Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0152025 (polyneuropathy)
 7,862 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty one patients with confirmed bronchial carcinoma were checked by clinical, electromyographical and electroneurographical methods. None of these patients underwent cytostatic therapy. Clinical findings were: 4 patients suffered from polyneuropathy (PNP) and myelopathy (MP). 3 patients had PNP alone, 3 had MP. We could support these findings by EMG in 7 patients with PNP. 4 of these cases had a lowered motor nerve conduction velocity (MNCV). In 4 cases without clinical symptoms we could show a lowered MNCV at the distal legs and affection of the motor neuron by EMG. 3 further cases without clinical symptoms showed only a lowered MNCV. 5 patients had proximal pareses. Signs of MP were not found in these cases. In conclusion we found a significantly lowered MNCV in 5 cases: only two of these showed clinical signs of PNP. Pathological EMG changes were mostly found in patients with squamous cell carcinoma, sometimes also in patients with oat cell carcinoma. Thus, clinical, electromyographic and electroneurographic findings did not always correlate in our cases.
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PMID:[Electromyographic and electroneurographic findings in bronchial carcinoma]. 21 56

A sural nerve biopsy was performed on an 8-year-old boy with a chronic, slowly progressive polyneuropathy. Light and electron microscopy as well as teased nerve-fiber preparations demonstrated numerous giant axons filled with closely packed neurofilaments. Both myelinated and unmyelinated fibers were involved. Segmental demyelination, remyelination, and onion-bulb formation by multiple Schwann cell processes were observed, suggesting recurrent Schwann cell dysfunction. Abundant aggregates of cytoplasmic microfilaments occurred in Schwann cells, endothelial cells, perineurial cells, endoneurial fibroblasts, and endomysial fibroblasts. These findings support the proposal that giant axonal neuropathy is a generalized disorder of cytoplasmic microfilaments and that segmental demyelination occurs concomitantly with axonal and Schwann cell disease. The pathogenesis of this rare disorder is discussed with reference to experimental toxic neuropathies.
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PMID:Giant axonal neuropathy: a childhood disorder of microfilaments. 21 18

Peroneal motor nerve conduction velocities (MNCVs) were performed on 58 children aged 20 months to 12 years undergoing chronic hemodialysis. No patient had any clinical manifestations of uremic polyneuropathy. The mean MNCV in 21 children at the onset of dialysis was 42.0 m/sec; significantly slower than the control group of 51.4 +/- 5.3 m/sec (p less than 0.001). 16 studied performed between the 1st and 6th month had a mean MNCV of 43.2 +/- 5.7 m/sec, also slower than the normal controls (p less than 0.001). We conclude that peroneal MNCVs are reduced in most children at the initiation of chronic hemodialysis and do not change significantly during the next 6--12 months and that the routine practice of obtaining such studied is of no value in the clinical management of children undergoing chronic hemodialysis.
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PMID:Peripheral motor nerve conduction velocities in children undergoing chronic hemodialysis. 21 41

Purification of b4-2 sub-peak obtained on DEAE Sephadex A25 chromatography gave us the possibility of quantifying the plasma concentration of the neurotoxin present in uraemic patients with active polyneuropathy. From the purified neurotoxin isolated by kieselguhr and cellulose chromatography we calibrated analytic columns for b4-2 analysis. Plasma concentration, measured in 6 uraemic neuropathic patients, is between 13 and 19 mg/litre. In 52 uraemic patients without neuropathy, the plasma concentration is between 3 and 9 mg/litre. In 20 healthy subjects the plasma concentration is less than 1 mg/litre. The weekly neurotoxin removal in uraemic patients without neuropathy, treated by a five hours RP6 session 3 times a week, is of the same order of magnitude as the weekly urinary excretion in healthy subjects. Preliminary results of a tentative identification of this purified product indicate that it is not a polypeptide but an acid-polyol with carbohydrate structure.
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PMID:Evaluation of plasma neurotoxin concentration in uraemic polyneuropathic patients. 21 89

The incidence of TIA, stroke, and neuropathy was studied in a community-based maturity-onset diabetic population. The frequencies of TIA and stroke were increased in maturity-onset diabetic patients as compared to the population of Rochester, Minnesota. The median age of occurrence of TIA and stroke in diabetics was 74 years, not significantly different from that in non-diabetics. Diabetic patients with hypertension at the time of diagnosis of diabetes mellitus had an increased frequency of TIA and stroke. Control of hypertension and/or diabetes mellitus was associated with a decreased frequency of TIA or stroke. Obesity, clinical coronary heart disease, and an abnormal electrocardiogram at the time of diagnosis of diabetes mellitus were not associated with a significantly increased frequency of TIA or stroke. The most common type of peripheral neuropathy in diabetes mellitus was distal polyneuropathy. Mononeuropathy and autonomic neuropathy were much less frequent. The frequency of distal polyneuropathy increased with the duration of diabetes mellitus. The frequency of neuropathy was increased in patients with poor control, reemphasizing the importance of diabetic control in the prevention of diabetic complications.
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PMID:Neurologic complications of diabetes mellitus: transient ischemic attack, stroke, and peripheral neuropathy. 21 54

