Hexacarbon neurotoxicity.
The neurotoxicity of hexacarbon solvents has become apparent only recently, but an extensive literature has already developed as a result of the clinical and epidemiological implications of the human disease, and the advantages of small animal models of hexacarbon neurotoxicity in investigation of experimental neuropathies. This review selectively summarizes the literature, focusing on clinical manifestations and pathological alterations in the peripheral nerves. The clinical manifestations are dominated by a distal, symmetrical, sensorimotor polyneuropathy. Pathological changes include distal axonal degeneration and formation of neurofilament-filled axonal swellings in early or moderately severe exposure. A late manifestation in severely affected experimental animals is recurrent demyelination and remyelination.
D000293:Adolescent; D000818:Animals; D001369:Axons / Q000187:drug effects / Q000473:pathology; D001519:Behavior / Q000187:drug effects; D004781:Environmental Exposure; D006168:Guinea Pigs; D006586:Hexanes / Q000378:metabolism / Q000633:toxicity*; D006801:Humans; D007659:Ketones / Q000633:toxicity*; D008297:Male; D008742:Methyl n-Butyl Ketone / Q000378:metabolism / Q000633:toxicity*; D009410:Nerve Degeneration / Q000187:drug effects; D009413:Nerve Fibers, Myelinated / Q000187:drug effects; D009420:Nervous System / Q000187:drug effects*; D010523:Peripheral Nervous System Diseases / Q000139:chemically induced; D051381:Rats
D006586:Hexanes; D007659:Ketones; D008742:Methyl n-Butyl Ketone