Facial nerve paralysis associated with psychosocial distress, poor self-image and interpersonal relationship impairment.
Functional concerns primarily involve adequate protection of the eye, with a risk of keratitis.
Swallowing, drooling, and speech difficulties may arise.
Repair of the facial nerve is reserved for permanent complete facial paralysis.
Facial paralysis has many causes, and the etiology determines the likelihood of spontaneous return of function, as in most cases of idiopathic facial paralysis.
The transected or severely damaged nerve requires repair in order to achieve return of function.
Weakness and synkinesis is a component of the healing process.
Repair of the facial nerve involves several choices of procedures including: direct repair, cable nerve grafting, and nerve crossover techniques.
The causes of facial paralysis divided into congenital, neoplastic, traumatic, inflammatory, and idiopathic.
Congenital facial paralysis is uncommon.
Traumatic injuries, which include blunt and penetrating trauma, iatrogenic injury during surgery are common causes of facial nerve palsy..
The site of injury to the facial nerve may be intracranial, intratemporal, or external to the stylomastoid foramen.
Neoplastic causes of facial paralysis commonly involve tumors of the parotid gland.
Facial nerve schwannomas, acoustic neuromas, and neoplasms of the brain are rare causes of facial paralysis.
Infectious agents implicated include herpes zoster (eg, Ramsey Hunt syndrome), mumps, Coxsackie virus, and mononucleosis.
Bacterial infections include sequelae of otitis media and Lyme disease.
Inflammatory conditions include sarcoidosis.
The facial nerve undergoes degeneration of the distal segment after injury.
Injuries to the nerve are classified by 5 degrees.
First-degree injury is ref2242ed to as neurapraxia, and is produced by increased intramural pressure, as occurs by external compression injury.
In first degree facial nerve injury the covering layers of the nerve, endoneurium, perineurium, and epineurium are not disrupted, and the nerve is capable of return of function without synkinesis.
Second-degree injury involves compression of the facial nerve, which is unrelieved, and results in degeneration of the nerve axons, but excellent return is expected, although recovery may take several months.
Second-degree injury is associated with compromised nerve stimulation.
Third degree injury involves the loss od endoneural function.
Fourth degree injury involves perineural dysfunction.
Fifth degree injury involves epineural injury.
Fourth- and fifth-degree injuries imply partial or complete transection of the nerve.
With more advanced degree injuries facial nerve regeneration is incomplete, and synkinesis occurs.
Transected nerves produce the best result when reapproximated due to an intact motor nerve supply from the facial motor nucleus in the pons to the muscle endpoint.
If the direct repair cannot be completed a cable graft may be inserted to produce a tensionless connection of the proximal nerve stump to the distal branch or branches.
If the proximal nerve stump is inadequate or inaccessible a nerve crossover technique can be utilized.
In most instances the sooner the facial nerve is repaired the better the long-term results, as nerve fibrosis, fibrosis of the motor endplate and muscle atrophy are prevented.