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

All five members of a family developed subacutely mental confusion and/or truncal ataxia. Symptoms and signs of polyneuropathy were seen later. The well water in the patients' home contained 400 ppm acrylamide. The present cases are unique in that they are cases of acrylamide poisoning induced by oral intake and percutaneous penetration, and that central nervous system symptoms were prominent.
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PMID:Acrylamide encephaloneuropathy due to well water pollution. 16 22

After the long-term exposure to cadmium chloride in drinking water, the Wistar rats developed peripheral polyneuropathy. The main lesion was of myelin degeneration. Ultrastructural examination of the roots and sciatic nerves revealed segmental demyelination beginning from the node of Ranvier. There was the active autophagocytosis of Schwann cells which contained a number of myelin remnants and dense bodies. There was, on the other hand, the evidence of remyelination with toxic damage, in which the thinner myelin sheaths and abnormal myelinations were observed with increase of Schwann cells containing rich ribosomes. Axoplasmic changes were minimal, but consisted of accumulation of glycogen particles which very often produced glycogenosomes in characteristic appearance with axoplasmal dysfunction.
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PMID:An ultrastructural study of chronic cadmium chloride-induced neuropathy. 20 91

Sixty-day-old virgin female Swiss CD1 mice were treated with 1.5% 2,5-hexanedione in their drinking water; control mice received tap water; duration of treatment was either 4 or 6 weeks. Under these conditions the treated mice did not show any clinical symptoms although electromyography revealed some signs of polyneuropathy. Protein and DNA content per mg of ovarian tissue in treated mice were not significantly different from controls. Histological examination of ovarian sections at the light microscope level showed no significant alterations after exposure. A morphometric study revealed a statistically significant reduction in the number of growing oocytes after 6 weeks of treatment. For fertility studies three groups of 15 female mice each were treated for 0, 4 or 6 weeks as above and then permanently housed with untreated proven breeder male mice (one male per female); cages were checked daily for newly born mice. All litters appeared normal by gross examination. During the first 14 weeks of continuous mating the mean litter size (number of newborns per litter) remained about 11.4 in all groups; this number subsequently began to decrease. Control and 4-week treatment regression curves did not differ statistically, while the slope of the 6-week line was significantly steeper, indicating a faster decrease in litter size over time and a shortening of fertile life in the latter group of treated females.
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PMID:Effects of 2,5-hexanedione on the ovary and fertility. An experimental study in mice. 145 23

2,5-Hexanedione is a main metabolite of n-hexane and is considered as the cause of n-hexane polyneuropathy. Therefore, it is useful to measure 2,5-hexanedione for biological monitoring of exposure to n-hexane. The analytical methods existing for n-hexane metabolites, however, were controversial and not established enough. Hence, a simple and precise method for determination of urinary 2,5-hexanedione has been developed. Five ml of urine was acidified to pH 0.5 with concentrated hydrochloric acid and heated for 30 minutes at 90-100 degrees C. After cooling in water, sodium chloride and dichloromethane containing internal standard were added. The sample was shaken and centrifuged. 2,5-Hexanedione concentration in an aliquot of dichloromethane extract was quantified by gas chromatography using a widebore column (DB-1701). Urinary concentration of 2,5-hexanedione showed a good correlation with exposure to n-hexane (n = 50, r = 0.973, p less than 0.001). This method is simple and precise for analysis of urinary 2,5-hexanedione as an index of exposure to n-hexane.
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PMID:Determination of urinary 2,5-hexanedione concentration by an improved analytical method as an index of exposure to n-hexane. 187 15

The article contains results of clinical studies of dimethylsulfoxide (DMSO) therapeutic application at vibration disease (VD) cases caused by local vibration and in comparison with the generally accepted complex therapy. 30% DMSO water solution skin compresses were used applied to the affected zones of the upper extremities for 1-1.5 hours daily with 12-15 procedures in the whole course. It was established that DMSO effects are positive in most VB manifestations: regional angiodystonia, sensor and vegetative--sensor polyneuropathy, arthroses, and particularly in cases of muscle dystonia and myodistrophy, humeroscapular periarthrosis. This kind of technique simplifies VD therapy as it excludes physiotherapy procedures and limits medication to a great extent, doing with no drugs at all in some cases. Treatment costs and clinical course duration are also lowered.
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PMID:[Dimethyl sulfoxide in the therapy of vibration disease]. 261 22

