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Facial paralysis presents a complex challenge to the reconstructive surgeon. Since Sir Charles Bell first described the course of the facial nerve in 1821, our understanding has led to the development of the vast array of surgical options used to treat patients with facial paralysis.
Sir Harold Gillies stated in 1919 that the aim of surgical reconstruction is to restore the normal form; this primarily aims to preserve function and then subsequently address the esthetics. The fundamental problem when considering facial paralysis is that there is currently no conceivable way to restore the 17 muscles of facial expression successfully. The second challenge facing the surgeon is that no patient is the same as another. Not only the etiology behind facial paralysis dictates which operations are available, the age group, the anatomy available and, most importantly, what the patient wants all make the decision-making process vital.
The presentation of facial nerve paralysis also adds to the conundrum, ranging from an isolated marginal branch palsy to a complete bilateral palsy. The approach to the management of any patient with facial paralysis should be to break the face down into three units: the forehead, the eyes, and the mid- and lower face. In a young child, the skin quality is far superior to that of an elderly patient and thus problems encountered are different to the adult population. Frequently, there is minimal asymmetry at rest and therefore focus needs to be directed at restoring dynamic function. In the elderly patient, skin elasticity is poorer and asymmetry at rest may be strikingly obvious and static treatment options may yield the desired outcome.
What is the importance of facial palsy reconstruction? This is not cancer surgery and patient survival is not the main outcome being measured. The impact facial paralysis has on an individual can be devastating and can be broken down into functional and psychological factors. If a patient is unable to close their eye and the cornea is insensate, the globe will dry leading to ulceration and ultimately blindness. Diminished oral continence and poor speech are other functional problems encountered. A child who is unable to smile or convey emotion effectively may be subject to bullying and psychological trauma and an adult with profound asymmetry at rest make be mistaken for being angry by another individual, causing the patient to become socially reclusive. ,
The aim of this chapter is to give the reader a strategy on how to tackle facial paralysis. The anatomy of the facial nerve and other important structures of the face will be reviewed as this provides the foundation on which the evolution of surgical techniques have been based. The information provided should enable a surgeon to have a methodical approach to patient management; however, it must be stressed that the information should be used as a guideline and that each patient will require a customized approach to a greater or lesser extent. This makes facial palsy surgery one of the most fascinating and challenging aspects of reconstructive surgery; not only are the technical aspects pushing the limits of modern surgery but the decision-making process is equally as difficult and one must select the correct tools from the surgeon’s vast armamentarium to complete the task at hand. To the reconstructive surgeon it combines the epitome of what we seek to achieve: a functional outcome in which one has to consider the esthetic result, as the face is the center of human interaction.
Anatomy of the Facial Nerve
The facial nerve develops embryologically from the second pharyngeal branchial arch, the hyoid arch. The motor division derives from the basal plate of the embryonic pons whilst the sensory division arises from the cranial neural crest. The sensory portion, known as the intermediate nerve, is responsible for supplying taste to the anterior two-thirds of the tongue, secretory and vasomotor fibres to the lacrimal, submandibular, and sublingual glands, the mucous membranes of the nose and mouth, and finally, sensation over the external auditory meatus and posterior skin of the ear. The cortical fibers of the facial nerve arise from the lower third of the motor cortex, passing through the internal capsule and the middle third of the cerebral peduncle to supply the seventh nucleus in the lower pons and is closely related to the abducens and vestobulocochlear nerves. Of clinical importance, the supranuclear innervation is bilateral to the muscles of the forehead and eyes, but only contralateral to the muscles of the lower face; this accounts for the sparing of the forehead muscles in cases of supranuclear lesions in comparison to nuclear or infranuclear lesions. The course of the nerve can be simply divided as follows.
As the facial and intermediate nerves leave the brainstem, they course laterally towards the cranium, entering the petrous temporal bone through the internal auditory meatus. Here, within the facial canal, the intermediate nerve forms the geniculate ganglion. After a tortuous course it emerges through the stylomastoid foramen.
Greater superficial petrosal nerve is the first branch given off from the geniculate ganglion within the facial canal, and is responsible for the parasympathetic innervations of multiple glands. The second branch is the nerve to stapedius, providing motor innervations of the stapedius muscle. The final branch is the chorda tympani, responsible for taste sensation in the anterior two-thirds of the tongue.
