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Brian A. Francis, James D. Weiland, Nicholas A. Sachs, Eli L. Chang; Benzalkonium Chloride–Induced Denervation of Orbicularis Oculi Muscle in Rabbits. Invest. Ophthalmol. Vis. Sci. 2013;54(3):1868-1872. doi: 10.1167/iovs.12-10792.
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To examine the potential for benzalkonium chloride (BAK) to cause denervation of the orbicularis oculi muscle (OOM) in a rabbit model.
Pigmented rabbits were separated into five groups consisting of five rabbits each. Group 1 was injected with 1 mL of BAK 0.25% in the OOM of the upper eyelid. Group 2 was injected with 1 mL of BAK 0.5%. Group 3 included untreated controls. Groups 4 and 5 underwent surgical severing of the facial nerve (to cause complete paralysis of the OOM). Strength-duration curves for electrical stimulation of muscle twitches were measured for each group and chronaxie values were calculated to determine innervation status. Groups 1 and 4 were stimulated at 1 week postintervention while groups 2 and 5 were stimulated at 4 weeks postintervention. The rabbits were then sacrificed and the eyelids sent for histological analysis.
In group 1, all five rabbits demonstrated denervation of the OOM in the injected area. In group 2, one rabbit developed an abscess at the injection site and was sacrificed at 1 week. Of the remaining four rabbits, two showed complete denervation and two showed denervation with evidence of partial reinnervation. The histology demonstrated marked atrophy of the OOM for BAK-treated rabbits when compared with controls. In group 3, all five rabbits showed normal OOM function. In groups 4 and 5, all rabbits showed denervation of the OOM and histological evidence of muscle atrophy similar to groups 1 and 2.
BAK causes denervation when injected into the OOM in rabbits. The clinical relevance of this finding may be the onset of lagophthalmos and eyelid retraction in patients with chronic BAK exposure.
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