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Query: UMLS:C0152025 (polyneuropathy)
 7,862 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Single fibre electromyography was carried out in patients with polyneuropathy due to uraemia, diabetes, and alcohol. In the two former groups the fibre density within the motor unit and the impulse transmission were mainly normal. In the latter group the fibre density was significantly increased as signs of reinnervation. Impulse transmission was impaired in a number of the action potential complexes, which is typical of active reinnervation. The results may indicate that the diabetic and uraemic polyneuropathies are characterized in the main by demyelination, whereas the alcoholic type is dominated by axonal lesion even at an early stage.
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PMID:Single fibre EMG findings in polyneuropathies of different aetiology. 17 47

One case each of pernicious anemia and folic acid deficiency with chronic malabsorption with disease of the cord and histologically demonstrated concomitant disease of the peripheral nerve system in the sense of a polyneuropathy are described. The histological findings of nerve obtained by biopsy show, in both cases, the loss of individual nerve fibers as an expression of a chronic axonal degeneration. The pathogenetic basis to be considered in these cases is presented.
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PMID:[Polyneuropathy in vitamin B 12 and folic acid deficiency. Clinical and histopathological study with electron-microscopy analysis of the sural nerve]. 17 62

Motor units in patients with motor neurone disease and polyneuropathy were studied with a new multielectrode technique allowing fibre mapping. In these disorders which are characterised by reinnervation the motor unit fibre distribution is changed from a normal scattered pattern to grouping often in clinically uninvolved muscles without definite EMG abnormalities. The changes found with this multielectrode technique in man are in accordance with those found in reinnervated motor units studied histochemically in the experimental animal.
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PMID:The reinnervated motor unit in man. A single fibre EMG multielectrode investigation. 17 38

A study of the sequential morphological changes in the peripheral nerve induced by experimental inhalation exposure of methyl n-butyl ketone (MBK) revealed that the earliest change was an increase in the number of neurofilaments in the large myelinated nerve fibers. This change occurred prior to axonal swelling or myelin thinning. As the duration of exposure lengthened the number of neurofilaments gradually increased and ultimately produced axonal swelling with secondary thinning of the myelin sheath. This appears to be the pathogenesis of the "giant axonal" neuropathy. Another change observed early in this neuropathy was the presence of inpouchings of the myelin sheath, which also increased in number in parallel to the duration of exposure. A careful study of the sequential changes in the entire motor unit did not show a predilection for early morphological changes at the axon terminal. Abnormalities at the neuromuscular junction occurred only after a full spectrum of changes were seen in the main nerve trunk, nerve roots and intramuscular nerves. An important observation was the marked potentiation of peripheral neurotoxicity observed when animals were exposed to MBK in combination with methyl ethyl ketone (MEK) at a ratio of 1:5, MBK:MEK. The latter solvent showed no neurotoxic effect alone. This might help explain a recent outbreak of a polyneuropathy affecting many workers. One further observation was that the sural nerve of a patient with prolonged exposure to MBK showed changes similar to those induced experimentally.
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PMID:Peripheral nerve changes induced by methyl n-butyl ketone and potentiation by methyl ethyl ketone. 17 32

The bulbocavernosus reflex was investigated electrophysiologically in 14 normal adult male subjects and in 80 patients with neurogenic bladders and/or impotence due to various neurological causes as well as in patients with functional impotence. The glans penis was stimulated superficially by single electrical shocks and the reflex responses were recorded from the bulbocavernosus (BC) and the striated anal sphincter muscles by means of concentric needle EMG electrodes. In all normal subjects, the BC reflex was recorded from the BC muscle as a stable and constant response having a mean latency of 36.1 msec. A response from the external anal sphincter was obtained in only 21% of the subjects investigated. In 13 patients with cauda equina lesions, the BC reflex was either absent or was present with a prolonged latency. Twenty-two patients with polyneuropathy of various causes were also investigated; in these patients the latency of the BC reflex was significantly greater than in the normal controls, but the most abnormal results were obtained in cases of alcoholic polyneuropathy. In the 19 cases of spinal cord disease with spasticity the BC reflex response was very intense, often with after discharges but latency values were within normal limits. In the 16 cases with functional impotence, the BC reflexes were basically normal; but in 3 cases, the threshold of the reflex was significantly raised, and in 1 case a prolonged latency was observed. The value and the practical application of the BC reflex in the BC reflex in the differential diagnosis of bladder dysfunction and of impotence was stressed.
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PMID:Bulbocavernosus reflex in normal men and in patients with neurogenic bladder and/or impotence. 18 Feb 61