After emerging from the stylomastoid foramen, the facial nerve passes through the parotid gland. The most immediate branch given off is the posterior auricular nerve that innervates the small muscles of the posterior ear and branches to the posterior belly of the digastric and stylohyoid muscles. The nerve divides into temporo-facial and cervico-facial divisions approximately 1.3 cm from the stylomastoid foramen. A useful clinical landmark for locating the trunk is at a point slightly anterior and inferior to the tip of the tragus ; the nerve typically lies between 1 cm and 1.5 cm deep to this. The nerve separates into the five principal branches at the pes anserinus.
The temporal branch courses cranially to cross the zygomatic arch within the superficial musculoaponeurotic system (SMAS), lying deep to frontalis but superficial to the deep temporalis fascia. The temporal branch is responsible for the innervation of frontalis, orbicularis oculi, and corrugators supercilii. An important efferent limb from this branch is responsible for the corneal reflex.
The zygomatic branch proceeds cranially, angled towards the lateral angle of the orbit. Here it supplies the orbicularis oculii.
The buccal branch is the largest branch and passes forward below the orbit and divides into deep and superficial divisions. The superficial branches lie superficial to the SMAS and supply procerus. The deep branches pass beneath zygomaticus and quadratus labii superioris, supplying them both. Further deeper branches go on to supply buccinator and orbicularis oris.
The marginal mandibular branch courses beneath the SMAS towards the chin, passing beneath depressor angulis oris (which it supplies). Here it branches to innervate the depressor labii inferioris and mentalis.
The cervical branch is the most inferior branch and passes towards the neck over the mandible beneath the SMAS. It primarily innervates the platysma.
There is much variability in the branching patterns of the facial nerve and numerous interconnections between them, and caution must always be exerted when making a surgical approach to expose the nerve.
There are 23 facial muscles, of which 17 are activated in facial expression. Broadly speaking, the musculature of the face can be divided into superficial and deep as described by Freilinger. The most superficial layer consists of zygomaticus minor and orbicularis oris. The deepest layer consists of buccinator, mentalis, and levator anguli oris, and it is important to note that these three muscles are the only ones to be innervated via their superficial surface; the remaining muscles receive their supply from their deep surface.
Anatomy of Potential Donor Nerves for Facial Reanimation
Whilst discussing the anatomy of the facial nerve it is worth spending some time to consider other local nerves of the face. Frequently, another donor nerve is required when either there is absence of a functioning facial nerve or if it is inappropriate to consider its use. Here, three other potential donor nerves will be considered.
The masseter is one of the principle muscles of mastication. It arises from the zygomatic arch and the maxilla and inserts into the coronoid process and the ramus of the mandible. The muscle is divided into a superficial and deep portion and is innervated by a branch of the mandibular division of the trigeminal nerve. The masseteric nerve arises from the anterior division of the mandibular nerve which arises from the cranium through the foramen ovale. The masseteric nerve passes laterally in front of the temporomandibular joint lying deep to the temporalis tendon. It crosses the mandibular notch with the masseteric artery and enters the masseter on its deep surface and branches within the muscle, reaching the anterior border. The nerve can be found intraoperatively by delicately spreading the muscle fibres of the masseter which are oriented downwards and backwards superficially, then downwards and forwards in the deep portion of the muscle. , It is important to isolate suspected branches and use a nerve stimulator to confirm its function.
The hypoglossal nerve is the twelfth cranial nerve and its nucleus is located in the medulla oblongata. It passes through the cranium to emerge from the hypoglossal canal. The extracranial course is closely related to the vagus nerve and passes between the internal carotid artery and jugular vein, lying on the carotid sheath. It passes deep to the posterior belly of the digastric muscle and enters the submandibular region, coursing lateral to the hyoglossus muscle and inferior to the lingual nerve before it branches to innervate the tongue. It innervates all of the muscles of the tongue except palatoglossus, which is innervated by the vagus nerve. When considering using the hypoglossal nerve as a potential donor nerve, it is advocated that a terminal branch is used to minimize any loss of function.
Spinal Accessory Nerve
The spinal accessory nerve is the eleventh cranial nerve and is responsible for the innervation of the sternocleidomastoid and trapezius muscles. The nerve is unlike other cranial nerves in the fact it arises from the upper cervical spinal cord and enters the skull through the foramen magnum. Its intracranial course leads it to emerge from the jugular foramen. In the neck it crosses the internal jugular vein at the level of the posterior belly of digastric muscle and continues to travel caudally, piercing and supplying sternocleidomastoid and then terminating to supply trapezius.
