Facial paralysis can be a debilitating condition from psychological, aesthetic, and functional points of view. Those affected by such pathology suddenly see the disfigurement of their face and often lose self-confidence in their social life. The tissues of the face on the affected side (bilateral cases are rare, and primarily congenital, as in Moebius Syndrome), no longer supported by the underlying mimetic muscles, tend to collapse as if there had rapid aging on only one side of the face. This is less evident in children because of the elasticity of their skin, but is evident in adults and the elderly. The tissues of the forehead, eyebrow, cheek, lips, and submandibular region literally fall downwards (ptosis). Spontaneous closure of the eyelids and, moreover, blinking (constant involuntary eyelid closure), essential to lubricate the eyes, are lost. Nasal breathing from the side of the lesion is hampered by collapse of the nostril, no longer dilated by the lateral nasal muscles. The tone-free cheek is often unintentionally chewed and interferes with appropriate voice function. Sometimes, food, particularly liquids, is not retained completely due to incomplete lip closure.
The most evident feature of this pathology is the inability to smile, because activation of the mimetic muscles on the healthy side increases the deformity of the face, and patients often prefer to hide this with a hand.
The treatment of this disease is extremely specialised and, to achieve optimal results, in depth knowledge of the pathology is essential, as is mastery of the most sophisticated techniques by the microsurgeon, to offer a patients the most up-to-date and customised, designed solution.
THERAPY
For simplicity, treatments can be divided into non-surgical, early surgical, and late surgical.
Medical treatment, surgical or not, is reserved for situations where the nerve has the potential to recover its function spontaneously, as in cases of Bell’s palsy or post surgery, in which the continuity of the facial nerve was preserved. The therapy is based on the administration of corticosteroids, antiviral drugs (in cases of Bell’s palsy), neurotrophic vitamins, and/or mild electrical stimulation. During the entire process of nerve function recovery, the patient should be monitored closely by the physician, and repeated serial electromyography examinations should be performed.
Eyelid incompetence may cause corneal lesions. To avoid this, the patient must use artificial tears and highly protective glasses. It may also be necessary to perform a temporary tarsorrhaphy (eyelid closure in anticipation of nerve functional recovery) or to temporarily apply a small weight to the upper lid. These procedures are temporary because long-term remedies must be much more refined.
If at the end of the phase of spontaneous nerve recovery, facial spasms and/or synkinesis (involuntary movements of the face related to aberrant nerve regeneration) occur, the use of botulinum toxin, selective neurectomies, and other means can improve the clinical picture.
After major surgery for facial reanimation has taken place, minor remaining defects may be addressed under local anaesthesia. These most frequently include reducing eyebrow drooping, enlarging the eyelid, and addressing slight ptosis in the upper lip.
Early surgery is carried out by directly microsuturing the facial nerve severed during parotid or skull base operations, or because of other trauma. If a tract of the facial nerve is missing and the two stumps of the facial nerve do not come into contact with each other, a less important nerve, such as the suralis, may be used as a graft to bridge them.
When direct repair of the facial nerve is not feasible, usually after brain or skull base operations, a new motor source is required. The hypoglossus nerve, responsible for lingual motility, has long been the nerve used for this purpose (hypoglossus-facial anastomosis), but the side effects are considered too serious because of consequent deficits in the motility of the tongue, swallowing, speech, and chewing. It is surely preferable to perform an anastomosis with the masseteric nerve, which leads to similarly positive results but carries almost no negative consequence for the patient.
Late surgical treatment is so called because it is executed beyond 18-24 months from the onset of palsy, when the mimic muscles have atrophied irreversibly. In such cases, it is futile to provide new neural input to the facial nerve using a donor nerve, like the masseteric. The better choice consists of transferring, microsurgically, into the face segments of healthy muscles taken from other sites in the body (typically, the latissimus dorsi and gracilis muscles). The neural stimulus is provided by a neural connection with the healthy facial nerve of the opposite side of the face (not paralysed), rather than the masseteric nerve or the deep temporalis.
For eyelid reanimation, a small temporalis muscle flap is rotated or the thin platysma muscle is transposed after harvesting from the neck.