The effects of acrylamide intoxication were studied both in peripheral (PNS) and central (CNS) nervous system of rats. The animals were sacrified at different time intervals from the beginning of the intoxication. Histological and ultrastructural studies of peripheral nerves and long tracts of the spinal cord revealed a severe axonopathy, characterized by swelling of axons, particularly in the paranodal regions due to accumulation of neurofilaments with almost complete disappearance of neurotubules. There was also aggregation of dense bodies, swollen mitochondria and multivescicolar bodies in subaxolemmal regions. Presynaptic endings in the anterior horns of the spinal cord and in the cuneate nuclei were swollen and filled with packed filaments. Fiber degeneration at different stages was seen both in PNS and in CNS. These changes are not specific for acrylamide intoxication, having been observed in other experimentally induced neuropathies (n-hexane, Mn-BK, CS2, ...), as well as in a variety of diseases both genetically determined and due to exposure to toxic substances (glue-sniffing, leather cement poisoning, antiblastic therapy, ...). Accumulation of filaments in peripheral and central axons is the pattern of fiber degeneration characterizing the dying-back neuropathies. These axonal changes are particularly marked in the pacinian bodies as well as in the distal segments of the fibres. These data support the hypothesis that a dying-back neuropathy might depend on the direct effect of the toxic substance on the most vulnerable segments of the fibres, rather than on the perikaryon of the nerve cell, as previously supposed.