Vascular Supply of the Face
The arterial supply of the face is predominantly via branches of the external carotid artery and the ophthalmic artery. The ophthalmic artery branches to give rise to the supraorbital and supratrochlear arteries to supply the forehead. Consideration here will be given to the branches that arise from the external carotid artery as these are of more practical use when free muscle transfer is proposed. The three main facial arteries most suitable for arterial anastomosis are the facial artery, the superficial temporal artery, and the transverse facial artery.
The facial artery arises in the carotid triangle just distally to the lingual artery behind the ramus of the mandible. It passes deep to the digastric and stylohyoid muscles and along the posterior border of the submandibular gland, superficial to the hypoglossal nerve. At the point of the anteroinferior angle of the masseter it crosses over the body of the mandible and proceeds tortuously towards the angle of the mouth. In the face it branches to give rise to the inferior and superior labial arteries and terminates as the angular artery and the lateral nasal artery.
The superficial temporal artery arises from the external carotid artery when it bifurcates to also give rise to the maxillary artery. The superficial temporal artery originates at the level of the parotid gland behind the neck of the mandible. It then courses cranially just anterior to the tragus, crossing superficially to the zygomatic process, and is covered by the auricularis anterior muscle and a dense fascia. The temporal and zygomatic branches of the facial nerve cross the artery and it is accompanied closely by the auriculotemporal nerve, which lies immediately posteriorly. It terminates by branching to form the parietal and frontal arteries.
The transverse facial artery arises from the superficial temporal artery before it emerges from the parotid gland. It travels transversely across the face, running between the zygomatic arch superiorly and the parotid duct inferiorly superficial to the masseter muscle.
When planning free functional muscle transfer good knowledge of the vascular supply is critical. Facial anatomy is by no means consistent and frequently secondary options are required ; in some cases even direct end-to-side anastomosis to the external carotid artery may have to be considered to prevent flap failure. Preoperative assessment with a Doppler can offer the surgeon some reassurance.
Etiology of Facial Paralysis
There is an incidence of 1.8 out of every 1000 children born with facial nerve paralysis in Northern America. Several factors increase the chance of facial nerve injury during childbirth, including instrumentation, birthweight over 3.5 kg and primigravida status. The exact mechanism of injury is unknown but likely to be caused by traction being placed on the nerve. The prognosis is excellent, with over 90% of children recovering completely without intervention. In the rare case where complete transaction is suspected, surgical exploration may be beneficial.
Möbius syndrome is characterized by concomitant bilateral facial nerve and abducens nerve (CN VI) palsies. This leads to complete, bilateral facial paralysis leading to extreme difficulty in expressing emotion as well as oral incontinence and social ostracism.
CHARGE association was first described in 1981 by Pagon et al and may involve Coloboma, Heart anomalies, choanal Atresia, Retardation of growth and development, Genital and Ear anomalies. Although not all anomalies may be present, at either least four major features or three major and three minor features must be present. The major features are: coloboma, chonal atreisa, cranial nerve abnormalities, and auditory anomalies. The minor features include distinctive facial dysmorphology, facial clefting, tracheoesophageal fistula, congenital heart defects, genitourinary anomalies, developmental delay, and short stature.
Hemifacial microsomia covers a variety of congenital facial anomalies which arise as a lack of development of one side of the face. It is characterized by a hemifacial soft tissue deficiency, the poor development of the mandible, maxilla, and external ear.
With developmental facial palsy patients, the management is best looked after with a multidisciplinary approach. Individual cases may require the input of the cleft, ear or craniofacial surgeon whilst needing ongoing medical support. In these situations careful planning of the timing of procedures is required.
Bell’s palsy represents 80% of the case load of a facial palsy surgeon. There is no known causative factor, however there is evidence herpes simplex virus plays a role. Incidence is around 30 cases per 100,000 per year, and is slightly higher in pregnant women (45 per 100,000). Eighty percent of people will completely recover within 2 years. Of the 20% remaining, the problem ranges from having a complete dense facial paralysis to synkinesis.
Ramsay Hunt Syndrome
This syndrome is caused by varicella zoster virus involving the facial nerve. It is distinguished clinically from Bell’s palsy by the presence of vesicles and pain in the ear, along with a myriad of other less common symptoms. Although far less common than Bell’s palsy, the prognosis is worse and most patients do not recover from the facial paralysis and develop chronic neuralgia.
