after prenatal glucocorticoid treatment. 相似文献
13.
Equine chronic back pain (CBP) has been linked to different pathologic processes, which directly or indirectly involve spinal structures. Thus, making diagnosis and management very challenging with most horses with the condition recommended for early retirement from athletic activity. This study described the spinal cord lesions and the development of reactive microgliosis and astrocytosis in the spinal cords of horse with CBP. Thoracolumbar spinal cord segments from three horses euthanized because of unresolved CBP were dissected and grossly and histopathologically examined. The expression of activated microglia and astrocytes were demonstrated immunohistochemically using polyclonal rabbit anti-Iba-1 and anti-glial fibrillary acidic protein antibodies, respectively. All horses had radiological evidence of varying degrees of kissing spine involving six to nine vertebrae with the majority of the lesions graded between 2 and 5. Grossly, there was myelomalacia with intramedullary hemorrhages. The gray matters of the spinal cords were characterized by hemorrhagic malacic lesions with medullary disintegration. Reactive microgliosis and astrocytosis were evident in the spinal dorsal horns. White matter lesions include axonal swollen and/or loss, satellitosis, and varying degrees of dilation of myelin sheaths with some containing macrophages. In conclusion, the presence of reactive microgliosis and astrogliosis in the spinal dorsal horn indicates that they are possible precipitating factors in the development of equine CBP. 相似文献
14.
The clinical and pathological features of 19 neonatal Holstein-Friesian calves affected with moderate to severe neurological disease are presented. Most calves were recumbent from birth, and many developed variable neurological signs including hyperaesthesia or depression, limb extension, head tremor, nystagmus, apparent blindness, and opisthotonos when stimulated. Consistent lesions of moderate to severe, diffuse, axonal swelling and loss, with Wallerian-type degeneration and myelin depletion in the spinal cord and brainstem, and occasionally in the midbrain and peripheral nerve roots, were observed. The lesions indicated a pre-natal insult affecting mainly motor areas of the foetal neuraxis, however the aetiology of the disorder remains undetermined. It is suggested that the calves may have been affected by a hitherto unrecognised disease entity for which we propose the term, degenerative axonopathy. 相似文献
15.
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
16.
Stierstorfer B Eichhorn W Schmahl W Brandmüller C Kaaden OR Neubauer A 《Journal of veterinary medicine. B, Infectious diseases and veterinary public health》2002,49(1):37-41
An outbreak of neurological disease occurred in a well-managed riding school. Ataxia and paresis were observed in several horses, five of which became recumbent and were euthanized. Post-mortem analysis revealed scattered haemorrhages along the spinal cord, that were reflected by multiple haemorrhagic foci on formalin-fixed sections, with the thoracic and lumbar segments being the most affected. Pathohistologically, perivascular mononuclear cuffing and axonal swelling, especially in the white matter, were evident. Parallel to the course of disease, alterations in myelin sheets and activation of astrocytes and microglial cells were also observed. Virological findings confirmed an acute equine herpesvirus type 1 infection and virus was isolated from the spinal cord of a 26-year-old mare. 相似文献
17.
B. STIERSTORFER W. EICHHORN W. SCHMAHL C. BRANDMÜLLER O.‐R. KAADEN A. NEUBAUER 《Zoonoses and public health》2002,49(1):37-41
An outbreak of neurological disease occurred in a well‐managed riding school. Ataxia and paresis were observed in several horses, five of which became recumbent and were euthanized. Post‐mortem analysis revealed scattered haemorrhages along the spinal cord, that were reflected by multiple haemorrhagic foci on formalin‐fixed sections, with the thoracic and lumbar segments being the most affected. Pathohistologically, perivascular mononuclear cuffing and axonal swelling, especially in the white matter, were evident. Parallel to the course of disease, alterations in myelin sheets and activation of astrocytes and microglial cells were also observed. Virological findings confirmed an acute equine herpesvirus type 1 infection and virus was isolated from the spinal cord of a 26‐year‐old mare. 相似文献
18.
