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One of the major complications of a peripheral facial nerve palsy (PFP) is the occurrence of corneal ulceration due to lagophthalmos—that is, incomplete closure of the affected eyelid. It is widely accepted that lagophthalmos after PFP is directly caused by paresis of the orbicularis oculi muscle (eyelid closure muscle). Yet, some of the signs and symptoms, which may be observed in patients with PFP cannot be explained by paresis of the orbicularis oculi muscle alone. First of all, gentle closure of the eyelid, as for example occurs when a person falls into sleep, is completely brought about by inhibition of the tonic activity of the levator palpebrae muscle (eyelid opener muscle).1 Secondly, upward and downward saccadic lid movements, accompanying saccadic eye movements, are mainly due to modification of the tonic activity of the levator palpebrae muscle. Finally, the downward and upward smooth pursuit movements of the lids are again secondary to alterations in the level of activity of the levator palpebrae muscle. If these above mentioned movements of the lids are not caused by the orbicularis oculi muscle activity, what is then the reason that patients with PFP are unable to perform these movements properly? Furthermore, gold implantation in the affected upper eyelid or injection of the botulinum toxin into the levator palpebrae muscle is helpful in closing the affected lid, while no modification of the orbicularis oculi activity occurs with these treatment modalities.
As the orbicularis oculi and the levator palpebrae muscles have a reciprocal antagonistic activity,1 we hypothesised that stiffness of the levator palpebrae is the cause of lagophthalmos. In a recent paper, we reported on the positive effect of stretch of the levator palpebrae muscle on lagophthalmos in a group of patients with PFP.2 In the video report we present two patients showing the effect of our intervention on lagophthalmos.
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