An acute infection of the middle ear or mastoid bone can very rarely lead to facial nerve paralysis. This is likely to be secondary to localized inflammation and compression of the nerve in the facial canal. Prompt recognition and treatment yields favorable outcomes and in select cases mastoidectomy may be indicated.
A cholesteatoma is a nonmalignant slow-growing skin cyst. It causes destruction of the inner ear through chronic infection and by local pressure effects as the cyst grows. Facial paralysis develops in less than 3% of cholesteatomas.
Lyme disease is caused by Borrelia burgdorferi , which is transmitted to humans by infected ticks. The symptoms are initially nonspecific, including headache, malaise, and fever; however, facial paralysis can develop in up to 11% of cases. The prognosis is excellent, with more than 99% of patients going on to full recovery without surgical intervention.
Trauma to the face or cranium represents the second most common cause of acquired facial palsies. The type of injury is the most important prognostic factor. In blunt trauma with no associated bony involvement, the type of injury is likely to be a neuropraxia and full recovery is to be anticipated. A penetrating injury where there is a transaction of the nerve warrants urgent surgical exploration and an attempt at primary nerve repair within 3 days. When there is an injury of the temporal bone the prognosis is less favorable unless the onset of the facial palsy is delayed. In temporal fractures the incidence of associated facial nerve injury is between 5% and 10%, of which 40% will recover poorly. In this group of patients, the diagnosis of a facial nerve injury may be difficult due to other intracranial injuries, making the assessment difficult or impossible.
Iatrogenic injuries may occur with soft tissue, bony or intracranial surgery. The injury may be unavoidable, however, prompt recognition and careful reconstructive planning is required.
The facial nerve may be prone to compression at any point along its course by a space-occupying lesion. The most common cause is secondary to compression by an acoustic neuroma followed by glomus, facial neuromas, and carcinomas. Manipulation of the facial nerve is frequently required in the removal of these tumors which may lead to further injury.
Systemic and Neurological
A brainstem injury may result in permanent facial paralysis due to disruption of the motor nucleus. A central facial palsy may be caused by a lacunar infarct that affects the fibers of the internal capsule going to the facial nucleus. The nucleus itself may be prone to ischemic injury secondarily to an infarct of the pontine arteries.
Many systemic diseases may lead to facial paralysis as a consequence of disease progression. Conditions include multiple sclerosis, Guillain–Barré syndrome, autoimmune disease, and diabetes. Treatment of the underlying cause is the primary management in this category.
Clinical examination of the facial nerve is best undertaken in a logical routine, working from the top of the face downwards. Most pertinent information can be ascertained almost immediately by observing a patient as you greet them and they talk. Resting asymmetry may be difficult to assess in the pediatric population as the skin quality is superior to the more elderly patient group and therefore asymmetry may only become apparent during interaction with a child and attempting to get them to smile or speak. It is important to bear in mind that what a clinician views as being the major problem may not be perceived as such by the patient.
Simple examination of the face is usually sufficient to assess the facial nerve. Beginning at the brow, look for asymmetry of the wrinkles of the forehead at rest and then ask the patient to raise their eyebrows to exaggerate this. A particular area that requires close examination is the eye. Ask the patient to close their eyes as tightly as possible. Eye closure is predominantly achieved by the upper eyelid and the lower eyelid acts to maintain the lid margins in contact with the globe and assist tear drainage. Begin with assessing the condition of the globe; are there signs of epiphora, corneal irritation or ulceration? During the introductory period of the consultation it should be possible to see if the blink reflex is still intact and whether the Bell’s reflex is effective. The height of the palpebral aperture should be compared between the two sides and measured during eye closure. When assessing the lower eyelid, the position of the lacrimal duct should be assessed as it normally should be lying pressed to the globe, however, when there is a moderate degree of ectropion it may be ineffective at lubricating the globe, leading to epiphora. The assessment of corneal sensation is paramount as an insensate eye that is unable to close effectively carries a high risk of corneal damage, ulceration, and scarring, which may ultimately result in blindness.
