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As we do for most of our human functions, we take facial movements for granted. Quick, complete, and frequent blinks of the eyelids keep the cornea healthy. Narrowing of the eyelid fissures, or guarding, protects an irritated eye. Reflex closure of the lids is a spontaneous reaction to avoid trauma to the eye. However, problems of both overactivity and underactivity of the facial muscles are common. Conditions related to overactivity of the facial muscles include:
Aberrant regeneration of the facial nerve
Problems of underactivity of the facial muscles are seen as well. A loss of facial expression is seen in patients with many of the myogenic ptoses that we have discussed and in patients with Parkinson disease. Facial nerve palsy can occur with a number of conditions and results in typical anatomic and functional abnormalities, including incomplete eye closure and corneal exposure, ectropion, and brow ptosis. You may see localized areas of facial weakness resulting from traumatic damage to facial nerve branches and muscles. We have already discussed ptosis syndromes associated with generalized muscle weakness, including myotonic dystrophy, chronic progressive external ophthalmoplegia (CPEO), and oculopharyngeal dystrophy. If you have not already become a student of facial expression, you surely will as your experience grows!
These are situations that an oculoplastic surgeon sees daily in practice. The conditions are easily differentiated on a clinical basis and rarely require any sophisticated testing to confirm your clinical impression. Each condition of overactivity or underactivity requires a different therapeutic approach.
In this chapter, we review the normal anatomy and function of the facial nerve and the muscles of facial expression. The pathologic conditions involving overactivity and underactivity of the facial muscles are discussed separately. In each section, we look at the important findings in the history and physical examination to help you make the correct diagnosis and formulate an appropriate treatment plan. Last, we explore the options for medical and surgical therapy for each disorder.
Anatomy and Function
Facial Nerve Anatomy
The facial nerve extends from its origin in the brainstem to the innervation of the facial muscles. There are two areas of particular interest to us. The first is the point at which the facial nerve leaves the brainstem in close proximity to the fifth and eighth nerves. The second location is distal to the appearance of the facial nerve trunk in the face anterior to the tragus of the ear. From this point, the facial nerve trunk divides into five branches ( Figure 9.1 ):
These branches innervate groups of the facial muscles selectively. Depending on the cause, facial nerve weakness may involve the entire nerve or individual branches. Bell palsy or any injury to the nerve proximal to the branching of the facial nerve involves the entire face. Accidental or surgical trauma to the face can result in injury localized to one or more branches. All nerves have the ability to regenerate. Unfortunately, regeneration of the facial nerve occurs in a nonanatomic manner known as aberrant regeneration of the facial nerve. You may see this in a patient after a cheek laceration heals. If you look carefully, you may see that the entire cheek moves as a whole or may move in synchrony with eyelid movement. Similarly, after facial nerve palsy, all branches of the facial nerve receive the same innervation. A signal to any branch of the facial nerve causes the entire face to move a bit. Pursing of the lips narrows the patient’s palpebral fissure ( Figure 9.2 ). Blinking causes the movement of the entire face, most noticeable at the corner of the mouth. You soon become aware of facial asymmetries in your patients. Remember, your examination begins when the patient enters the room. Your conversation as you get to know the patient often gives you clues to the type and cause of the patient’s problem. At some point, view the accompanying videos to this chapter to give you a better understanding of these movement abnormalities.
The Facial Muscles
All the muscles of the face are innervated by branches of the seventh nerve. The orbicularis muscle is responsible for eyelid closure. The orbicularis is divided into three areas: The orbital orbicularis causes forceful squeezing of the eye, and the preseptal and pretarsal portions of the orbicularis are responsible for the quick blinks that lubricate the cornea. The orbicularis muscle receives innervation from several branches of the facial nerve such that localized trauma has to be fairly extensive to cause a significant paralysis of the orbicularis muscle. You can test for eyelid closure weakness by asking the patient to forcefully close the eyes. Normal forceful closure buries the eyelashes ( Figure 9.3 ). As you become an experienced observer, you recognize that some patients have a weak or incomplete blink. This is easiest to see in a patient with a unilateral facial palsy. This may be clinically insignificant, or it may reveal itself as inferior corneal exposure with fluorescein staining seen on slit lamp examination. In our discussion of levator function, we mentioned the speed of the upper eyelid excursion. This is a similar observation; a patient with orbicularis palsy has a slower-than-normal velocity of closure.
