Nerve conduction studies velocity

A meta-analysis of 32 pubhcations of nerve-conduction studies and occupational lead exposure foimd BLL to be a weak predictor of peripheral nerve impairment (Davis and Svendsgaard 1990). Nerve-conduction testing includes analysis of latent period (time it takes for stimulatory impulse to initiate an evoked potential), conduction velocity, and amplitude. Reduced nerve-conduction velocities in lead-exposed subjects revealed that the median motor nerve was most sensitive. 

Nerve-conduction studies of workers in a lead-battery factory (Kovala et al. 1997) found that sensory amphtudes of the median and sural nerves correlated negatively with long-term exposure (CBLI and dirration of exposure). Chia et al. (1996b) also foimd the strongest dose-effect relationship between median sensory conduction velocity and CBLI, whereas He et al. (1988) foimd sensory-... 

Inhibitors of AR have been demonstrated to prevent a wide variety of biochemical, functional and structural alterations in animal models of diabetes. Early studies demonstrated arrest of both early cataract development and nerve conduction velocity. At least 30 clinical trials of AR inhibitors have been published involving nearly 1000 patients in total. However, there is little impressive data of their efficacy up to now but, rather than undermine the hypothesis linking excess polyol pathway activity to diabetic complications, it may reflect methodological difficulties and trial design errors. 

The intermediate-duration effects of hydrogen sulfide on neurological function were examined by the measurement of motor and sensory nerve conduction velocities of the tail nerve or morphology of the sciatic nerve (Gagnaire et al. 1986). Male Sprague-Dawley rats were exposed to 0 or 50 ppm hydrogen sulfide for 5 days a week, for 25 weeks. The study authors did not report the duration of exposure to hydrogen sulfide per day. No neurotoxic effects were observed in the rats. 

Yokoyama K, Araki S. 1986. Alterations in peripheral nerve conduction velocity in low and high lead exposure An animal study. Ind Health 24 67-74. 

In axonal neuropathies, the velocity of action potential propagation in surviving axons is well maintained but the number of axons capable of conducting action potentials is diminished. Transcutaneous nerve stimulation and recording, the method routinely used for studying nerve conduction in the clinic, does not permit evaluation of the function of autonomic or unmyelinated sensory axons. These smaller, slow-conducting axons can be analyzed, in research studies, by intraneural recording with needle electrodes. 

A decrease in the amplitude of the sensory nerve action potential has also been observed in a group of 20 asymptomatic workers exposed to -hexanc (Pastore et al. 1994). The subjects of this study were selected on the basis of urinary levels of the n-hexane metabolite 2,5-hexanedione (See Sections 2.3 and 2.7) exceeding 5 mg/L and compared to a group of unexposed laboratory workers. Mean years worked was 8.13 (range, 1.5—23 years). Sensory and motor nerve conduction velocities and distal latencies were normal in all nerves tested. However, significant decreases were found in sensory nerve action potential amplitude in the median, sural, and ulnar nerves. Neither the level of 2,5-hexanedione in urine nor age correlated with the changes in amplitude however, there was a significant correlation between years worked and amplitude. 

It is not entirely clear whether the acetone co-exposure in the Sanagi et al. (1980) study contributed to the observed effects. Indirect evidence from an occupational study (Cardona et al. 1996) showed that workplace acetone concentrations had a statistical correlation with the ratio of urinary -hexane metabolites to /i-hcxanc air concentration, although it did not correlate with measured urinary metabolites. No animal studies are available describing the effects of inhalation co-exposure to acetone and -hexane, although there are several studies which report interactions between acetone and the neurotoxic metabolite of -hexane 2,5-hexanedione (See Section 2.4, Mechanisms of Action). Oral administration of acetone has been reported to potentiate the neurotoxicity caused by oral exposure to the neurotoxic u-hexane metabolite 2,5-hexanedione in rats (Ladefoged et al. 1989, 1994). Oral exposure to acetone alone in rats at 650 mg/kg/day resulted in a statistically significant decrease in motor nerve conduction velocity after 6 weeks co-exposure to acetone and 2,5-hexanedione resulted in greater effects... 

In a study where both peripheral and central nervous system effects were measured in rats co-exposed to u-hexane and toluene (Pryor and Rebert 1992), toluene exposure at 1,400 ppm for 14 hours a day for 9 weeks prevented the peripheral neurotoxicity (decreased grip strength and nerve conduction velocities) caused by exposure to 4,000 ppm 77-hcxanc alone. There was no reciprocal action of 77-hexane on the motor syndrome (shortened and widened gait and widened landing foot splay) and hearing loss caused by toluene. Brainstem auditory response amplitudes were decreased by 77-hcxanc, co-exposure to toluene did not block this effect. 

---