The midface must be examined at rest and during animation. At rest the position of the nose, alar symmetry, the presence of a nasolabial fold, the position of the philtrum and mouth must all be noted. This should be repeated whilst asking the patient to perform a closed mouth smile, an open mouth smile, and whilst attempting to show all their teeth. Internal examination of the mouth is prudent as it will give the surgeon a better idea of dental hygiene and the presence of dental caries. Functional assessment of speech should be performed by asking the patient to repeat labial sounds of “b,” “p,” and “m”. The patient should be asked to pucker their lips and blow out their cheeks.
Not all patients will have a dense unilateral palsy and more subtle signs should be observed. The presence of synkinesis is particularly trouble for a patient and the most common symptom is involuntary eye closure during smiling. Dyskinesis may also be present and signs of involuntary muscle twitching must be observed.
An important part of the examination should be to examine other cranial nerves, particularly if they are to be considered as donor nerves in reanimation. The nerve to masseter can be examined by asking the patient to bite whilst palpating the muscles of mastication. Examination of the hypoglossal nerve is performed by asking the patient to protrude their tongue and observing that it does not deviate. Asking the patient to shrug their shoulders will confirm the function of the spinal accessory nerve.
A thorough discussion with the patient should then be performed if possible to illicit the symptoms they suffer from. Typically this will start with the patient listing the symptoms in order of severity. In the pediatric patient this discussion mainly involves the parents and what they have noticed. It is often useful to ask the parents to bring photos or videos of the child from home, as they may be somewhat apprehensive during the consultation. Parents can often feel negative emotions of guilt if their child has difficulty smiling; it is important to consider the psychological support a family may require before, during, and after treatment of their child. In the adult group, patients’ primary concern may be with the eye with persistent watering or recurrent infections. With regard to the mouth, they may report function or psychological symptoms; drooling, difficulty eating or poor speech may be the primary concern. For some, the psychological implications of not being able to smile may be more concerning or the feeling that they are being perceived as angry or hostile may lead them to social isolation.
Once the clinical examination has been performed, discussion regarding the management with the patient or their parents is undertaken. It is important to ascertain the patient’s or parents’ expectations and modify this at an early stage if appropriate. A tailor-made approach that is patient-focused usually provides the most successful outcomes. After the consultation it is useful to ask the patient to have both photographic and video documentation. Each unit varies in their requirements, but this serves as a vital tool in assessing outcomes of intervention.
Many scoring systems have been proposed over time and the general consensus is that there is no ideal system. The most popularized is the House–Brackmann scale, originally described in 1985 and modified in 2009 to form the basis of the Facial Nerve Grading System 2.0. It is a widely accepted system, simple, sensitive, accurate, and reliable, which grades facial function in six steps from normal (HB I) to total paralysis (HB VI). Multiple scoring systems are present and there is no universal opinion as to which is the most accurate.
Diagnostic studies can play a critical role in the assessment of cranial nerves, either preoperatively, postoperatively, or during the monitoring nerve recovery. If there is any doubt regarding a facial nerve paralysis or a potential donor nerve paralysis, it is prudent to perform further testing.
Radiological imaging in the form of a computed topography (CT) scan or a magnetic resonance imaging (MRI) scan can be useful to exclude a space occupying lesion. Typically this has normally been performed prior to referral. Physiological MRI scans can be used to assess cortical remodeling for situations where relearning how to use a nerve to carry out a different function needs to be assessed.
Several electrophysiological tests can help guide the clinician. Electromyography (EMG) is most commonly used to assess the function of different branches of the facial nerve or potential donor nerve in comparison to the normal side. EMG is often combined with electroneurography (ENoG) which assesses nerve conductivity in comparison to muscle activity. The Nerve Excitability Test (NET) is used mainly to determine the prognosis of nerve recovery in unilateral facial nerve palsy. The facial nerve is stimulated at the angle of the jaw with increasing current until a barely perceptible twitch is seen in the face. This is compared with the normal side and a difference of more than 2–3.5 mAmp is considered abnormal. Due to the invasive nature of these tests, patients may not be able to tolerate the investigation, particularly in the pediatric group.
When considering the management of facial paralysis the clinician must have a set of priorities to which they adhere. First, protection of the eye is paramount. Drying out of the globe can lead to corneal ulceration and ultimately blindness if untreated. Second, oral continence and speech should be restored. Third, facial symmetry should be restored to address the esthetic appearance of the patient and, consequently, the psychological impact of the paralysis.
