Dr. Pulley of the University of Florida, Jacksonville, received honorariums from Alexion, CSL Behring, and Grifols for consulting work.)
Dr. Weimer of Columbia University has received consulting fees from Roche.)
The authors discuss the clinical manifestations of acrylamide neuropathy. This toxic neuropathy has served as a model for studying the effects of toxins on the nervous system. Recently, new information has emerged regarding the potential mechanism of the neuropathy. This may completely change the approach to research of toxic neuropathies.
• Acrylamide causes a central-peripheral distal axonopathy.
• The neuropathy in animals is predictable and has been used as a model for other forms of central peripheral distal axonopathy.
• As with many toxic neuropathies, the manifestations are dose dependent, and the prognosis is dependent on the degree of central axonal degeneration.
Historical note and terminology
The neurotoxic effects of acrylamide have been known for over 50 years (Kuperman 1958; Fujita et al 1960). Acrylamide is used in grouting agents for soil and sealing applications (Kjuus et al 2004), and polyacrylamide is used in flocculating wastewater treatment plants (Feldman 1999). The monomer is the toxic form, whereas the polymer is innocuous. However, the polymer may be contaminated by up to 2% monomer and can, thus, be a source of toxicity. Acrylamide is readily absorbed by inhalation, ingestion, or dermal contact. Acrylamide neuropathy has been a popular experimental animal model for studying the processes of axonal transport (Miller and Spencer 1984; Gold et al 1985), dying-back neuropathy (Schaumburg et al 1974), and axonal swelling. More recently, studies have raised doubts about the basic underlying mechanism of acrylamide neuropathy (LoPachin and Gavin 2015).
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