Both the corrugator and the procerus muscles are also innervated by the facial nerve ( Figure 9.4 ). These muscles are known, respectively, for the creation of the vertical (or slightly angled) wrinkles and the horizontal glabellar wrinkles. The corrugator muscle also plays a prominent role in the forceful eyelid closure of essential blepharospasm.
The frontalis muscle lifts the eyebrows and forehead. This muscle is innervated by a single branch of the facial nerve, the temporal branch. Injury to the temporal branch (also called the frontal branch) can cause a permanent brow ptosis.
Loss of function of the lower facial muscles results in a drooping of the midface and lip, as well. In patients with mild weakness, you see slight facial asymmetry and a shallowness of the nasal labial fold. This asymmetry can be brought out by asking the patient to make a broad smile.
Overactivity of the Facial Muscles
Orbicularis myokymia is a common condition. It generally occurs in younger patients who note an involuntary twitching of the upper or lower eyelid. The abnormal movements are quick, lasting a second or less. The movements are easily noticed by the patient but require your close observation to see them. The movements result from spasm of individual bundles of muscle fibers. The muscle as a whole is not in spasm. Orbicularis myokymia is related to stress, fatigue, use of alcohol, or use of excessive caffeine. On rare occasions, the spasm becomes prolonged and botulinum toxin (Botox) injections can be used to relieve it; only a tiny amount is needed, such as 1 unit, in one or more areas.
Facial tics are voluntary movements of a group of facial muscles. In most situations, the patient is actually not aware that he or she is controlling the movements. The condition may be a unilateral movement of the eyelids and side of the face or may be simply a bilateral increase in blinking rate. Some tics may be more complex. There is often some secondary gain obtained with the tic, although that is difficult to identify. Tics occur most commonly in children but can also be seen in adults ( Figure 9.5 ). Probably you have already seen patients with tics. We discuss their diagnosis in more detail later.
Hemifacial spasm is an involuntary movement of one side of the face ( Figure 9.6 ). The movement may be a quick apparent twitch or may be seen as a sustained spasm involving all the facial muscles on the side. The etiology of facial spasm is thought to be vascular compression of the facial nerve where the nerve leaves the brainstem. Frequently, the hemifacial spasm is accompanied by signs of mild facial weakness and aberrant regeneration (movement of the lower face causes movement of the upper face, and vice versa).
Essential blepharospasm presents as an uncontrolled blinking or spasm of both eyes ( Figure 9.7 ). Essential blepharospasm results from progressive degeneration of the central nervous system thought to occur in the basal ganglia. It is most commonly seen in elderly patients. Initially, the disorder may start as increased blinking, but it generally progresses to a more sustained spasm of both eyes with prominent orbital orbicularis and corrugator muscle activity. Botox injections make a tremendous improvement in the spasm for most patients.
As the disorder progresses, patients lose the ability to open the eyes ( apraxia of eyelid opening ). The brain is sending uncontrolled impulses to close the eyes, including both orbicularis muscle contraction and levator muscle relaxation . In the early phases of the disorder, the spasm seems to predominate. Following the Botox injections, the spasm is diminished but the patient is left with eyes that have forgotten how to open. The patient no longer has a spasm that predominates. The patient just finds that it is more comfortable to keep the eyes closed because it is a struggle to open them.
Apraxia is difficult to treat. There is no known treatment to stimulate the levator muscle. The frontalis sling procedure can benefit some patients by increasing the efficiency of the frontalis muscle in opening the eyes. I have seen patients that improve significantly, but many patients show no benefit whatsoever. Some doctors inject a tiny amount of Botox into the pretarsal orbicularis (1 unit or so) as a supplemental treatment for apraxia. I have done this and cannot say whether it helps or not.
Abnormal movements of the lower face may be seen in association with essential blepharospasm, known as Meige syndrome ( Figure 9.8 ). Another, more descriptive, term for Meige syndrome is oral facial dystonia.
History and Physical Examination of the Overactive Face
When diagnosing abnormal movements of the face, your history taking and physical examination occur at the same time. You learn to watch the patient as you take the history. As you see the type of spasms occurring, you are able to tailor your questions to make a diagnosis.
Several factors are important in arriving at the correct diagnosis:
Character of the spasm
Quadrants of the face involved
Orbicularis myokymia and tics tend to occur in younger patients. Essential blepharospasm and hemifacial spasm occur in older adults. Orbicularis myokymia has an abrupt onset and usually lasts less than a week. The onset of facial tics may follow a particular event, and they frequently disappear spontaneously over a variable period of time, especially in children. For other patients, a tic may be present for life. Hemifacial spasm and essential blepharospasm generally do not have a specific onset and tend to progress. As you watch the patient, you are able to get a feel for the character of the movement problem. Is the muscle activity a quick twitch or a sustained spasm? Are you seeing an involuntary muscle activity (myokymia, hemifacial spasm, or blepharospasm), or is the abnormal facial movement the result of a voluntary coordinated movement of a group of muscles (a facial tic)? Most of all, you want to determine which parts of the face are involved. This leads the way to determining the diagnosis ( Box 9.1 ).