Patients should be treated differently on age criteria. In the pediatric group the eye and forehead do not usually require surgical intervention and the focus of attention should be on smile restoration. In the aging patient, treatment options begin to become more limited as the ability of a nerve to regenerate diminishes with age, as does the chance of retraining the brain if a different nerve is used. The gold standard should be to recreate symmetrical spontaneous movement; this may not be possible in all cases, and many treatment options exist to help improve the circumstance.
In cases where a spontaneous recovery is expected this represents the mainstay of treatment. In permanent partial or complete facial paralysis, this is a key adjunct to the operative management and is by no means exclusive. In patients complaining of the difficulty in eye closure at night, particularly in the absence of Bell’s phenomenon, simple taping of the eyelids closed may be all that is required to relieve the symptom. Often, it is crucial to keep the eye hydrated and this may be achieved by using topical eye drops or lubricants.
Botulinum type A provides a reversible chemical method of denervation and may be used for two different patient groups; first, in patients complaining of asymmetry, and second, those complaining of synkinesis. When focusing on brow asymmetry or overactivity of the depressor, botulinum type A is often the initial first step in a patient’s management as it is minimally invasive, provides rapid visual results, and is reversible. It is important to recognize that the dose is variable between patients and that it should be administered to the unaffected side. Typically, patients achieve a maximum response at 2 weeks and the dose should be repeated every 3 months and titrated as necessary. Botulinum A is effective in treating synkinesis, and the affected muscle groups may be directly injected to diminish their action. Dyskinesis is what a patient will complain of if there is involuntary twitching of muscle groups as they recover or fail to completely recovery. Botulinum type A is administered directly, typically requiring a lower dose, to the affected muscle groups and similarly repeated every 3 months and titrated as necessary. The key is to avoid paralyzing the muscle as this may increase asymmetry and lead to an unhappy patient outcome; if this arises it is important to reassure the patient that full recovery is expected.
Management is best approached by addressing the subunits of the face. In addition, some differences in treatment are preferred depending on the age of the patient, the etiology of the facial paralysis, as well as the degree of paralysis that exists.
Management of the Brow
The only management options available for the brow are static; resting symmetry is the goal of treatment. With a unilateral paralysis the drooping of the brow increases with age and decreased skin elasticity. All brow lifts are static, and currently there are no useful procedures that can provide dynamic forehead movement. Correction of brow ptosis may be approached surgically either directly or via an endoscopic approach. Direct brow-lift incisions include brow, coronal or midforehead approaches. The direct brow lift through a superciliary brow incision is well recognized as the favored method in the setting of facial paralysis and can correct large discrepancies at the expense of a visible scar. An ellipse of skin and frontalis muscle is excised and pexy of orbicularis to the periosteum is performed for durability of the lift. The supraorbital nerve is at risk and must be carefully preserved, but even so, patients often complain of numbness. A coronal brow lift is approached through an incision in the scalp 4–6 cm posterior to the anterior hairline extending to the pinna. Elevation in the subgaleal plane is performed and 1–2 cm of scalp is removed by incising anterior to the initial incision. The scars are usually inconspicuous but the amount of lifting is much less than the direct brow incision and patients often complain of paresthesia posterior to the incision. A receding hairline, or family history of male-pattern baldness, may be a relative contraindication to a coronal brow lift, in which case a midforehead brow lift through a deep brow rhytid may be more appropriate.
Endoscopically-assisted brow lifts may be useful for small amounts of brow ptosis and are therefore not satisfactory in older individuals with significant ptosis. In contrast to the direct methods involving skin excision, endoscopic brow lift suspends the periosteum in an elevated position until adherence by healing is obtained. Elevation of both brows and the complete frontal region appears necessary to address the hyperfunction observed in the unparalyzed side, producing the best symmetry. An alternative is to weaken the contralateral normal frontalis muscle by frontal nerve denervation with or without frontalis muscle resection or chemodenervation with botulinum toxin A. Preservation of the supratrochlear and supraorbital nerves is also achieved by direct visualization endoscopically and incisions are smaller with less sensory disturbance and less alopecia.
Management of the Eye
The goal of corrective surgical procedures is to achieve complete eye closure, thereby providing corneal protection, with minimal ptosis in the open position. In principle, the upper eyelid needs to be lowered (unopposed action of levator palpebrae superioris) and the lower eyelid needs to be elevated. Standard static procedures include lid loading (upper lid) and tarsorrhaphy (upper/lower lid) as well as lower eyelid slings, whereas the palpebral spring implant (upper lid) and the temporalis muscle transfer (upper/lower lid) are classified as dynamic.