Jolly RD Johnstone AC Williams SD Zhang K Jordan TW 《New Zealand veterinary journal》2006,54(5):210-217
AIM: To investigate an axonopathy of Merino sheep that caused progressive hindlimb ataxia and slight to moderate paresis, with the purpose of understanding its pathogenesis. METHODS: Tissues were fixed in buffered paraformaldehyde or paraformaldehyde and glutaraldehyde, processed into wax and epoxy resin, respectively, and examined by light and electron microscopy. Fresh frozen spinal cord and trigeminal nerve roots were subjected to homogenisation, centrifugation and two-dimensional electrophoresis. Selected protein spots were identified using matrix-assisted laser desorption ionisation (MALDI) mass spectrometry. RESULTS. By light microscopy, there were large pale foamy spheroidal axonal swellings affecting peripheral as well as central axons. By electron microscopy, these were shown to contain many membrane-bound vesicles. The main abnormalities in expressed proteins involved cytoskeletal elements and myosin heavy chain, the latter interpreted as associated with the molecular motor myosin Va. CONCLUSIONS: The disorder is the same as that described in Merinos in Australia as segmental axonopathy, and believed to have an inherited aetiology. The lesions and protein changes indicate abnormalities of the cytoskeleton, its relationship with the myelin sheath, and myosin Va molecular motor. The consequence appears to be abnormal axonal transport and inability to maintain the integrity of axons and their myelin sheaths. 相似文献
19.
Experimentally induced thiamine deficiency in beagle dogs: pathologic changes of the central nervous system 总被引：1，自引：0，他引：1
Brain and spinal cord were examined in twenty-two 2- to 5-month-old Beagle dogs fed a purified thiamine-deficient ration for 84 +/- 42 (range, 32 to 134) days. Eleven dogs were used as principals, 6 were pair-fed controls, and 5 were controls fed ad libitum. Thiamine at 300 micrograms/kg of body weight was administered IM to control groups once a week. Lesions occurred in 2 topographic patterns in the brain of 8 of the principals. In pattern I, only the caudal colliculi were involved. In pattern II, the suprasplenial gyri of the cerebral cortex and the claustra, caudal colliculi, cerebellar nodulus, and medial vestibular nuclei were commonly involved. In both patterns I and II, gray matter was primarily involved, and in bilateral structures, the 2 sides were affected. Lesions were not limited to a given cerebral lamina or layer of the cerebellum, whereas sulcal areas were relatively spared, and the cingulate gyri were completely spared. Microscopic appearance of the lesions varied greatly among locations and individual principals. Collectively, regressive and reparative changes indicated that there was a progressive process which began with spongiosis and ended with tissue necrosis. These included hydropic vacuolation of the neuropil and myelin sheaths followed by demyelination, neuronal cell body necrosis, hypertrophy and hyperplasia of endothelial cells, necrosis of glia, neutrophil infiltration, disintegration of neuropil, and, finally, accumulation of lipid-containing phagocytes. Axonal degeneration was variable. Neuronal necrosis in the brain stem was characterized by acute swelling and lysis and by shrinkage of the cell body in cerebral and cerebellar cortex and basal ganglia. 相似文献
20.
RD Jolly AC Johnstone SD Williams K Zhang TW Jordan 《New Zealand veterinary journal》2013,61(5):210-217
AIM: To investigate an axonopathy of Merino sheep that caused progressive hindlimb ataxia and slight to moderate paresis, with the purpose of understanding its pathogenesis. METHODS: Tissues were fixed in buffered paraformaldehyde or paraformaldehyde and glutaraldehyde, processed into wax and epoxy resin, respectively, and examined by light and electron microscopy. Fresh frozen spinal cord and trigeminal nerve roots were subjected to homogenisation, centrifugation and two-dimensional electrophoresis. Selected protein spots were identified using matrix-assisted laser desorption ionisation (MALDI) mass spectrometry. RESULTS. By light microscopy, there were large pale foamy spheroidal axonal swellings affecting peripheral as well as central axons. By electron microscopy, these were shown to contain many membrane-bound vesicles. The main abnormalities in expressed proteins involved cytoskeletal elements and myosin heavy chain, the latter interpreted as associated with the molecular motor myosin Va. CONCLUSIONS: The disorder is the same as that described in Merinos in Australia as segmental axonopathy, and believed to have an inherited aetiology. The lesions and protein changes indicate abnormalities of the cytoskeleton, its relationship with the myelin sheath, and myosin Va molecular motor. The consequence appears to be abnormal axonal transport and inability to maintain the integrity of axons and their myelin sheaths. 相似文献