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Pediatric myasthenia gravis exacerbation associated with permethrin cream

We describe an unusual and previously uncharacterized presentation of medication-induced worsening of pediatric myasthenia gravis (MG). A 7-year-old girl who had a history of ocular myasthenia gravis (OMG) diagnosed at age 4 following 1 month of right eye ptosis, underwent neurologic evaluation. A diagnosis of OMG at age 4 was made when she was found to have an acetylcholine receptor antibody (ARCA) titer of 0.51 (nl< 0.24). She had no response to pyridostigmine 30 mg 4 times daily, and it was subsequently discontinued. She was started on prednisolone 2 mg/kg and achieved complete clinical resolution within a month. Over the next 2 years, prednisolone was tapered to 5 mg daily, and azathioprine 1.5 mg/kg was added, with excellent control except for an episode during an upper respiratory infection. Her right ptosis redeveloped and became constant for weeks. It resolved a few days after infusion of 1 g/kg of intravenous immunoglobulin (IVIG). The OMG was stable until the patient contracted head lice at age 7 and was given permethrin shampoo. The next day, her mother noticed severe right eye ptosis. The ptosis worsened over the next 3 days. Physical exam was only significant for profound right eyelid ptosis; extraocular movements were intact, and proximal strength was normal, even on sustained activation. There was no dysphagia, dysarthria, or dyspnea. As her symptoms had not improved spontaneously after 4 days, she was given IVIG 1 g/kg. Within a week, the right eyelid ptosis had resolved, and she continued using azathioprine and prednisolone. Permethrin is an anti-parasitic agent that is used to treat head lice and scabies infestations. It works by inhibiting Na influx through nerve cell membranes, resulting in delayed repolarization. It acts on the cell membranes of parasites, causing paralysis and death. It is known to have very poor skin penetration in humans, and there have been limited reports of mammalian toxicity caused by permethrin use alone. One percent of military personnel serving in Desert Storm who were exposed to pyridostigmine bromide, DEET, and permethrin complained of various neurologic symptoms, without known etiology. However, any neurologic dysfunction may be due to concurrent exposure to all 3 toxins, which reduces the breakdown of each. Permethrin by itself has not been shown to cause toxicity in humans. From the history and course of treatment of this patient, it seems very likely that permethrin caused an exacerbation of the right eyelid ptosis. We hypothesize that its ability to block sodium influx channels extended to the muscle membrane, which led to the prevention of depolarization by means of sodium channels and release of Ca from the sarcoplasmic reticulum, resulting in exacerbation of her OMG. It is unusual that our patient’s symptoms persisted for over a week. This may be partly explained by the fact that permethrin, once absorbed, resides in fatty tissue, sometimes with half-lives of 4–5 days in brain and fatty tissue. Alternatively, there could have been focal infiltration of the permethrin that affected only the levator palpebrae muscle. As there were no other new exposures or precipitating illness, it is most likely that permethrin was the factor in the MG exacerbation. Furthermore, there may not have been prompt recovery after removal of the drug, because she apparently required more aggressive treatment with IVIG for MG exacerbations, as in her previous episode of ptosis after infection. Her symptoms only improved following IVIG administration in both instances. There have been no reports of permethrininduced OMG exacerbation. Drug-induced MG exacerbations have been widely studied and reported. The proposed mechanism for many of these drugs is their interference with neuromuscular transmission. We report here the effect of a common lice treatment that worsens MG symptoms and should be added to the list of medications that may exacerbate MG.