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1.
The clinical and electrophysiological findings in 14 Boxer dogs with progressive axonopathy (PA) are described. The salient clinical features are hind-limb ataxia which may later involve forelegs, proprioceptive defects, hypotonia, patellar areflexia, absence of muscle atrophy and, in a few instances, ocular tremor and head bobbing. The outward signs are often observed by 2–3 months of age but clinical testing can reveal patellar areflexia at 1 month of age. After an initial progression, the signs may stabilize and dogs are alive at 4 years of age having shown no deterioration over the previous 2 years. The electrophysiology shows reduced motor nerve conduction velocities and evoked potential amplitudes after about 4 months of age. The F-wave latency is considerably increased. Sensory nerves also show a marked reduction in the amplitude of their evoked potentials and eventually cease to conduct. Abnormal spontaneous activity is not a feature on electromyography. The conduction defects probably reflect to some degree the reduced nerve fibre diameters and myelin sheath changes found in PA although other factors may also be operating. The study shows that PA can be diagnosed with reasonable confidence by routine clinical testing at an early age.  相似文献   

2.
雏鸡核黄素缺乏症的外周神经酶细胞化学   总被引：3，自引：0，他引：3  
为进一步探讨核黄素缺乏时外周神经变化的发生机理,对琥珀酸脱氢酶、酸性磷酸酶、腺苷三磷酸酶、碱性磷酸酶进行了酶细胞化学研究。结果表明,核黄素不足的鸡,雪旺氏细胞和轴突中琥珀酸脱氢酶活性下降,酸性磷酸酶活性明显升高,定位于雪旺氏细胞膜上的腺苷三磷酸酶和碱性磷酸酶活性均下降。通过对琥珀酸脱氢酶、腺苷三磷酸酶、碱性磷酸酶活性变化的动态观察,证明轻症鸡自愈的现象以及雪旺氏细胞中琥珀酸脱氢酶活性下降可能是形成脱髓鞘、外周神经水肿、导致雪旺氏细胞膜上的腺苷三磷酸酶和碱性磷酸酶活性下降的原因之一,而增生的雪旺氏细胞中琥珀酸脱氢酶活性增强则可能是修复损伤的一种代偿。腺苷三磷酸酶活性下降与神经水肿密切相关。  相似文献   

3.
The motor cortex was transcranially and peripheral nervous structures (motor roots, plexus, peripheral nerves) were percutaneously stimulated by magnetic pulses in awake dogs and in dogs awaking from general anesthesia. The compound muscle action potentials were recorded by surface or needle electrodes. The central motor conduction time as an information about central motor tracts was obtained by subtracting the peripheral latency from the corticomuscular latency. The peripheral latency was assessed by high voltage electrical and magnetic stimulation of motor roots and by the F-wave technique. The motor conduction velocity of the tibial nerve was measured by percutaneous magnetic and by electrical stimulation and the resulting values were compared.  相似文献   

4.
Electromyographic (EMG) examinations were performed on Beagles before and for 7 days after oral administration of one of the following organophosphate (OP) compounds; ronnel (55.0 or 110.0 mg/kg), dichlorvos (29.7, 59.4, or 148.5 mg/kg), or cythioate (24.8 or 33.0 mg/kg). The EMG values determined were evoked potentials, after-discharge activity, F-wave activity, nerve conduction velocity, and motor unit potential activity associated with interosseous and pectineal reflexes. Erythrocyte cholinesterase (ChE) activities were measured in some dogs. Ronnel did not have an effect on ChE activity, whereas dichlorvos and cythioate, at all dosage levels, had an inhibitory effect. Some dogs had minor signs of OP toxicosis. The EMG changes for individual OP compounds were not statistically significant (P greater than 0.05), but pooled results revealed an increased duration of evoked potentials, increased after-discharge activity, and decreased F-wave activity; however, only the effect on duration was significant (P less than 0.05). Reflex motor unit potential activity and nerve conduction velocities were not affected. Effects of neostigmine (0.1 to 0.4 mg/kg) given IV to anesthetized, atropinized Beagles were similar to those effects shown by pooled data for the OP compounds, but considerably more muscle fasciculation was produced. Results of this study indicate that even when erythrocyte ChE activity is reduced by OP compounds at dosage levels that produce no or minimal visible signs of toxicosis, EMG reveals little evidence for increased motor unit irritability.  相似文献   