Divide the face into four quadrants.
First ask yourself if one or both eyes are involved.
If one eye is involved, ask yourself whether the whole side of the face is involved.
If the eye alone is involved, the problem is probably myokymia.
If one eye and the whole side of the face are involved, the diagnosis is probably hemifacial spasm.
If you have identified spasm in both eyes, the patient has either a form of blepharospasm or a facial tic.
Rule out a cause of reflex spasm.
If the patient with bilateral eyelid spasm is younger than 50 years of age, the spasm is probably a tic.
If the patient is 50–60 years or older, the spasm is probably essential blepharospasm.
If the upper and lower regions of the face are involved, the patient has Meige syndrome.
Facial tics can be unilateral or bilateral.
The movements involve a group of muscles under voluntary, but unconscious, control. In many cases, you can trick the patient into stopping the tic for a minute or so to confirm the diagnosis.
It is helpful to divide the face into four quadrants when evaluating patients with movement abnormalities ( Figure 9.9 ).
First ask yourself whether one eye or both eyes are involved.
If the answer is one eye, ask yourself whether the whole side of the face is also involved. If the eye alone is involved, the problem is probably myokymia, and you should ask about stress and fatigue. Frequently, the patient tells you that this is a very busy time at school or work. Probably you have had an episode of orbicularis myokymia yourself.
If one eye and the whole side of the face are involved, the diagnosis is probably hemifacial spasm. In general, patients with hemifacial spasm are older than 50 years, but this condition can occur in the 40s. Beware of diagnosing hemifacial spasm in a patient younger than 40 years of age. As you initially examine the patient with hemifacial spasm, there may be no apparent abnormal movements. You may notice that as the patient talks, the spasm starts. This is typical of hemifacial spasm where the so-called cross-talk of nerve fibers initiates the facial spasm. This phenomenon is bothersome to patients because the spasm often starts when they are talking to friends or business acquaintances. If you suspect hemifacial spasm but do not see movements elsewhere in the face, look closely at the chin for dimpling of the mentalis muscle or at the neck for subtle movement of the platysma muscle. You may be able to confirm the diagnosis of hemifacial spasm by asking the patient if the spasm occurs while sleeping. Hemifacial spasm is the only diagnosis where spasms continue in the patient’s sleep.
A tic can involve one side of the face, as well. Patients with a unilateral periocular tic often show bilateral orbital orbicularis activity because it is difficult to lightly blink one eye voluntarily. In most patients, it is easy to identify a tic because the movements seem somewhat bizarre and for some reason you get the idea that the patient is actually causing them. Sometimes I pass by the examination room a few times to see if the movements are occurring in my absence. Frequently, when I enter the room, the facial movements of the tic start. We say the tic is voluntary, but in fact, many patients with tics are not aware that the movements are occurring. The patient is often able to stop the movements for brief periods of time. There are patients, both children and adults, where the movements are intentional, likely providing some secondary gain. If you have identified spasms in both eyes, the patient has either a form of blepharospasm or a facial tic. If the patient with bilateral eyelid spasms is younger than 50 years, the diagnosis is probably a tic. We talk more about tics a few paragraphs from now.
In all patients, you should rule out the possibility of a reflex blepharospasm from some cause of ocular irritation. The reflex spasm is usually obvious in a young patient but may be more difficult to identify in an older patient, who may have an element of dryness in the eye. Ask if the patient has any sensation of a foreign body or burning in the eye. If there is a question of surface irritation causing the spasm, a drop of topical anesthetic should relieve the spasm. If you remain uncertain about the possibility of a reflex component, try lubricants or punctal plugs before proceeding with any other treatment.
