Key points
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Optimal facial rehabilitation must address each affected zone of the face: lower lip, oral commissure, midface, ocular region, and brow.
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Since its introduction, the gracilis free muscle flap has revolutionized facial reanimation by achieving the critical goals of restoring spontaneous facial motion and functionality to the paralyzed face.
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Reconstruction after radical parotidectomy involves both facial nerve reconstruction and volume restoration of the surgical defect commonly with free tissue transfer.
Introduction
Facial nerve paralysis is a debilitating condition that affects an estimated 20 to 30 per 100,000 people per year. The facial nerve is responsible for the innervation and control of the muscles of facial expression, or the facial mimetic muscles. With loss of this function, there is a pathologic relaxation and droop of the eyebrow, eyelid, cheek, and corner of the mouth. Speech, oral competence, vision, and expression of emotion may be compromised, with significant effects on the overall quality of life of affected patients. The psychological and social implications of this disorder cannot be understated, because facial expressions play a pivotal role in interpersonal communications. Facial paralysis can encumber this critical function, giving rise to feelings of social isolation and depression in affected individuals.
A facial paralysis is referred to as acute paralysis within the first year of onset and chronic paralysis thereafter. Pathologic conditions that target structures along the course of the facial nerve such as brainstem masses, temporal bone trauma, parotid neoplasms, or traumatic injury to the face may impair the function the facial nerve, resulting in facial paralysis. Given its divergent origins, the variety of settings on which it may first be diagnosed, and its wide-ranging effects on the affected individual, facial nerve paralysis is best managed through a multispecialty, team-oriented approach. The goal of the current review is to provide a contemporary summary of the surgical management of facial nerve paralysis, procedures that are collectively referred to as facial reanimation.
Introduction
Facial nerve paralysis is a debilitating condition that affects an estimated 20 to 30 per 100,000 people per year. The facial nerve is responsible for the innervation and control of the muscles of facial expression, or the facial mimetic muscles. With loss of this function, there is a pathologic relaxation and droop of the eyebrow, eyelid, cheek, and corner of the mouth. Speech, oral competence, vision, and expression of emotion may be compromised, with significant effects on the overall quality of life of affected patients. The psychological and social implications of this disorder cannot be understated, because facial expressions play a pivotal role in interpersonal communications. Facial paralysis can encumber this critical function, giving rise to feelings of social isolation and depression in affected individuals.
A facial paralysis is referred to as acute paralysis within the first year of onset and chronic paralysis thereafter. Pathologic conditions that target structures along the course of the facial nerve such as brainstem masses, temporal bone trauma, parotid neoplasms, or traumatic injury to the face may impair the function the facial nerve, resulting in facial paralysis. Given its divergent origins, the variety of settings on which it may first be diagnosed, and its wide-ranging effects on the affected individual, facial nerve paralysis is best managed through a multispecialty, team-oriented approach. The goal of the current review is to provide a contemporary summary of the surgical management of facial nerve paralysis, procedures that are collectively referred to as facial reanimation.
Surgical management
The facial nerve has a long, circuitous course, traveling from the brainstem through the temporal bone to eventually emerge via the stylomastoid foramen. The nerve then enters into the parotid gland and divides into 5 major branches: temporal, zygomatic, buccal, marginal mandibular, and cervical. Facial nerve paralysis may affect some or all branches of the facial nerve. The facial nerve innervates the facial musculature in a zonal pattern, and as such, the specific disabilities suffered are contingent on the affected facial subunits. Historically, the goals of facial reanimation were simply to provide eye closure for corneal protection and oral competence to prevent drooling. However, advances in facial reanimation techniques have made it possible to achieve these basic goals as well as to attain facial symmetry both at rest and with movement. To this end, attempts at optimal facial reanimation must address each affected zone of the face: lower lip, oral commissure, midface, ocular region, and brow. Furthermore, defects following radical parotidectomy offer unique challenges for the reconstructive surgeon.
Lower Face and Midface
The facial musculature acts to provide oral competence, express emotion through smiling, and augment nasal breathing by flaring of the nostrils. With loss of this function, patients may suffer from drooling, nasal airway obstruction, esthetic deformity, and emotional distress. Surgical interventions are therefore targeted at restoring or replicating the native function of the facial musculature.
Static reconstruction
Generally, facial paralysis reconstructive techniques may be classified as static or dynamic. Static reconstruction techniques have historically acted as the workhorse of facial reanimation by repositioning the pathologically relaxed soft tissues of the face to counteract the effects of gravity (ie, facial droop) and provide symmetry at rest. In addition, static reconstruction can restore oral competence as well as improve external nasal valve collapse. Static reconstruction of the lower face can be accomplished with the use of “sling” suspension techniques. Using a facelift approach, a skin flap is elevated in the subcutaneous plane medial to the oral commissure and nasolabial fold, exposing the muscle fibers of the orbicularis oris if present. A “static sling” is then sutured medially to the oral commissure, lower lip, and nasolabial fold. The lateral aspect of the sling is then secured to the temporalis fascia or the zygomatic arch, to provide appropriate elevation of the soft tissue and symmetry at rest ( Fig. 1 ).