Lid loading was first described over 50 years ago and is well tolerated and highly efficacious. Gold and platinum have been the most widely used materials for implantation because of their high density and excellent side effect profile. The amount of weight required for complete closure is frequently too large, and a large weight is more likely to detach and erode through the skin. Test weights attached to the upper eyelid with double-sided tape are used preoperatively to determine the lightest weight that will bring the eyelid within 2–4 mm of the lower lid. The most commonly selected weights are 1.0 g and 1.2 g, though standard sizes range from 0.6 g to 1.8 g. For the best results, they should be placed at least 4 mm above the lid margin (to decrease visibility). Care must be taken not to damage the levator insertion during the dissection for placement to avoid ptosis. Patients are advised that eyelid closure is a slow rather than a rapid blink and that they must practice holding the closure. Complications include a visible lump (capsule formation), ulceration, and/or extrusion, migration of the weight and irritation of the cornea. More recently, a flexible platinum chain has been described as an alternative to rigid gold weights, with multiple links allowing flexibility to adapt to the shape of the globe. Platinum has a better biocompatibility profile and a higher density compared to gold and can thus be made into a smaller implant with improved cosmesis. In terms of static support for the lower lid, the use of autologous conchal cartilage grafts can be an effective procedure to improve the function and appearance of the atonic lower eyelid.
A tarsorrhaphy results in support of the lower eyelid and decreases the amount of corneal exposure by lowering the upper lid. Mclaughlin’s lateral tarsorrhaphy is a quick and simple procedure involving resection of the posterior lamellar of the upper lid (tarsal plate and conjunctiva) as well as an identical area of anterior lamellar of the lower lid (skin and muscle). The two denuded areas are overlapped and both tarsal plates are sutured. It is especially indicated in older patients with concomitant senile ectropion but may result in the appearance of a smaller eye and difficulty when looking laterally. If this fails to achieve the desired result, then a fascial or palmaris longus tendon sling is used to support the lower lid with fixation points at the medial canthal ligament and supraorbital margin laterally. Proper placement of the tendon 1–2 mm below the lid margin is crucial as low placement will exacerbate an ectropion and high placement may result in an entropion. Canthoplasties are rarely performed as they tend to stretch over time in patients with facial paralysis.
The palpebral spring implant is a wire shaped by the surgeon in the form of an open safety pin. The lower arm is attached to the lid margin and the upper arm to the superior orbital rim. When the eye is opened by contraction of the levator muscle, the spring is compressed. When the levator is relaxed, the spring expands and forces the eyelid to a closed position. It has an advantage over upper lid weighting in that it will function equally well in the upright or supine position, but the results depend on the experience of the operator and the spring may loosen or fracture with time.
The transfer of a strip of temporalis muscle was first described by Gillies to provide a dynamic closure of the eyelid using autologous tissue. A 1.5-cm strip of temporalis muscle is detached superiorly, turned anteriorly, and extended with two strips of tendon or fascia, passed through the upper and lower eyelids, and fastened to the medial canthal ligament. Alternatively, a static sling can be placed in the lower lid as previously described and a dynamic temporalis transfer applied to the upper lid as this eyelid requires more movement. The temporalis muscle transfer is activated by closing the jaw and therefore frequent biting throughout the day results in frequent corneal lubrication. It does result in a bulge over the lateral orbital margin and a slit-like appearance to the eye, and is technically demanding to perform, but it can provide forceful and full eyelid closure, especially if the tension of the transferred muscle has been set correctly. It is also especially useful if sensibility of the cornea is diminished.
In order to restore the blink reflex, free functional muscle transfer (FFMT) must be considered. This should ideally be performed as part of a two-stage reanimation process where two cross-facial nerve grafts (CFNG) are harvested, one being attached to a functioning buccal branch, the other to a zygomatic branch of the contralateral side. At the second stage, a free platysma flap may be raised with its neurovascular pedicle, tunneled through the upper and lower lids and attached to the medial canthal ligament medially and temporal fascia laterally ( Fig. 22.1 ). The neurovascular pedicle is then typically joined to the CFNG from the functioning zygomatic branch and the superficial temporal vessels. This provides the patient with true spontaneous eye closure and restoration of the blink reflex.