The neurobehavioural and morphologic changes and the reversibility in 2,5-hexanedione-induced polyneuropathy in rats were studied. The potentiation and influence of acetone on the reversibility of the induced neurotoxicity was also evaluated. Male rats were treated for 6 weeks with 0.5% w/v 2,5-hexanedione alone or in combination with 0.50% w/v acetone in the drinking water. During the treatment period, neurobehavioural tests (ambulation and rearing in open field, balance on the accelerating rotarod and fore-and hindlimb muscle strength measurements) were performed weekly. After 6 weeks half of the rats was sacrificed and histopathological lesions in the sciatic nerve and tibial nerve were evaluated by morphometry. Neurotoxicity was induced by 2,5-hexanedione, and acetone caused a potentiation of this effect in open field ambulation and rearing and in the rotarod test. In the pathological evaluation, giant axonal swelling was observed after 2,5-hexanedione and 2,5-hexanedione plus acetone. In nerve fibre cross sections, a significant change of the distribution of fibre area size was observed in animals treated with 2,5-hexanedione. Aggravation of the lesions was seen in rats treated with both 2,5-hexanedione and acetone. The other half of the animals was used to study the reversibility of the neurotoxic effects within a dose-free period of 10 weeks. Reversibility of the effect on ambulation was complete within the recovery period, but the effects on rearing and balance in the rotarod test were only reversible within the 10 weeks in the 2,5-hexanedione-treated rats and not in the combined 2,5-hexanedione and acetone-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acetone potentiation and influence on the reversibility of 2,5-hexanedione-induced neurotoxicity studied with behavioural and morphometric methods in rats. 809 Jul 2

The effects of warming on nerve conduction variables and electromyography were studied in 15 patients with a polyneuropathy associated with monoclonal gammopathy of undetermined significance. In each patient median nerve (motor, sensory) and tibial nerve (motor) conduction parameters were measured before and after warming in water at 36 degrees C. Warming: (1) increased the conduction velocity (CV); (2) decreased the distal motor latency, amplitude, and duration of the compound muscle or nerve action potential; and (3) caused fibrillations to appear in 1 patient. The increase in CV with temperature depended upon the CV after warming: the lower this CV, the smaller the increase in CV with temperature (delta CV/delta T). Correction of median nerve motor CV before warming with 2.2 m/s per degree C yielded CV values which were higher than the CV values after warming, because in most patients delta CV/delta T was less than 2.2 m/s per degree C. Because of differences in delta CV/delta T values, it is more accurate to warm the extremity than to correct for temperature.
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PMID:Temperature dependence of nerve conduction and EMG in neuropathy associated with gammopathy. 815 82

Deficiency and/or altered metabolism of vitamins in CRI is caused by uremic toxins, dietary restrictions, catabolic illness, losses during dialysis and drug interaction. There are no reports of consistent studies on vitamin status of water soluble vitamins in CRI. Vitamin B1 (thiamine) deficiency several authors found most frequently in CAPD patients. The cause of this deficiency depends probably on increased requirement of vitamin B1 due to high glucose intake with peritoneal dialysis solution. In patients with polyneuropathy high doses of thiamine pyrophosphate (Cocarboxylase), given i.v., can be helpful in this respect. There are conflicting reports concerning plasma level of vitamin B2 (riboflavin) in CRI patients. Some authors recommend its supplementation. The majority of patients with CRI exhibit biochemical and clinical signs of vitamin B6 deficiency. There exists an univocal opinion that supplementation of this vitamin effects the cellular immune system and the amino acid metabolism as well. An adequate dose of vitamin B6 is still a matter of dispute. Evidence of vitamin B12 deficiency has been reported rarely, thus, only few authors recommend the supplementation of it, mainly in CAPD patients. According to most authors the losses of folic acid and ascorbic acid during dialysis require oral supplementation. Despite the divergences in opinions concerning the deficiency of water-soluble vitamins in CRI patients, the supplementation of these vitamins is practised in many nephrological centers. The amount and the route of vitamins, administered to CRI patients, should be individualized.
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PMID:[Vitamin disturbances in chronic renal insufficiency. I. Water soluble vitamins]. 883 46

