Facial paralysis can be a consequence of traumatic facial nerve injury, iatrogenic causes, malignancy, congenital syndromes, and viral infections. Prolonged paralysis can result in ocular complications, articulation difficulties, impaired feeding, and difficulty in conveying emotion through expressive movement.
Numerous reanimation techniques are available to restore function and are based on the cause of the facial paralysis, type of injury, its location, and the anticipated duration.
These methods are broadly classified into 4 types as follows: (1) neural methods, (2) musculofascial transpositions, (3) microneurovascular transfer (4) facial plastic procedures, and (5) prosthetics.
The most desirable procedures to reestablish the mimetic control of the face are based on a sequence of operations. The surgeon chooses the procedure that has the highest likelihood of achieving the best functional and cosmetic result.
Dynamic procedures for total unilateral facial paralysis are as follows:
Direct facial nerve anastomosis
Anastomosis to other motor nerves
Dynamic musculofascial transpositions
Dynamic free flap reconstruction
Static procedures for total unilateral facial paralysis are as follows:
Static musculofascial transpositions
Facial plastic procedures
Dynamic procedures aim to restore some voluntary movement and, thus, are more desirable. Free flap reanimation and static procedures are reserved for patients whose motor endplates are not viable, typically from congenital syndromes or after long-term denervation. Combinations of the above procedures may be appropriate depending on the circumstances.
An image depicting the facial nerve can be seen below.
History of the Procedure
Attempts to correct facial paralysis date back to 200 AD, when Galen actually discussed the possibility of nerve regeneration. However, the first documented suture repair of a nerve is attributed to Paul of Argina in 600 AD. A. Waller, who recognized that peripheral nerves could regenerate, rediscovered this work in the 1850s.
With experience from World War II, H.J. Seddon is credited with introducing the use of cable grafts after it was noted that the primary repair would lead to unacceptable tension and poor results. With the introduction of magnification, including the operating microscope and loupes in peripheral nerve repair, results greatly improved. Evidence of this improvement was reflected in many other papers published after this time.
As early as the turn of the century, Alexer in Eden recognized the transposition of muscles in lieu of primary nerve anastomosis. Reuben, Baker, and Connelly repopularized this intervention in the late 1970s by using either the temporalis or masseter muscle.
Techniques for facial reanimation have a long and protracted history, but it was not until the modern era with the advent of finer sutures, magnification, and better understanding of physiology that results from reanimation techniques dramatically improved.
Total disruption of the facial nerve does not permit restoration to complete normalcy. Therefore, realistic expectations must be established at the initial encounter and candidly discussed between the physician and the patient.
Choice of reanimation procedure is dictated by the duration of paralysis and the status of the mimetic musculature’s motor endplates. Neural procedures are indicated if the duration of paralysis is less than 24 months and the electromyography (EMG) shows fibrillations, indicating denervation with intact motor endplates. If the motor endplates are not viable (electrical silence on EMG) or immediate restoration of some movement is desirable, muscle transposition techniques should be considered.
To perform the reanimation procedures, the surgeon must have a thorough knowledge of the anatomy of the facial nerve.
The facial nerve originates within the pons and exits between the olive and inferior cerebellar peduncle. At this location, the nerve forms a 12-14 mm intracranial portion within the cerebellopontine angle, as shown below.
The facial nerve then enters the temporal bone, where it is confined within a bony conduit. As it enters the internal meatus, the nerve lies in the anterior superior quadrant, traveling about 10 mm before reaching the lateral end of the meatus superior to the crista transversalis and anterior to the vertical crista (Bill's bar). Exiting the internal auditory canal, the nerve gradually curves anteriorly around the basal turn of the cochlea where it enters the infratemporal portion and travels 2-4 mm. This segment of the facial nerve courses through the narrowest portion of the fallopian canal, making it the most susceptible to damage from inflammatory conditions.
The geniculate ganglion is then formed by the union of the facial nerve and the nervus intermedius into a common trunk. The greater superficial petrosal nerve, the lesser petrosal nerve, and the external petrosal nerve all branch off of the geniculate ganglion while the facial nerve exits and takes a 40-80° turn, marking the first genu of the facial nerve.
The nerve then courses posteriorly and slightly inferiorly, traveling 11 mm across the tympanic cavity. This horizontal course lies superior to the oval window then makes its second genu as it leaves the oval window niche, passing anteriorly and caudal to the lateral semicircular canal. It then passes lateral to the sinus tympani and the stapedius muscle to form the vertical (mastoid) portion within the temporal bone.
At the end of this 13-mm segment, the facial nerve exits from the stylomastoid foramen, where it becomes the extracranial segment. The nerve first innervates the posterior belly of the digastric muscle and then travels 15-20 mm to enter the parotid gland. In the parotid gland, it divides at the pes anserinus into 2 main branches, namely, the temporofacial and cervicofacial. Terminal ramifications of these branches to the temporal, zygomatic, buccal, mandibular, and cervical regions are variable. Terminal branches of the facial nerve are depicted below.
Terminal branches of the facial nerve are depicted below.
The nerve fibers travel in groups called fascicles, which vary according to the level. The fibers are surrounded by 3 types of connective tissue: endoneurium, perineurium, and epineurium. The structure of the fascicles varies considerably throughout the course of the nerve. For this reason, direct repair of the fascicles is not feasible and may be counterproductive.
No contraindications exist for facial reanimation, unless a patient is not able to tolerate general anesthesia; however, specific guidelines must be followed. If the possibility of spontaneous facial nerve recovery exists, then any procedure that involves transsection of the nerve must be avoided until lack of recovery is certain.
Any attempt to restore facial function by reestablishing nerve continuity requires intact motor endplates. Nerve continuity can be re-established by direct facial nerve anastomosis, interpositional grafts, or anastomosis to other cranial nerves. Selection of these procedures cannot be considered up to 3 years following the original insult. The possibility still exists for motor endplates to survive from 1-3 years after the original insult. An EMG can be obtained to determine viability of the motor endplates.
Cross-over technique cannot be used if the donor nerve is essential to the overall function of the patient.