A morphological study of the effect of glucocorticoid treatment on delayed organophosphorus neuropathy.
The delayed neuropathy caused by the organophosphate diisopropylfluorophosphate (DFP) can be minimized by a high dose glucocorticoid regimen started after exposure to DFP. In cats 21 days after an intraarterial injection (2 mg/kg) of DFP, morphologic alterations of neuromuscular junctions and myelinated intramuscular axons are evident. These alterations include the presence of extensive lamellar whorls in nerve axons and terminals, the disruption and retraction of nerve terminals from the synaptic cleft and a widening of secondary junctional folds with coincident dispersion of the basal lamina. The pathologic changes while more intense in the DFP-treated leg are also evident in the contralateral leg. Only 2% of motor nerve terminals from the soleus of DFP-treated legs were rated as normal in morphologic evaluations. In contrast 90% were rated normal in cats exposed to DFP and subsequently treated with one dose of methyl prednisolone (90 mg/kg, i.v.) and 7 doses (8 mg/kg, i.m.) of triamcinolone over a 20 day period. The mechanism whereby glucocorticoid therapy exerted this effect during the time interval studied remains unresolved. However, this observation may be important in the further definition of both the normal and diseased state.
D000818:Animals; D001369:Axons / Q000187:drug effects; D002415:Cats; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology*; D007531:Isoflurophate / Q000633:toxicity*; D008297:Male; D009410:Nerve Degeneration / Q000187:drug effects; D009469:Neuromuscular Junction / Q000166:cytology / Q000187:drug effects* / Q000473:pathology; D010523:Peripheral Nervous System Diseases / Q000139:chemically induced* / Q000517:prevention & control
D005938:Glucocorticoids; D007531:Isoflurophate