Ultrastructure of carbon disulphie neuropathy.

Adult Wistar rats were exposed to carbon disulphide (CS2) vapour at a concentration of 2.4 mg/l of air for 5 days a week (6 h a day), and the ultrastructure of peripheral nerves, neuromuscular junctions and muscles was investigated after 6 months of exposure to CS2. Numerous giant axons, i.e. paranodal or internodal swellings, were seen in the peripheral nerves. At the swollen paranodes, the myelin sheath was thinned, in other regions large intramyelinic vacuoles indicative of more dramatic demyelination were observed at axonal enlargements. Axonal enlargements consisted essentially of whorls of tightly packed neurofilaments. A number of nerve fibres underwent complete degeneration, but at the same time there was evidence of nerve regeneration. Nerve terminals were affected in a similar way following CS2 exposure. At neuromuscular junctions, filamentous swellings of nerve terminals preceded their degeneration and eventual denudation of synaptic gutters. As a rule, the postsynaptic part of neuromuscular junctions remained unimpaired by CS2 treatment. Muscles were affected by both atrophy and degeneration. Clusters of dense and lamellar bodies and numerous autophagosomes indicative of direct myotoxic effect of CS2 were frequently encountered in the investigated muscles. Some muscle fibres apparently underwent necrosis judging from the occurrence of myotubes characteristic of muscle degeneration and regeneration. The pathomorphology of CS2 neuropathy resembles that of other toxic neuropathies which presumably have a common origin in impaired energy metabolism.