Lead neuropathy.
The still unexplained nature of the neurotropic action of lead has prompted this chronological survey of the course of development of the medical attitude towards the problems of lead neuropathy all along the centuries--from ancient times up to the present. Once a conspicuous, severe, and even frequent clinical type of plumbism, peripheral lead neuropathy has received due attention in the early classics (Tanquerel des Plances, Duchenne, Aran, Remak, Romberg, Erb, etc.) and of the pioneers in industrial medicine (Legge, Aub, Teleky, Hamilton). Even the modern era, however, has not come further than to state that lead produces different neurological effects in different animal species and even in humans--different patterns of neuromuscular involvement. With the advent of electrophysiology, conflicting and inconsistent findings have also appeared, particularly in regard to overt and latent lead neuropathies. Theories regarding the mode and site of the neurotoxic action of lead are reviewed and data which might be used as arguments both in favor and against are presented.
D000622:Aminolevulinic Acid / Q000378:metabolism; D000818:Animals; D004576:Electromyography; D004594:Electrophysiology; D006801:Humans; D007854:Lead / Q000097:blood; D007855:Lead Poisoning / Q000473:pathology / Q000503:physiopathology*; D009046:Motor Neurons / Q000502:physiology; D009431:Neural Conduction / Q000187:drug effects; D009787:Occupational Medicine; D010525:Peripheral Nerves / Q000503:physiopathology; D010523:Peripheral Nervous System Diseases / Q000139:chemically induced* / Q000473:pathology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D007854:Lead; D005680:gamma-Aminobutyric Acid; D000622:Aminolevulinic Acid