Myopathy, organophosphate-induced

Karalliedde, L., Baker, D., Marrs, T.C. (2006). Organophosphate-induced intermediate syndrome aetiology and relationships with myopathy. Toxicol. Rev. 25 1-14. 

Gupta, R.C., Dettbam, W-D. (1992). Potential of memantine, d-tubocurarine and atropine in preventing acute toxic myopathy induced by organophosphate nerve agents soman, sarin, tabun and VX. NeuroToxicology 13 500-14. 

Treatment was mainly symptomatic. Atropine did not seem to influence the course of IMS. No definite mechanism of IMS was identified, but the authors wondered whether the necrotizing myopathy induced by acute organophosphate poisoning in patients (De Rcuck and Willems, 1975 Weeker et ai. 1986 Tattersall, 1990) and in experimental animals (Ariens el al., 1%9 Dettbarn, 1984 Inns et al, 1990 Dc Bleecker et al., 1991, 1992b, 1998) might underlie the. selective muscle weakness. 

A myopathy has been described post mortem in cases of human poisoning with organophosphates inter alia with parathion and also noted in experimental animals with soman, paraoxon and sarin " and it has been suggested that there might be a connection between this myopathy and IMS (see section 10.3.1.2). The myopathy appears to be initiated by calcium accumulation in the region of the motor endplate as a result of OP-induced acetylcholine accumulation. Karalliedde et al concluded that IMS was probably caused by down-regulation of cholinergic receptors and that there was no direct relationship of IMS and the myopathy. 

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