Essential blepharospasm occurs as a degenerative disorder seen mainly in patients older than 60 years. It may occur in the 50s, however. Although patients think of the disorder as a spasm disorder, essential blepharospasm is really a loss of the ability to keep the eyes open. Eyelid closure involves simultaneous initiation of the orbicularis muscle activity and suspension of the levator muscle activity. In the early stages of the disorder, increased orbicularis activity, blinking, is the predominant symptom. Over time, the blinking becomes forceful spasms, which can interfere with all activities of daily life. Typically, the symptoms decrease when the patient is busy with an activity such as work or a hobby. Symptoms seem to be worst when the patient is at rest or while the patient is driving or reading. Frequently patients note that they pry their eyelids open to be able to drive. Often, this represents a sensory trick to keep the eyes open. Touching the periocular tissue somehow turns off the spasm through some unknown sensory feedback loop. It is real and is a helpful diagnostic sign (see Figures 9.6 to 9.8 ).
On examination, you see an increased rate of blinking in the early stages of the disease. Usually, the orbital orbicularis muscle is involved. In later stages, the corrugator muscle pulls the eyebrows toward the midline and spasms are sustained. Often, lower facial involvement is noted, with mild abnormal movements of the face, frequently, lip pursing. If present, this lower facial movement helps to confirm the diagnosis of essential blepharospasm. As we said earlier, patients with lower facial involvement and blepharospasm are said to have Meige syndrome.
Sometimes patients tell you that their eyes feel much more comfortable if they are just closed, a symptom that apraxia is developing. Ongoing botulinum injections have improved the spasm, but the patient is left with the inability to open the eyes. As apraxia develops, the patient may think that the botulinum injections are not working because the patient cannot open the eyes. You recognize this in the patient that cannot open the eyes but really has no spasm. When you ask the patient to squeeze the eyelids closed, you see little movement, demonstrating that the injections are, in fact, reducing the orbicularis activity. There is no medical or surgical treatment that can stimulate the levator muscle activity in these patients.
Treatment of the Overactive Face
The treatment of facial spasm was revolutionized by the introduction of botulinum toxin (Botox Allergan, botox.com ; Dysport, Galdermadysport.com ; Xeomin, Merz xeomin.com ). The toxin serotype A is produced by Clostridium botulinum and is a potent muscle-paralyzing agent. Injection of botulinum toxin into the orbicularis muscle of the eyelids and eyebrow provides symptomatic relief of spasm for 3 to 4 months (average being 14 weeks), depending on the disease process. Botulinum toxin is the primary treatment for hemifacial spasm and essential blepharospasm. All brands of botulinum toxin can be used to treat these movement disorders ( Table 9.1 ). In this text, the approximate dosing equivalents are given in Botox units. The toxins give similar results. There can be differences in the diffusion properties of the toxins owing to the different molecular weight of each toxin molecule. I suggest that you get familiar with one toxin first. Later you can add the others to your treatment choices. There are some practical considerations regarding cost and wastage that come into play, depending on your particular practice situation.
|Brand Name||Chemical Name||Dose Equivalent|
|Botox||Onabotulinumtoxin A||1 unit|
|Dysport||Abobotulinumtoxin A||2.5–3 units|
|Xeomin||Incobotulinumtoxin A||1 unit|
Orbicularis myokymia is a self-limited condition. The spasm usually lasts a few days and rarely more than a week. Botulinum toxin can be used, but be careful that you do not miss a more serious diagnosis if the myokymia persists. Very small amounts of Botox should be used (1 to 2 units per site).
Tics usually start in childhood. Blinking, twitching, or facial grimacing may show. Usually, these signs are transient, but they may become chronic and last into adulthood. Facial tics are treated with reassurance. In most children, the tic is simply a way to get attention from the parents. I encourage the parents to ignore the tic, if possible. If the tic persists for more than a few months, I recommend that the family discuss the situation with the family pediatrician, because the tic may be a sign of a more serious problem in the family or at school.
Facial tics are seen in Tourette syndrome, a neurologic disorder, characterized by repetitive, stereotyped, involuntary movements and vocalizations. The syndrome usually appears in childhood and peaks in the teen years. These tics are classified as simple or complex tics. Simple motor tics are sudden, brief, repetitive movements that involve a limited number of muscle groups. Some of the more common simple tics include eye blinking and other eye movements, facial grimacing, shoulder shrugging, and head or shoulder jerking. Complex tics involve several muscle groups and may be of the head, shoulder, or extremities. Vocalizations are a part of Tourette syndrome but are not seen in all cases. Simple vocalizations can be barely recognized, such as sniffing, grunts, or throat clearing. These vocalizations may be of socially unacceptable words, known as coprolalia (present in only a small number of patients). Most patients with Tourette syndrome have an associated anxiety disorder such as attention deficit disorder, attention deficit hyperactivity disorder, or obsessive-compulsive disorder. There seems to be a familial component in many cases of Tourette syndrome.