A kinship is described in which there was slowly progressive wasting and weakness of the muscles of the upper and occasionally of the lower limbs. Some members had hyperreflexia. There were no sensory abnormalities. Electrophysiological study suggested the presence of motor peripheral polyneuropathy. The condition appeared to be inherited as an autosomal dominant. The disorder does not appear typical of any of the known hereditary polyneuropathies and it is possible that it may represent a unique hereditary, dominantly motor, polyneuropathy. The significance of the hyperreflexia is uncertain, but raises the possibility of minor central involvement as well as peripheral neuropathy.
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PMID:Hereditary motor peripheral neuropathy predominantly affecting the arms. 18 Feb 64

Seven men aged 17 to 22 years developed severe distal symmetrical predominately motor polyneuropathy after repeated inhalation of a commercially available brand of lacquer thinner. Motor nerve conduction velocities were markedly slowed. Fascicular biopsy specimens of sural nerve showed a striking loss of myelinated nerve fibers. Prominent neurofilamentous masses resulted insegmental paranodal distention of axons with secondary thinning and retraction of myelin from the node of Ranvier. Autopsy material from one case revealed central chromatolysis of anterior horn cells in the lumbosacral enlargement and axonal swellings in the fasciculus gracilis. One or more volatile hydrocarbons contained in the lacquer thinner involved may be neurotoxic if inhaled to excess any many cause a neuropathy with characteristic pathological features.
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PMID:Pathology of lacquer thinner induced neuropathy. 18 61

A motor polyneuropathy developed in a woman with subcorneal pustular dermatosis of 16 years' duration, who had received at least 300 gm of dapsone over a five-year period and 80 gm during the four-month period of progression of her neurologic symptoms. Although the patient believed her muscle power had returned to normal four months after the drug was stopped, a slight peripheral neuropathy remained. Electrodiagnostic and clinical features during the period of greatest weakness and the subsequent 16 months were consistent with a polyneuropathy of the axonal type. The neurotoxicity of dapsone appears to be dose-dependent, but the mechanism by which it occurs is unknown.
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PMID:Dapsone-induced motor polyneuropathy. A complication of prolonged treatment of subcorneal pustular dermatosis. 18 85

A new SER recording system using the bilateral simultaneous peripheral nerve stimulation on cervical, thoracic and lumbar segments was found to be helpful as a diagnostic aid for the localization and the level diagnosis of sensory neuronal lesions including peripheral nerves. SER abnormalities were observed in 32 (76.2%) of the 42 cases with cerebrovascular disease, in 11 (64.7%) of the 17 cases with spinal cord lesions and 12 (75.0%) of the 16 cases with peripheral nerve lesions. As an interesting finding, marked SER abnormalities corresponding with the level and the distribution of the lesions were observed in cases with spinal cord tumor, myelopathy and polyneuropathy. In a case with recurrent myelitis, lesions of different levels of spinal cord were suggested from the SER changes. The recording system gives also valuable information about chronological modifications of the lesions, and may reveal subclinical neuronal damage in a certain neurological disorder.
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PMID:Clinical application of somatosensory cerebral evoked response for the localization and the level diagnosis of neuronal lesions. 18 24

Symmetrical polyneuropathy developed in two patients after they had been in contact with acrylamide and methyl n-butyl ketone, respectively. In sural nerve biopsy material from both patients, electron microscopy showed frequent focal axonal swellings containing masses of neurofilaments. Some axons undergoing axonal degeneration also were seen. These morphologic features are identical to those produced in experimental animals after exposure to these chemicals and are similar to those found in n-hexane neuropathy and in the three reported cases of giant axonal neuropathy. Sural nerve biopsy is an important diagnostic test in identifying cases of peripheral neuropathy caused by these chemicals.
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PMID:"Giant axonal neuropathy" caused by industrial chemicals: neurofilamentous axonal masses in man. 18 68


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