| Abstrakt: |
Facial nerve paralysis can result from a number of causes, including neoplasms, Bell΄s palsy, infections, trauma, congenital conditions, and idiopathic processes. Both the medical and social consequences of facial nerve paralysis can be distressing for patients. The most significant ophthalmic consequence of facial nerve paralysis is loss of function of the orbicularis oculi muscle. The complete assessment of a patient with facial nerve paralysis includes clinical evaluation of the resting tone and active function of the facial muscles, as well as determination of the extent of dry eye and the function of the lacrimal gland and lacrimal drainage system. The goal of medical therapy is symptomatic relief of dry eye and exposure keratopathy. Botulinum toxin can also be employed to treat other symptoms, such as synkinesis, hypertonicity, and spasms. The goal of surgical therapy is improved protection of the cornea, as well as a more symmetric static and dynamic appearance. Lagophthalmos and exposure keratopathy can be addressed with procedures such as surgical closure of the eyelids, known as tarsorrhaphy, or other alternatives, such as placement of an alloplastic gold weight in the upper eyelid, injection of hyaluronic acid gel into the upper eyelid, or palpebral springs. Ectropion also commonly results from facial nerve paralysis and can be improved with lateral or medial canthal procedures. Reanimation of the midface can be accomplished by any of several surgical techniques; some provide static support for the midface, while others attempt to restore dynamic movement to the paralyzed face. [ABSTRACT FROM AUTHOR] |