5.
Common peroneal and ulnar nerves of 21 dogs between 2 and 15 years of age with malignant tumors were examined for possible paraneoplastic effects. Percent of abnormalities in single-teased fiber studies exceeded the confidence limits (P = 0.99) established for age-matched control dogs in 16 of 21 dogs (76%) with malignancies, none of which manifested clinical signs of polyneuropathy. The incidence of abnormalities was higher in common peroneal nerve (73%) than in ulnar nerve (57%). Lesions were characterized by a mixture of demyelination/remyelination and axonal degeneration; however, the former lesions predominated in most affected dogs. The severity of the neuropathy varied with different tumors, with the most severe lesions observed in a bronchogenic carcinoma (59%), a mammary adenocarcinoma (59%), a malignant melanoma (48%), and an insulinoma (47%).  相似文献   

6.
Background: Acute canine polyradiculoneuritis (ACP) is considered to be an animal model of the acute axonal form of Guillain‐Barré syndrome (GBS) in humans. Various antecedent events have been associated with GBS, including bacterial or viral infection. The relationship between ACP and previous infection requires additional attention. Hypothesis: We hypothesized a relationship between ACP and serological evidence of exposure to Ehrlichia canis, Borrelia burgdorferi, Toxoplasma gondii, Neospora caninum, Campylobacter jejuni, and canine distemper virus (CDV). Animals: Eighty‐eight client‐owned dogs, 44 with ACP, 44 age‐matched controls. Methods: Retrospective study with stored serum samples. Serum antibodies against the target organisms were measured with commercially available assays. Sera from dogs with and without ACP that were positive for T. gondii IgG by ELISA were assayed by an IgG heavy chain‐specific, Western blot immunoassay. Results: Dogs with ACP (55.8%) were more likely to have T. gondii IgG serum antibody titers than dogs without ACP (11.4%). Serum antibodies from 8 affected dogs and 11 control dogs bound to T. gondii antigens with apparent molecular masses of 67, 61, 58, 45, 33, 24, 9, and 6 kDa. An antigen with an apparent molecular mass of 36 kDa was recognized by 2 dogs with ACP but none of the control dogs. Conclusions: Results of this study suggest that ACP in some dogs, like GBS in some humans, may be triggered by T. gondii and a prospective study should be performed to further evaluate this potential association.  相似文献   

7.
OBJECTIVE: To establish a method of F-wave examinations and to determine values of F-wave conduction velocity (FWCV) and F-wave latency for the tibial nerve of clinically normal dogs. ANIMALS: 21 clinically normal dogs. PROCEDURE: The F-waves were elicited from the interosseous muscles via stimulation of the tibial nerve. The FWCV was determined by using the F-wave shortest value and the surface distance corresponding to the tibial nerve length. Correlation between the smallest latency value of the F-wave and the length of the tibial nerve and between the FWCV and rectal temperature were closely examined. RESULTS: F-wave latency was proportional to the length of the tibial nerve (correlation coefficient, 0.929). Mean +/- SD FWCV was 77.98 +/- 8.62 m/s. Regression equation was as follows: F-wave latency = 2.799 + (0.029 X length of the tibial nerve).The FWCV was increased when the measured rectal temperature was high. Correlation coefficient between FWCV and rectal temperature was 0.665. CONCLUSIONS AND CLINICAL RELEVANCE: In the study reported here, we established a reliable method for clinical evaluation of the F-wave. When assessing nerve conduction velocity, it is essential to measure nerve length along the pathway that the nerve impulse travels. This method of F-wave examination is a useful diagnostic tool for the evaluation of suspected dysfunction of the peripheral nervous system.  相似文献   

