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Query: UMLS:C0031117 (peripheral neuropathy)
 10,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In mammalian species lead acts primarily as a neurotoxin. Lead poisoning is common in avian species but lesions in the nervous system have not been associated with it. This paper describes a peripheral neuropathy with fragmentation and segmental demyelination of fibers in the sciatic nerves of an adult guinea hen (Numida meleagris) which died of lead poisoning.
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PMID:Demyelinating peripheral neuropathy in a guinea hen associated with subacute lead intoxication. 20 80

This report summarizes the results of baseline neurologic testing in a group of apparently healthy workers from a secondary lead smelter and a group of controls from nearby aluminum processing plants. The test battery included a standard neurologic examination nerve conduction measurements, quantitative oculomotor function tests and detailed audiologic studies. Lead workers and controls were intermixed so that the examiners were unaware of the status of any individual being tested. Although the lead workers reported significantly more neurologic symptoms than the controls, relatively few differences were found on quantitative neurologic testing. Decreased deep tendon reflexes occured more frequently in the lead workers than in the controls (22% vs. 11%) but the difference was of borderline significance (p=0.06) and other signs of peripheral neuropathy occurred with equal frequency in both groups. The mean motor conduction velocity and sensory latency measurements were not significantly different in the lead workers and in the controls and, of the six oculomotor function measurements, only the mean accuracy of saccadic eye movements was significantly (p less than 0.01) different in the two groups. High frequency hearing loss occurred with equal frequency and severity in both groups, consistent with the level of noise exposure in the lead and control plants.
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PMID:Subclinical effects of chronic increased lead absorption--a prospective study. II. Results of baseline neurologic testing. 46 15

Lead poisoning resulting from exposure to lead in a domestic car battery workshop is reported in 10 children in 2 families. 2 girls, aged 2 10/12 and 1 8/12 years, respectively, from 1 of the families were hospitalized for investigation of nausea, vomiting, progressive muscular weakness and peripheral neuropathy. Serum lead levels were 52 and 49 mcg/dl, respectively. Subsequent screening of all members of this family, as well as those of the other family who lived in the same house, revealed abnormally elevated levels of serum lead in all the members of both families. The 2 girls were treated with chelating agents and improved clinically and their serum lead levels decreased to 29 and 34 mcg/dl, respectively. The domestic workshop was closed and the 2 families moved to another neighborhood. These cases illustrate the need to screen all family members and contacts of patients with lead poisoning, as well as the hazards of the uncontrolled use of lead in domestic workshops.
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PMID:[Lead poisoning in two families from a car battery workshop]. 270 78

Lead induces peripheral nerve segmental demyelination in rats. Arsenic and thallium produce a peripheral neuropathy characterized by axonal degeneration in humans. Mercury and thallium appear to damage both the peripheral and the central nervous system. It is not known whether this difference in effect is due to different molecular forms of the elements, to differential access to various compartments of the nervous system, or to intrinsically different properties of the elements. Using an in vitro model system of dorsal root ganglion neurons and morphometry of neurite outgrowth and myelination, we demonstrated that mercury and arsenic produce 50% inhibition of neurite outgrowth at 3.9 and 9.6 X 10(-6) M, respectively, whereas the same degree of inhibition is produced by 1.3 X 10(-4) M thallium and 3.3 X 10(-4) M lead. Lead also produces complete inhibition of myelination at 1 X 10(-6) M, suggesting that a primary effect on myelination is present in this model system as well as in the intact rodent.
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PMID:Specific inhibition of myelination by lead in vitro; comparison with arsenic, thallium, and mercury. 375 80

Lead causes peripheral neuropathy, which may lead to radial palsy or other peripheral palsy. In milder cases weakness has been reported especially in the wrist extensors. Several reports have confirmed that even in neurologically symptom-free lead workers motor and sensory conduction velocities slow down and also electromyographic abnormalities like denervation activity and loss or changes in the motor unit potentials appear. When individual exposure to lead has been monitored for long term, an exposure-effect relationship and also an exposure-response relationship have been shown concerning lead exposure and slowing of nerve conduction velocities and also concerning frequency of abnormally slow conduction velocities.
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PMID:Lead poisoning: neurophysiological aspects. 696 50

As far as is known, lead is not required by animals. Lead poisoning is almost always caused by the oral ingestion of too much lead (alimentary contamination). Less than 44 mg lead per kilogram dry weight of feed is considered safe for cattle. Lead intoxication presents in a gastrointestinal form, an encephalic form, a haematological form, and as peripheral neuropathy. Zinc-protoporphyrin (ZPP) and zinc levels in blood should be measured to diagnose lead poisoning. The acceptable range of ZPP is 2.5 to 3.0 micrograms/g Hb(Fe) or less than 150 micrograms/l; more than 250 micrograms/l is too high. Benelux regulations from 1991 give acceptable concentrations for meat, kidneys, liver (between 0.3 and 0.1 mg Pb per kilogram), and milk (0.05 mg Pb per kilogram) destined for human consumption. The treatment for lead poisoning is described.
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PMID:[Lead and health]. 816 Jan 68

