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The facial nerve is involved in ocular protection, articulation, oral continence and greatly affects the aesthetic appearance of the face. Impairment of this nerve is therefore associated with significant morbidity and social withdrawal. Despite significant advances in therapy, the multitude of problems associated with the paralyzed face can only be targeted with a broad spectrum of additional procedures. Common to all surgical techniques is the need for an exact anatomical knowledge.
Facial nerve anatomy
The facial nerve consists of a branchial motor component for voluntary motor control of the facial musculature and a visceral motor component for parasympathetic control of lacrimal, submandibular, and sublingual glands. Besides, there are two sensory components for the innervation of the external auditory canal and for the taste in the anterior two third of the tongue. The course of the facial nerve can be subdivided into three segments: intracranial, intratemporal, and extratemporal. In the intracranial segment, the upper group of neurons that innervate the frontalis muscle and the periauricular region receives bilateral cortical input. Neurons that innervate the remaining facial muscles receive contralateral cortical input exclusively. As a consequence, frontalis function is maintained in ipsilateral supranuclear lesions. The intratemporal segment can be further divided into three segments. In the labyrinthine segment, the greater petrosal nerve leaves the trunk to supply the lacrimal gland with parasympathetic fibers1.
In the mastoid segment, the thin stapedius nerve runs to the correspondent muscle. Parasympathetic branches innervate the submandibular, sublingual and anterior lingual glands, whereas the anterior two thirds of the tongue are supplied with gustatory fibres (chorda tympani). The main stem of the facial nerve exits the bony canal through the stylomastoid foramen. This is the beginning of the extratemporal segment, however arborisation does not start before entering the parotid gland. The nerve is first divided into 3 to 4 motor divisions that form the intraparotid plexus and ultimately give rise to the temporal, zygomatic, buccal, mandibular and cervical branches2.
Differential diagnosis of facial paralysis
As etiology of facial paralysis is broad and hard to classify, the division that is affected should be considered first.
Intracranial facial paralysis can be caused by lacunar infarcts or tumors of the intracranial cavity. Bacterial and viral infections, cholesteatoma and Bell’s palsy can be reasons for intratemporal nerve damage. Neoplastic malignancies and associated surgical therapy are the dominant causes for extratemporal facial paralysis. Although Bell’s palsy represents the most common diagnosis in patients with facial paralysis, most patients recover completely without sequelae and do not need surgery3. The second most common cause of facial paralysis is trauma. Here, fractures to the temporal bone are the predominant trauma mechanism4.
Treatment types of facial paralysis
Numerous surgical options exist for the treatment of facial paralysis and they may be classified into reinnervation, static reconstruction and dynamic reconstruction. Typically, two years are considered to be the time from injury in which function after reinnervation can be regained satisfactory with reinnervating procedures5. Later on, denervation atrophy of facial muscles precludes their usefulness for further reconstruction. Reinnervation can be obtained by primary nerve repair, interpositional nerve grafts, cross-facial nerve grafting or cranial nerve transfer. Static reconstruction techniques are directed to correct functional disabilities, (protection of the cornea, improvement of nasal airflow, and prevention of drooling) and to improve symmetry at rest. Typical procedures are browlift for brow ptosis, or canthoplasty for lower lid ectropion. Static reconstruction is preferred in elderly patients with significant comorbidities or in massive facial defects secondary to trauma or cancer resection.
The surgical techniques of dynamic reconstruction can be subdivided into regional muscle transfer and free microneurovascular muscle transfer with either coaptation to the masseter motor branch or cross-facial nerve grafting. The latter represents the criterion standard for the reconstruction of the smile in facial paralysis, as no other treatment option reliably achieves a spontaneous smile that is crucial to improve social handicap. Coaptation to the masseter motor branch is the treatment modality of choice for patients with bilateral paralysis, however indications have extended, as elderly patients or patients with significant comorbidities usually prefer a single-stage procedure6.
Gracilis flap
Regional anatomy
The gracilis muscle is a rather superficial muscle of the medial thigh, representing the longest muscle of the adductor muscles. It originates from the lower symphysis and the inferior ramus of the pubis. Running distally, the muscle becomes narrow and inserts distal to the knee joint on the tibia that allows not only adduction of the thigh but also flexion of the knee. The gracilis muscle has a type II circulatory pattern after Mathes and Nahai with an arterial supply from a dominant and some minor vascular pedicles7. The dominant artery exits the muscle at the hilum to course laterally and usually terminates in the medial circumflex artery. Rarely, the dominant artery terminates directly in the deep femoral artery. Venous supply of the gracilis muscle is usually achieved through two venae comitantes, that course deep to the adductor longus muscle to follow the dominant artery. Innervation of the muscle is achieved through an anterior branch of the obturator nerve that enters the muscle 1-2 cm superiorly to the hilum.
Clinical use
The gracilis muscle is a valuable donor muscle for reconstructive microsurgery and has become the muscle of choice for many surgeons for functional free muscle transfer. This is owed to the fact that there is little donor site morbidity and the flap shows optimal proportions with regards to excursion of the muscle and vascular pedicle dimensions respectively. A long single innervated motor nerve alleviates functional flap harvest8.
We here demonstrate the case of a 49 year old female, who initially presented with a complete picture of left peripheral facial paralysis following resection of an acoustic neuroma (vestibular schwannoma) 2 years earlier. The patient was most afflicted by facial asymmetry, particularly when smiling. Other pre-existing comorbidities were not documented.
Upon clinical examination, the patient showed a complete paresis of the frontalis muscle, however a satisfactory forehead symmetry at rest. Lid closure was insufficient on the left with a lagophthalmos of 5 mm and Bell’s phenomenon. Signs of cornea irritation and ectropion were absent. At rest, the patient showed a moderate asymmetry of the corner of the mouth with a tragus-modiolus distance of 11 cm on the right and 11.5 cm on the left at rest. Upon smiling, tragus-modiolus distance scaled down to 9 cm on the right and elongated on the left to 12 cm. After extensive counseling, the patient wished for a single-staged dynamic reconstruction of the smile with a free functional gracilis transfer using the masseter as donor nerve. The patient was also informed about various techniques of lid closure reconstruction, however declined surgical treatment at this stage. The course of the treatment was uncomplicated. Signs of reinnervation were first noticed three month postoperatively. Four months after surgery, the patient presented with unremarkable scarring along the former modified facelift incision line. Symmetry at rest and deliberate smiling were excellent with a satisfactory definition of the nasolabial crease. The patient also showed a completely spontaneous smile. Pre- and 9-month postoperative range of excursion of the corner of the mouth was documented by videography.