8.
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   

9.
Giant axonal neuropathy is a newly discovered, neurological disease of the Alsatian which is probably inherited as an autosomal recessive trait. The clinical features of the disease, its differential diagnosis and pathology are discussed in this review. First signs of weakness and ataxia appear in the hind legs of affected dogs at 14–15 months with areflexia, atrophy and diminution of pain sensation. The development of mega-oesophagus appears to be a cardinal feature of the disease. Distal tibial nerve biopsy demonstrates multifocal axonal swellings which result from neurofilament accumulation. Similar lesions are seen at the ends of motor and sensory tracts in the central nervous system. The pathogenesis of this axonopathy is unknown but the possible causes are discussed and the comparative features of the disease presented.  相似文献   

10.
Insulinoma and Subclinical Peripheral Neuropathy in Two Dogs   总被引：1，自引：0，他引：1  
Two dogs with diffuse, subclinical polyneuropathy associated with insulinoma are reported. Seizures were the dominant sign of central nervous system disease. One dog had clinical signs of facial nerve paralysis. Lesions in selected appendicular and cranial nerves included a mixture of demyelination, remyelination, and axonal degeneration. The incidence (range: 18-47%) of these changes far exceeded that of comparable nerves from six control dogs (range 0-11%). Myopathic and electrodiagnostic findings were compatible with the nerve changes.  相似文献   

11.
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   

12.
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   

13.
A male 14-year-old Arab horse was pathologically diagnosed as equine motor neuron disease (EMND), which was kept as a breeding horse on a farm in Tokachi district of Hokkaido in Japan. On examination of the peripheral nerves, the most characteristic feature was Wallerian-type degeneration revealed by myelinoclasis associated with myelin ovoids which were sometimes infiltrated by macrophages. The other abnormalities were axonal swellings which were surrounded by thin myelin sheaths. Ultrastructurally, the axonal swelling was due to an accumulation of neurofilaments, and was accompanied by a thin and degenerating myelin sheaths. In teased nerve fiber preparations, the most conspicuous change was myelinoclasis represented by segmentation into myelin ovoids or balls. Occasionally, segmental demyelination and axonal degeneration characterized by multifocal axonal swelling were observed.  相似文献   

14.
Five Boxer dogs with a new neurological disease are described. There is a progressive ataxia and weakness, initially in the hind-legs but later involving forelegs. The onset of signs is usually around 6 months of age although an older dog was affected. Proprioceptive function, muscle tone and tendon reflexes are diminished or absent while pedal reflexes and pain sensation are preserved. Muscle atrophy is minimal. The peripheral nerves are depleted in myelinated fibres. Nerve roots and, to a lesser extent, peripheral nerves show demyelination/remyelination changes and in the cervical ventral roots in particular, regenerative clusters are present. Forelimb muscles show evidence of re-innervation. In the CNS numerous swollen axons are present. The dorsolateral and ventral columns of the spinal cord are affected throughout their length. In the brain a number of nuclei and tracts, particularly in the lower brain stem, are affected and the superior olives are severely involved. The cerebral cortex and subcortical white matter appear normal. Various portions of the auditory and optic pathways are affected pathologically as are a number of cranial nerves. The axonal swellings contain a number of organelles including smooth endoplasmic reticulum, disordered neurofilaments, vesicles and mitochondria. The disease may be specific to Boxer dogs and may be inherited.  相似文献   

15.
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16.
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   