Expanded polytetrafluoroethylene (ePTFE; Gore-Tex, W.L. Gore & Associates, Flagstaff, AZ) is a common synthetic material that has been used for static facial reanimation of the lower face. However, concerns have been raised regarding the high rate of complications, including loss of tensile strength with time, graft infection, and need for revision surgery. Alternatively, freeze-dried acellular human dermis (AlloDerm, Lifecell Corporation, The Woodlands, TX) and porcine dermis (Surgisis, Cook Surgical, Cook Biotech, Inc, West Lafayette, IN) are other commercially available options that may be used. Like ePTFE, use of acellular dermis spares the patient donor site morbidity; however, acellular dermis slings give less oral commissure support compared with ePTFE or autologous tensor fascia lata. Tensor fascia lata is the most common autologous material used for static suspension. Autogenous tissue carries the advantage of providing superb tensile strength while having no immunologic response but does have increased morbidity from a second surgical site.
Dynamic reanimation
Although static reanimation as a stand-alone procedure can improve facial symmetry at rest, it does fall short of the key goals of restoring voluntary facial movement and symmetric facial expressions. To this end, dynamic reanimation techniques have been developed with the goal of re-establishing voluntary facial movements. Dynamic reanimation techniques may be further divided into those that produce either volitional or spontaneous facial movement. With volitional movement, patients must be actively conscious of their attempts to move their face, as the patterns of innervation of facial musculature are different than that of the native face. As such, significant muscular retraining must take place for the patient to obtain optimal results. By contrast, with techniques that restore spontaneous facial movement, the patient needs only to attempt facial expressions as he or she normally would before onset of their facial paralysis.
Volitional reanimation
Dynamic facial reanimation techniques that reproduce volitional movement include cranial nerve substitution techniques and local muscle transfer. Importantly, cranial nerve substitution techniques may only be performed when the distal portion of the facial nerve is intact and facial musculature has not atrophied, thereby having the ability to reinnervate. This situation may arise when there is proximal injury to the facial nerve, as in the case of intracranial facial nerve injury during the extirpation of cerebellopontine tumors, or intratemporal facial nerve injury as a result of trauma or mastoid surgery.
The most well-described cranial nerve substitution technique is the hypoglossal-facial nerve transfer (XII-VII transfer). The XII-VII transfer ( Fig. 2 A–D) involves using the hypoglossal nerve, which controls the movement of the tongue, to reinnervate the distal facial nerve. The hypoglossal nerve may be split in half in a linear fashion, and the superior nerve bundle is then coapted to the recipient distal facial nerve stump ( Fig. 2 B). A split hypoglossal graft is preferred to sacrificing the entire hypoglossal nerve, because the latter may produce significant hemitongue atrophy and difficulty with speech articulation and swallowing. Alternatively, a “jump” graft may be performed in which the hypoglossal nerve is partially incised, and a donor nerve (typically the sural or greater auricular nerve) is interpositioned between the hypoglossal and the facial nerve ( Fig. 2 C).
Alternative donor nerves have also been suggested as candidates for nerve substitution procedures, with the masseteric branch of the trigeminal nerve showing particular promise ( Fig. 3 A, B ). Use of masseteric-facial transfer for reanimation is particularly advantageous because it provides robust neurotization of the facial nerve with minimal donor site morbidity. Most importantly, the masseteric nerve has demonstrated the ability to produce the most natural excursion of the oral commissure with smiling, providing an indispensible alternative to the hypoglossal-facial transfer ( Fig. 3 C, D).
Regardless of which technique is used, the nerve substitution procedures all aim to facilitate neurotization of the distal facial nerve. Grafting to the facial nerve, however, may be impossible in a variety of scenarios. These scenarios include situations in which sufficient time has passed since onset of the facial nerve injury that the facial muscle motor end plates have undergone fibrosis, or when a distal segment of the facial nerve was sacrificed for oncologic purposes. For these patients, muscle transfer (either local muscle flaps or microvascular free muscle flaps) provides an additional option for reanimation.
The temporalis muscle transfer is one technique that can restore volitional facial movement ( Fig. 4 A ). In this procedure, the central one-third of the temporalis muscle is elevated off the temporal fossa, transposed over the zygomatic arch, and sutured to the orbicular oris at the oral commissure. This procedure elevates the lower lip and provides volitional lateral and superior excursion of the corner of the mouth. Thus, by biting down and activating the temporalis muscle, the patient is able to mimic the action of the muscles normally used to produce smiling. Although efficacious, the temporalis muscle transfer is accompanied by significant donor site morbidity, including esthetic deformity secondary to depression of the temple and fullness over the zygomatic arch ; this has been addressed by development of the temporalis tendon transfer. In this procedure, the temporalis tendon is detached from its insertion at the coronoid process and transferred in an orthodromic fashion to the oral commissure ( Fig. 4 B), providing similar volitional movement of the face without the temporal donor site ( Fig. 5 ).
