Nerve induced myopathy

Emetine emetine is still used at high doses for the treatment of patients with severe amebiasis. Muscle damage is uncommon but when it does occur can be a severe generalized necrotizing myopathy. The outcome is, at times, fatal, especially when an emetine-induced cardiomyopathy is also present. Despite the suggestion that there may be neuritic changes, there is no evidence that emetine damages peripheral nerve. The myopathy is usually painful but reversible. The mechanism of action of emetine is unknown. 

Sripathi N, Wortmann RL, Phillips PS (2006) Genetic risk factors associated with lipidlowering drug-induced myopathies. Muscle Nerve 34 153-162... 

Isackson PJ, Ochs-Balcom HM, Ma C, Harley JB, Peltier W, Tamopolsky M, Sripathi N, Wortmann RL, Simmons Z, Wilson JD, Smith SA, Barboi A, Fine E, Baer A, Baker S, Kaufman K, Cobb B, Kilpatrick JR, Vladutiu GD (2011) Association of common variants in the human eyes shut ortholog (EYS) with statin-induced myopathy evidence for additional functions of EYS. Muscle Nerve 44(4) 531-538... 

Previous studies have demonstrated that the noncompetitive NMDA receptor antagoni.si memantine (MEM) provided protection against OP- or CM-induced myopathy by multiple mechanisms. In brief, these mcchanifsms include blockage of nAChR-ion channel complex (Masuo et al., 1986), prevention of neural hyperexcitability (McLean el ai, 1992), reduction of high-frequency repetitive activation of peripheral nerves (Wesemann and Ekenna, 1982). and reduced seizures induced by NMDA receptor blockage (Danysz el aL 1994 Carter, 1995 Parsons et ai, 1999). 

Weber M, Diener HC, Voit T, Neuen-Jacob E. Focal myopathy induced by chronic heroin injection is reversible. Muscle Nerve 2000 23(2) 274-7. 

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. 

Subsequent to the acute cholinergic manifestations of OP toxicity in humans, and approximately 24-96 hours after exposure, the onset of an "intermediate syndrome" which includes ocular effects has been recognised more recently for some OPs (Senanayake and Karalliedde, 1987 Karademir et aL, 1990). The associated clinical signs, which are characteristically different from those seen in OP-induced delayed pol)meuropathy, are paralysis and weakness of proximal limbs, respiratory, neck and cranial muscles, including those innervated by the oculomotor nerve. The occurrence of myopathy in rats exposed to diisopropylfluorophosphate, paraoxon or soman (Wecker et aL, 1978 Vanneste and Lison, 1993) resembled the features of the "intermediate syndrome". The severity and duration of the myopathy in rats appeared directly related to the degree of inhibition of AChE. 

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