17.
We conducted combined electrophysiological examinations including F-wave, motor nerve conduction velocity (MNCV), spinal cord-evoked potential (SCEP), and needle electromyography (EMG) in two cats involved in traffic accidents that consequently developed hind limb paralysis caused by lumbar hematomyelia. F-wave could no longer be elicited within 3 days after the accident, and the MNCV and compound muscle action potential (CMAP) amplitude decreased in a time-dependent manner, with CMAP no longer being evoked after 7 or 8 days. EMG showed abnormalities such as fibrillation and positive sharp waves after 6 to 8 days. These results suggest that such combined electrophysiological examinations may provide objective, quantitative data for motor nerve dysfunction in cats with lumbar hematomyelia.  相似文献   

18.
This report describes a rapidly progressive loss of motor function in a 16-month-old male neutered Bengal cat, beginning in the pelvic limbs and progressing to involve all limbs and rendering the cat non-ambulatory. The neurological examination revealed flaccid tetraparesis with decreased spinal reflexes but preserved conscious proprioception and skin sensation. Extensive electrophysiological tests were conducted including electromyography, motor and sensory peripheral nerves potential recordings and 'late' potentials, defining the electrodiagnostic characteristics of this disease. Based on the electrophysiological findings, a generalised proximal and predominantly axonal neuropathy affecting the ventral (motor) nerve roots was suspected. As no aetiology was identified, this disease was classified as idiopathic polyradiculoneuropathy. Over a year, the cat presented three separate episodes of tetraparesis, each with a spontaneous complete recovery, consistent with the reportedly good prognosis for this disease.  相似文献   

19.
Objective To develop fast and reliable testing routines for diagnosing retina and optic nerve diseases in canine cataract patients based on chromatic properties of the pupillary light reflex response. Procedures Seventy‐seven canine patients with a history of cataract and decreased vision (43 patients with cataracts and no evidence of retina or optic nerve disease, 21 patients with cataracts and retinal degeneration [RD], 13 patients with cataracts and retinal detachment [RDT]), 11 canine patients with optic neuritis (ON) and 23 healthy dogs were examined using chromatic pupillary light reflex (cPLR) analysis with red and blue light and electroretinography. Results Electroretinography analysis showed statistically significant deficits in a‐ and b‐wave amplitudes in dogs with cataracts and RD, or cataracts and RDT, when compared to dogs with cataracts without evidence of retinal abnormalities. Evaluation of b‐wave amplitudes showed that presence of 78.5‐μV (or lower) amplitudes had high sensitivity of 100% (95% CI: 87.2–100%) and high specificity of 96.7% (95% CI: 88.4–100%) in RD and RDT. Evaluation of cPLR responses using red light showed that presence of the pupil end constriction diameter of 5.5 mm (or higher) had moderately high sensitivity of 76.5% (95% CI: 50.1–93.2%) and high specificity of 100% (95% CI: 91.2–100%) in detecting RD and RDT. Optic neuritis patients had absent cPLR responses, regardless of the visual status. Conclusions and Clinical Relevance Chromatic evaluation of the pupillary light reflex is a rapid and accurate test for diagnosing retina and optic nerve diseases in canine patients.  相似文献   

20.
A group of ten dogs affected by an apparently identical denervating disease, is described. There was no breed or age predisposition but females were preferentially affected (70%). The rate of onset of signs was variable from a week to greater than 1 month. Quadriparesis was present to varying severities and in two dogs the head and neck could not be supported. Mastication, swallowing, respiration and bladder function were unimpaired. Pain sensation was normal, tone was usually decreased and the local limb reflexes depressed or absent. Muscle atrophy was often prominent. All cases bar one recovered but another dog was also destroyed. Electrophysiology revealed diffuse spontaneous activity in the muscles and the motor nerve conduction velocities were at the lower end of or just below the normal range. The evoked muscle potentials were reduced in amplitude. Sensory nerve potentials were normal. The pathology showed a degeneration of the distal intramuscular axons with collateral axonal sprouting. The muscle changes were typical of neurogenic atrophy. The disease has been called distal denervating disease (DDD) until the precise aetiology can be determined.  相似文献   

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