Lead has been known to be toxic to most living things at high dose. It is found naturally in earth and present in almost all parts of the environment, such as foods, air, water, dust, soil, paint, and tissues of living organisms including human. This metal is being used in various aspects including the manufacturing of storage batteries, production of chemicals, paints and gasoline additives. It is also used to make various metal products, e.g. sheet lead, solder, and pipes. Human exposure to lead is mainly from foods and other environments. However, it is expected that exposure to environmental lead is normally excessive and produces toxic effects. The well-known and excessive environmental exposures are air of industrial and heavy traffic areas. Use of leaded gasoline has caused the main lead pollution for years in almost every big city. Therefore, city inhabitants normally exposed to lead much more than those who live in the rural area. The most vulnerable groups at risk to lead exposure are fetuses and preschool age children. Young children in the 2-3 year-old age may be the most at risk for exposure to contaminated soil. Adults are affected when exposure is excessive in the working place and causing lead poisoning. Toxicities are mainly on heme biosynthesis, neurological effects including encepharopathy, peripheral neuropathy, and most importantly on I.Q. deficits. It also affects renal tissues to produce acute and chronic nephropathy and elevated blood pressure. There are studies of lead exposure of various means and the effects on human health, both in children and adults. Lead in environment and human exposure are expected to stay with us for long to come, due the still required lead use in many fields, particularly the use of lead in storage batteries and others. The magnitude of exposure will depend solely on the control of use by not allowing the contamination of lead in our environment to be excessive.
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PMID:Lead--the toxic metal to stay with human. 976 Apr 73

Clinical, electromyographic, and pathologic findings characteristic of lead toxicosis were detected in a turkey vulture (Cathartes aura). The bird had generalized lower motor neuron dysfunction that progressed over 5 days. Electromyography revealed diffuse denervation potentials and a presumed decrement in the sciatic-tibial nerve conduction velocity. Histologic examination of peripheral nerves obtained at necropsy revealed changes that could be compatible with lead-induced neuropathy. Lead toxicosis was confirmed by determination of blood lead concentrations. Lead toxicosis causing neurologic disorders in birds has been described. However, this report emphasizes the effects of lead on the peripheral nervous system and demonstrates the use of electromyography for diagnosis of peripheral neuropathy in birds.
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PMID:Peripheral neuropathy in a turkey vulture with lead toxicosis. 1021 87

The ubiquity and stability of metals in the environment make them unique as a pollutant or an essential dietary component. Metals are neither created nor destroyed by chemical processes but are redistributed in the environment. In combination with other elements, metal compounds and alloys are essential materials of the contemporary world. Inappropriate use or distribution in the environment leads to adverse health effects on all biologic systems, including horses. Gastrointestinal upset is a common feature of acute toxicosis with metals in general. Among the metals discussed, arsenic and inorganic mercury have a propensity to do severe damage to the gut. Deposition of cadmium on forage is the source most likely to intoxicate horses. This subchronic to chronic problem in horses is manifest as disease of the musculoskeletal system and kidneys. Iron-containing hematinics are widely used in racetrack horses and occasionally result in hepatopathy when excessive doses are administered. Lead continues to be recognized as the most significant environmental metal pollutant. Poisoning is encountered routinely in humans and animals. Of the animal species of veterinary concern, lead-poisoned horses are not a frequent encounter. Lead-intoxicated horses show signs of peripheral neuropathy (laryngeal hemiplegia), intermittent colic, and mild anemia. Acute mercury poisoning sometimes occurs from the common use of mercury-containing blistering agents, with most clinical findings related to acute renal failure. Chronic excessive intake of zinc by horses is uncommon but devastating in rapidly growing foals. The mechanism of chronic zinc toxicosis is coupled to the induced copper deficiency. The condition is a disease of cartilage in the articular and growth physes.
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PMID:Metal toxicosis in horses. 1178 Feb 84

The neurotoxic effects of inorganic lead are known to include peripheral neuropathy in adults and encephalopathy in children. The purpose of this study was to determine the effect of inorganic lead (PbCl2) administration on norepinephrinergic neurons of the locus ceruleus in neonatal rats by immunocytochemical and electron microscopic analyses. Lead chloride solutions, 0.05%, 0.1% and 0.2% in concentrations, were prepared in distilled water and administered orally via drinking water. After 4, 8, or 12 weeks of continuous administration, the rats were sacrificed and brains were immunostained with the tyrosine hydroxylase antibody. The number of immunoreactive cell bodies in the locus ceruleus was estimated. Densitometric analysis of immunoreactive profiles visualized by electron microscopy was performed using an image analyzer. The numbers of immunoreactive neurons in the locus ceruleus were increased statistically by lead administration. The intensity of the immunoreaction, both under the light and electron microscopes was also increased. Degenerative changes, including intra-axonal vacuole formation and widening of the extracellular spaces, were found by electron microscopy in and around the tyrosine hydroxylase immunoreactive axons. Increased tyrosine hydroxylase immunoreactivity may correlate with the hyper-reactivity of lead intoxicated children. Degenerative changes may account for the reported deficits in intellectual attainment and achievement in lead intoxicated children.
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PMID:Effects of postnatally administered inorganic lead on the tyrosine hydroxylase immunoreactive norepinephrinergic neurons of the locus ceruleus of the rat. 1200 10


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