Proteinases are widespread in neuronal or nonneuronal eukaryotic cells. They are suggested to play an important role in the turnover of proteins in neuronal perikaryon and axon, and digestion of the transported cytoskeletal proteins in synaptic terminals. We examined the effect of acrylamide (50 mg/kg, ip), carbon disulfide (700 ppm, 9 h, 7 d a week), and 2,5-hexanedione (2,5-HD) (1% in drinking water) treatment of rats on mCANP (2 mM Ca2+), microCANP (0.1 mM Ca2+), and CINP (Ca(2+)-independent) activity in telencephalon + diencephalon (FB), rhombencephalon + mesencephalon (LB), spinal cord (SC), and sciatic nerve (SN). The proteinase activity was determined in the 30,000g supernatant fraction of tissues using 14C-methylated casein as the substrate. mCANP activity in FB, LB, and SC was inhibited only by acrylamide. Acrylamide or 2,5-HD treatment had no effect on microCANP and CINP activities of SN, whereas carbon disulfide enhanced microCANP after 15 d and CINP activity after 10 d. It is suggested that alteration in in vitro calpain activity shown by these chemicals may not be directly related to their neurotoxic effect. However, calpain may still be playing a role in this polyneuropathy by alteration in activity through inflow of Ca2+, release of Ca2+ from intracellular organelles, or other factors. Modification of cytoskeletal proteins making them more susceptible to proteases and the role of some other proteinase is also possible.
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PMID:Alterations in the neutral proteinase activities of central and peripheral nervous systems of acrylamide-, carbon disulfide-, or 2,5-hexanedione-treated rats. 888 40

Autonomic dysfunction constitutes a prominent clinical feature of equine grass sickness (EGS). Significant injury to the nervous control of the alimentary system is life threatening, partly because of dysphagia but also because of the failure of the unique regulatory mechanisms in equine digestion involving water and electrolyte balance. The neuropathology also indicates the presence of a somatic polyneuropathy. The morphological features of EGS are similar to those of excitotoxic neuronal degeneration, which resembles neuronal apoptosis. It is difficult to ascertain from published accounts the degree of damage to central neurones: the distribution is well documented and selective but the proportion of damage is poorly quantified. If lesions involve a significant number of regulatory neurones they should produce functional deficits. Any clinical assessment of horses, especially those with chronic EGS, should include a thorough neurological examination. Although this will not necessarily improve the outcome of the case, it may enable the rational selection of animals with a reasonable prognosis for recovery which is partly determined by the extent of CNS lesions. The evidence supports the following pathogenesis. There is an initial lesion in the enteric nervous system of susceptible horses. In the acute form of EGS, massive enteric neuronal damage occurs first functionally, then structurally leading to generalized alimentary smooth muscle atony, enhanced secretions and altered fluid fluxes. Severe distension of the stomach and small intestines rapidly develops, which augments the intestinal ileus by intersegmental inhibitory reflexes and causes colic and dehydration. In subacute cases, failure of intestinal bicarbonate buffer together with alimentary stasis rapidly reduces caecal-colonic fermentation. Thus the osmolality of large intestinal digesta reduces and water travels out of the bowel along osmotic gradients. Water returns to the circulation, but is eventually lost in the gastric and small intestinal secretions. The observation that pathological lesions may not be seen in the prevertebral ganglia within the first few days of acute cases supports the view that a functional deficit precedes structural lesions which may be secondary to a retrograde degeneration. It is therefore possible to resolve the observations that less damage may be seen in prevertebral ganglia and elsewhere in peracute and acute cases with the more common finding that greater neuronal damage is present in acute than in chronic cases. These different observations are probably time dependent. Chronic EGS occurs when there is less initial enteric nerve damage which may lead to less secondary prevertebral ganglionic pathology, and more time for functional and structural compensatory mechanisms to develop. Denervation hypersensitivity develops at target sites both in the gut and in peripheral somatic nerves which may account, in part, for the clinical signs of patchy sweating and muscle tremors. Raised circulating adrenaline levels may also account for generalized sweating, may contribute to gastrointestinal atony and may affect pacemakers at the pelvic flexure. Many of the features of EGS make worthwhile the re-investigation of Clostridium botulinum Group III toxins, which are known to prevent vesicular exocytosis, stimulate neurosecretion, produce neuronal chromatolysis and inhibit neutrophil migration. Also, evidence from other species suggests that increased nitrergic neuronal activity can account for many of the clinical signs of EGS, namely dysphagia, generalized ileus, gastric dilatation, sweating, peripheral vasodilatation, tachycardia, salivary hypersecretion, muscle wastage and cachexia.
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PMID:The neurology and enterology of equine grass sickness: a review of basic mechanisms. 1032 May 95


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