OBJECTIVES: Rodenticide Vacor causes a severe peripheral neuropathy in humans. Electrophysiologic studies on a peripheral motor nerve-skeletal system of Vacor-treated rat showed decreased amplitude of muscle action potential without conduction velocity abnormalities. The ultrastructural studies of the neuromuscular junction were performed to clarify the anatomic site of the Vacor-induced peripheral neuropathy in male Wistar rats. METHODS: After oral administration of a single dose of Vacor, 80 mg/kg of body weight, to the experimental animals, neuromuscular junctions within the interosseous muscles of the hind foot were observed in time. RESULTS: No axon terminal change was noted until 24 hours after the administration of Vacor. Remarkable loss of presynaptic vesicles and swollen endoplasmic reticulum in the axon terminal were developed at 3 days after Vacor treatment. Progressive degenerative changes consisting of marked loss of presynaptic vesicles, focal disruption of membrane in the axon terminal with disappearance of the number of the damaged axon terminal appeared, and flattening of postsynaptic folds was also seen. CONCLUSIONS: These results suggest that degenerative changes in axon terminal at neuromuscular junction may contribute to the peripheral neuropathy developed in the early phase of Vacor poisoning.
Animal ; Diabetic Neuropathies/physiopathology ; Diabetic Neuropathies/pathology* ; Diabetic Neuropathies/chemically induced* ; Human ; Male ; Microscopy, Electron ; Neuromuscular Junction/ultrastructure ; Neuromuscular Junction/physiopathology ; Neuromuscular Junction/drug effects ; Peripheral Nervous System Diseases/physiopathology ; Peripheral Nervous System Diseases/pathology ; Peripheral Nervous System Diseases/chemically induced ; Phenylurea Compounds/toxicity* ; Rats ; Rats, Wistar ; Rodenticides/toxicity*

Compound nerve action potential (CNAP) of the mixed peripheral nerve is composed of A alpha beta, A delta, and C potentials. All components of CNAPs in the sciatic nerve were recorded by stimulating the tibial nerve of both control and lead-poisoned rats. Marked decrease of nerve conduction velocity and prolonged duration were found in A alpha beta and A delta fibers especially in large myelinated A alpha beta fibers. The amplitude decreased in A alpha beta potential, but the area did not change. In C potential produced by activation of unmyelinated fibers, nerve conduction velocity slightly decreased, but the amplitude and area did not significantly change. Pathologic correlates revealed prominent segmental demyelination with significant decrease of large myelinated fiber densities. Minimal axonal degeneration of unmyelinated fibers was present. We can conclude that electrophysiologic changes in the lead-poisoned rats correlate with pathologic changes in them.
Animals ; Electrochemistry ; Lead Poisoning/complications/*pathology ; Neural Conduction ; Peripheral Nervous System Diseases/chemically induced/*pathology ; Rats ; Rats, Inbred Strains ; Sciatic Nerve/pathology

OBJECTIVETo study the nerve electromyogram results by analysing the pathological characters of 4 cases diagnosed as peripheral neuropathy caused by n-hexane and arsenic.

METHODSThe nerve electromyogram examination and pathology data of 4 patients, who had been diagnosed as toxic chemicals peripheral neuropathy, were studied retrospectively.

RESULTSTwo patients in this group were exposed to n-hexane, their nerve electromyogram examinations and biopsy pathology of superficial peroneal nerve indicated the peripheral neuropathy was mainly manifests the lesion of medullary sheath. Another two patients were exposed to arsenic, their nerve electromyogram examinations showed axonal degeneration associated with demyelination, and their biopsy pathology showed the peripheral neuropathy was mainly axonal degeneration.

CONCLUSIONAxonal degeneration and demyelination always coexist in peripheral neuropathy caused by chemicals.

Arsenic Poisoning ; pathology ; physiopathology ; Female ; Hexanes ; poisoning ; Humans ; Male ; Middle Aged ; Peripheral Nervous System Diseases ; chemically induced ; pathology ; physiopathology ; Retrospective Studies ; Young Adult