A patient with postinfective cranial and peripheral polyneuropathy exhibited the electroencephalographic and behavioral features of "alpha coma". The relation of this form of extensive peripheral disconnection to those cases with central disconnection due to pontomesencephalic lesions is discussed. We conclude that in both situations further evaluation of brain stem and cortical function is necessary to determine whether or not consciousness is preserved, rather than relying solely on the presence of ocular movements and reactivity of the electroencephalogram.
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PMID:'Locked-in coma' in postinfective polyneuropathy. 21 18

We report a patient with IgM gammapathy, cryoglobulinemia, Raynaud's phenomena, purpura hyperglobulinemica of the legs and polyneuropathy. Endoneural vasculitis with infiltrations of eosinophilic and neutrophilic granulocytes and an extensive loss or Wallerian degeneration of myelinated nerve fibers were seen on histopathologic examination of a sural nerve biopsy specimen. The microscopic picture differed somewhat from that observed previously in cryoglobulinemic vasculitis. Although vasculitis is most often believed to represent an immunologically mediated lesion, we propose an alternate explanation, namely, that the disease manifestations in the present case were secondary to cold-induced effects of the cryoglobulin on the microcirculation.
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PMID:Peripheral neuropathy in monoclonal gammapathy with cryoglobulinemia and arteritis. 21 28

In patients with diabetes, a carefully taken history and meticulously performed neurologic examination enable the clinician to separate superimposed mononeuropathy from more generalized symmetric polyneuropathy. Recognition of mononeuroparhy is important, since often it is reversible.
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PMID:Mononeuropathy in diabetes mellitus: a phenomenon easily overlooked. 21 22

Although acute lead encephalopathy is rare in adults, the authors had the opportunity to observe a case in a patient who had been exposed to lead occupationally for 25 years. This patient was also seen to be suffering from anemia and polyneuropathy. The blood lead level was 591 micrograms/100 ml (28,52 mumol/l). A review of the literature concerning the principal sources of lead poisoning, routes of absorption, metabolism and consequences of poisoning is conducted. Treatment by chelating agents is discussed. CaNa2-EDTA was administered by i.v. infusion over 24 hours and a favorable evolution was rapidly observable in the encephalopathy and anemia. On the other hand, the polyneuropathy was intensified, a fact which may have been caused by redistribution of lead in the soft tissues.
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PMID:[Lead poisoning. Apropos of a case of acute encephalopathy in an adult]. 21 72

Some conclusions are drawn from findings in 167 consecutive patients with the ordinary "garden variety" of polyneuropathy; the aetiology was unknown in 15%. Histological findings in sural nerves were related to clinical and electrophysiological abnormalities. In some patients with discrete clinical abnormalities, sensory and motor conduction and amplitudes of evoked sensory and muscle action potentials were normal, whereas the nerve biopsy showed slight but definite abnormalities. The reverse, abnormal nerve conduction and normal histological findings, did not occur. Histological findings were rarely, and electrophysiological findings were not, specific for the aetiology or type of a neuropathy. Thus, neither conduction studies nor conventional or single fibre electromyography can identify the underlying pathology: loss of large myelinated fibres (greater than 7 micrometers) was equally prominent in nerves with de- and re-myelination as in those without them. Paranodal and segmental demyelination in less than 20% of the teased fibres occurred as often in nerves with as in those without disproportionate slowing in conduction. When the recorded conduction velocity was equal to that to be expected from the fibres with the largest diameter, slowing in conduction could be explained by axonal degeneration ("proportionate" slowing, 79% of the nerves). When the recorded velocity was disproportionately slower than that expected from fibre diameter (21% of the nerves), causes other than loss of the largest fibres must be assumed to explain the slowing in conduction. Myelin abnormalities in more than 50% of the teased fibres were found only in nerves from patients with the hypertrophic type of peroneal muscular atrophy and in postgastrectomy neuropathy and can probably explain the marked disproportionate slowing in conduction. The material contained, however, only one patient with acute idiopathic polyradiculoneuropahy. In diabetic neuropathy, segmental demyelination was present in only 8 of 502 teased fibres (9 nerves), remyelination was present in 135 fibres, and could not explain the disproportionate slowing in conduction. The mechanism of disproportionate slowing, when it is not due to demyelination, is still obscure.
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PMID:Polyneuropathy. Facts and fancies. 22 6


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