Nerve conduction velocity reduced

Chronic exposure to Pb has been shown to cause anaemia, neurotoxic effects, such as reduced cognitive performance and reduced peripheral nerve conduction velocity, and nephrotoxicity. Children are more sensitive to exposure to Pb than adults, especially during the first 2 years of life [41], For children, exposure to lead can cause growth retardation, affect the neuropsychological development and cause encephalopathy [39]. Adverse reproductive effects due to lead exposure have been observed for both men and women. Exposure of pregnant women to low concentrations of lead is associated with miscarriages and low birth weights [40],... 

A chronic-duration inhalation MRL of 0.6 ppm has been derived by ATSDR, based on a LOAEL of 58 ppm for reduced motor nerve conduction velocity in occupationally exposed workers (Sanagi et al. 1980). 

In streptozotocin-induced diabetic rats, OPB-9195 improved delayed motor-nerve conduction velocity by 60%, reduced stress-related DNA damage in the periphery of sciatic nerves, and reduced serum-AGE levels, but did not affect body weight, blood glucose levels, and glycated haemoglobin.600... 

Lithium also impairs the function of the peripheral nervous system, reducing motor nerve conduction velocity (Faravelli et al., 1999). It causes many metabolic adverse effects, resulting in hypothyroidism, hyperthyroidism (rare), hyperparathyroidism, and diabetes insipidus (Livingston et al., 2006). 

Diabetic patients and animals show reduced nerve conduction velocity. Julu... 

Saxitoxin binds to the sodium channels in the membranes of excitable cells (neurons and muscle cells) blocking synaptic transmission. Saxitoxin is connected to red tides. Saxitoxin reduces nerve conduction velocities. 

Case studies have associated exposure to mercury vapor with neurological effects (e.g., tremors, insomnia, shyness, emotional instability, decreased motor function and muscle reflexes, headaches, and abnormal EEGs) (Davis et al. 1974 Jaffe et al. 1983 McFarland and Reigel 1978). Some studies have examined the relationship between nerve function and mercury levels in blood, urine, and tissue. Tissue levels of mercury have also been found to correlate with impaired nerve function. Among 23 dentists with mercury levels greater than 20 g/g (measured in wrist tissue), 30% exhibited reduced nerve conduction velocity when compared with dentists with tissue levels of mercury below 20 g/g (Shapiro et al. 1982). The decrease in nerve conduction velocity was observed in both sensory and motor nerves. 

Biochemical indicators of possible renal dysfunction (increased urinary NAG levels, and elevated porphyrins) have been associated with increased urinary levels of mercury (Rosenman et al. 1986 Wada et al. 1969 Woods 1996). Functional indicators of adverse neurological effects (reduced nerve conduction velocity, prolonged nerve latency, increased tremor frequency, increased reaction time, reduced hand-eye coordination, and performance on memory and verbal intelligence tests) have also been correlated with increased urinary levels of mercury (Levine et al. 1982 Piikivi et al. 1984 Smith et al. 1970, 1983 Verberk et al. 1986 Vroom and Greer 1972 Williamson et al. 1982). Decreased nerve conduction velocity has been correlated with increased tissue levels of mercury (Shapiro et al. 1982). These biomarkers are not specific for mercury and may be induced by exposure to other metals and... 

Siblerud RL, Kienholz E. 1997. Evidence that mercury from silver dental fillings may be an etiological factor in reduced nerve conduction velocity in multiple sclerosis patients. Journal of Orthomolecular Medicine 12(3) 169-172. 

Reducing the serum magnesium concentration decreases the threshold of axonal stimulation and increases nerve conduction velocity. Magnesium also influences the release of neurotransmitter at the neuromuscular junction by compet-... 

There are additional changes in diabetic nerve of experimental animals that will not be considered in detail here. These include, but are not limited to, diminished Na, K -ATPase activity, which can have adverse effects on the maintenance of the nerve resting membrane potential and perturbation of neurotrophic support. All of these pathological processes, acting in concert, lead not only to decreased nerve conduction velocity but also to reduced nerve blood flow, a condition beUeved to induce endoneurial hypoxia. Over the... 

The neurotoxic effects after 10 years or more of long-term, low-level occupational exposure to carbon disulfide in workers at a viscose rayon plant were examined by assessing markers of the peripheral and autonomic nervous system (Ruijten et al. 1990, 1993). Reinvestigation of 44 of 45 exposed and 31 of 37 matched control workers revealed changes in the motor nerve conduction velocity (Ruijten et al. 1993). The exposure concentration in the two studies varied from 1 to 30 ppm. For peripheral nerves, a decrease in the conduction velocity in both fast and slow motor nerve fibers (peroneal nerve) was observed in exposed workers. Sensory conduction velocities were reduced and the refractory period of the sural nerve was increased. The effects on the sural nerve were pronounced. A small decrease in conduction velocities in the absence of symptoms of neuropathy and decreased response amplitudes suggest a mild presymptomatic nerve impairment. 

Neurological effects such as hind-limb motor difficulties, reduced nerve conduction velocity, and degeneration of nerve fibers were seen in rats exposed to 700 ppm of carbon disulfide for 5 hours a day,... 

An MRL of 0.3 ppm was derived for chronic exposure to carbon disulfide. This MRL was derived based on peripheral neuropathy (reduced motor nerve conduction velocity) in humans after prolonged occupational exposure to carbon disulfide. A LOAEL of 7.6 ppm was established for this effect. Although a dose response was achieved, the effect was considered minimal since the reductions in motor nerve condition velocity were within a range of clinically normal values. This concentration was divided by an uncertainty factor of 30 (3 for use of a LOAEL, 10 for human variability) to yield the calculated MRL of 0.3 ppm. 

A chronic-duration inhalation MRL was calculated on the basis of reduced motor nerve conduction velocity in humans after occupational exposure to an average of 7.6 ppm carbon disulfide, for individuals working approximately 8 hours a day, 5 days a week, for 12.1 years (the mean exposure period) (Johnson et al. 1983). The calculated chronic-duration inhalation MRL is 0.3 ppm. 

Damage to the peripheral nervous system may cause paralysis, as well as pain in the extremities. Chronic lead exposure may reduce nerve conduction velocity in peripheral nerves in adult subjects without clinical symptoms or signs of disease. In some studies, such effects have been recorded in subjects with B-Pbs as low as 1.5-2.0 pmol L (Skerfving 1993). 

A few studies have examined the effect of hypothyroidism on the conduction velocity of action potential propagation in mixed nerves. In both hypothyroid rats and humans, nerve conduction velocity was either unchanged (Quattrini et al., 1993) or modestly reduced (Dyck and Lambert, 1970 Rao et al., 1980). Since these studies examined mixed nerves, a selective effect on motor axons can be obscured. Indeed, as mentioned above, we found that hypothyroidism reduced axon diameters only in type S motor units in the rat diaphragm muscle (Prakash et al., 1996a). GhnicaUy, hypothyroidism results in prolongation of the deep tendon teflex (Swanson et al., 1981), likely related to the slowing of conduction velocities in sensory and/or motor axons. 

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