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In the lower part of the face, facial paralysis causes drooping and elongation of the lips, drooping of the ala of the nose, flattening of the nasolabial fold, and drooping of the corners of the mouth. The cheek is hollow and flaccid . The development of compensatory hyperactivity on the unaffected side deviates the tip of the nose and the philtrum. These deformities are exacerbated by facial expressions. Functionally, there may be difficulty eating, due to food accumulation in the gingivobuccal sulcus or cheek biting during chewing. In elderly individuals with loose skin, salivary incontinence is not uncommon. These abnormalities are more pronounced the longer the paralysis has been present.
At the orbitofrontal level, paralysis of the frontalis muscle leads to ptosis of the eyebrow, resulting in excess skin on the upper eyelid. The asymmetry of the forehead is accentuated by hypertonia of the frontalis muscle on the side opposite the paralysis.
Paralysis orbicularis oculi muscle leads to incomplete eyelid closure, elevation of the upper eyelid margin when the eyelids are open (the Müller's and levator palpebrae muscles – innervated by the third cranial nerve – no longer have antagonists), and relaxation of the lower eyelid, which becomes atonic. This results in lagophthalmos, exposing the eye to trauma . This risk of injury is greatest in the lower quadrant of the cornea and is exacerbated by the anesthesia of this small corneal area, whose sensitivity is dependent on the facial nerve. Keratitis will progress to scarring with permanent corneal opacity or to corneal perforation and blindness. Corneal lesions cause severe, debilitating pain that is resistant to minor analgesics and can become chronic. The spontaneous evolution of the hyperlax lower eyelid leads to ectropion (eversion of the eyelid) and epiphora (excessive tearing).
At the stage of post-sequelae facial paralysis , when all hope of recovery is abandoned, we propose a surgical strategy for the rehabilitation of the paralyzed face.
