Organophosphates have been implicated in delayed neuropathy resulting several days after the initial exposure. The delayed neuropathy has been attributed to demyelination of axons and phosphorylation of esterase in neurons. However, acetylcholinesterase and paraoxon do not produce delayed neuropathy.
Carbon disulfide induces axonopathies by interfering with transport of chemicals along axons. The interference is achieved by linking filaments within axons via covalent bonds. Acrylamide is another neurotoxin that has been shown to cause axonopathies, beginning at the terminals of axons and proceeding proximally. There is controversy on the exact mode of action, but several studies support the idea that impaired transport along axons is involved. Organic lead has been confirmed to cause myelinopathies which are characterized by chronic exposures. The myelinopathies produced by organic lead mostly affect motor neurons rather than the sensory neurons. Hexachlorophene also induces myelinopathies by oxidative phosphorylation within neurons, affecting the myelin sheaths of the axons. The compound is rapidly absorbed by human skin, and it affects both the CNS and PNS. One of the most common effects of this neurotoxin is edema in the central nervous system and peripheral nervous system. Myelinopathies lead to altered conduction of impulses along nerves. The properties of the alteration produced may be decreased speed of action potential, blockage or irregular transmission. It has also been shown that axonopathies mostly affect long axons of the central nervous system and peripheral nervous system.
