Neurophysiological aspects of the toxicity of organic solvents

Abstract

Symptoms after long-term exposure to organic solvents are nonspecific, and for both medical and insurance purposes objective demonstration of toxic damage would be desirable at the earliest possible stage of beginning disease. Axonopathy does not dramatically decrease nerve conduction velocities; however, epidemiologic studies may reveal slower conduction velocities, especially in the distal nerve segments, among workers exposed to organic solvents. Among patients with solvent poisoning abnormally slow nerve conduction velocities are detected. Electromyography reveals denervation activity in early axonopathy; loss of motor units is detectable at a later stage. Hexacarbons, eg, n-hexane, have caused changes in visual evoked potentials, namely, prolonged latencies and decreased amplitudes, probably due to axonal lesions within the central nervous system. Electroencephalography (EEG) has been applied in studies of individual patients or patient groups and in epidemiologic approaches. Among patients actual abnormalities, mainly diffuse or local slow wave abnormalities, are frequent. In epidemiologic studies the frequency of abnormal EEG findings is related to overall exposure levels in the studied populations.