Tics in adults may be a later manifestation of childhood tics. Tics starting in adulthood are usually not a serious medical problem and may be stress related. If the patient agrees with this assessment and expresses an interest in counseling, arrangements are made. There are unusual, more serious causes of adult-onset tics, so if the tics are persistent, help from a neurologist should be considered. Botulinum toxin injections are not recommended for facial tics.
If you diagnose hemifacial spasm, you should order a magnetic resonance imaging (MRI) scan of the brain to rule out any mass that may be causing compression of the facial nerve. A mass seen on an MRI scan is very rare. I have seen this only once, in a 20-year-old man with hemifacial spasm caused by an epidermoid tumor of the skull base. His spasm resolved upon removal of the mass. In most cases, the scan is normal or shows a long, dilated basilar artery in proximity to the facial nerve where it exits the brainstem, the so-called dolichoectatic basilar artery.
In healthy patients aged 50 to 60 years or younger, microvascular decompression of the facial nerve (Jannetta procedure) can be considered. In this low-risk intracranial operation, a pad is placed between the artery and the nerve. The reported success rate for this procedure varies significantly but can be as high as 75%. I discuss this as an option with my younger hemifacial patients, but few seem interested.
In my practice, botulinum toxin is the treatment of choice for most patients with hemifacial spasm. Five units of botulinum toxin are administered subcutaneously in five sites around the periocular region ( Figure 9.10 ). The choice of sites can be individualized after the initial injection, if the need arises. Most patients with hemifacial spasm have an element of facial weakness, making the effects of the injections last longer than for patients with essential blepharospasm; 4 to 6 months is common. Remind your patients to use artificial tears frequently throughout the day and lubricating ointment at night for the first few weeks after injection to prevent corneal exposure.
Essential blepharospasm is a difficult disorder to treat completely. Most of your patients see improvement with botulinum toxin injections, but very few are completely asymptomatic after treatment. The disease tends to be progressive and becomes a lifelong condition that will affect your patient for the rest of his or her life. I urge all patients to subscribe to the Benign Essential Blepharospasm Research Foundation newsletter ( blepharospasm.org ).
No oral medication has been proven to be effective for treatment of essential blepharospasm. Most patients have considerable improvement from botulinum toxin injections. Initially, 5 units of botulinum toxin are administered subcutaneously in five sites in the periocular area ( Figure 9.11 ). Injections are given subcutaneously above and below the medial and lateral canthal tendons. No injection is made within the orbital bony rims. An additional 5 units is given above the head of the brow in the area of the corrugator and procerus muscles. Each physician has his or her favorite pattern of injections. This seems to work well for my patients. After the first injection, I check the patient in 1 to 2 weeks. After subsequent injections, I do not see the patient before the next injection unless there is a problem. The muscle weakening gradually takes effect over 48 to 72 hours. The effect gradually diminishes. Most patients need reinjection in 3 months (most insurance companies cover treatment every 91 days). In some cases, you can modify the position of the injection to improve the effect or decrease a particular area of weakness (usually the mouth). I generally do not increase the dose, although some doctors do so.
Botulinum toxin has been used safely for more than 30 years. Some patients have temporary dryness related to the paralysis of the orbicularis muscle and resultant decreased blinking. Corneal exposure can be avoided by using topical lubricants for the first 2 or 3 weeks after injection. You notice some loss of animation of the face after botulinum toxin injection, as you would expect. Patients rarely complain of this. You also notice that the crow’s feet and other wrinkles of the skin around the eye diminish because the orbicularis muscle is not pulling on the skin (this is the basis for the use of botulinum toxin injections to eliminate glabellar wrinkles in the patient seeking cosmetic improvement). A very small number of patients develop upper eyelid ptosis or double vision secondary to botulinum toxin–induced paresis of the levator muscle or extraocular muscles. Ptosis and diplopia are rare, troublesome side effects, which may last for 6 weeks but resolve completely with time.
Most patients see reduction in the blepharospasm after the initial dose of botulinum toxin. If the injections seem to lose their effectiveness over months and years, apraxia of the eyelid opening may be developing. As you know, during eyelid closure, the orbicularis muscle contracts and the levator muscle relaxes. As we discussed above, your patients think of essential blepharospasm as a spasm condition. You may need to explain that there is an element of persistent levator muscle relaxation involved, as well. Remember that many of your patients with essential blepharospasm may tell you that they feel better with their eyes closed. This is because it is a struggle for them to overcome the inhibition of the levator muscle seen with the apraxia component of essential blepharospasm. Early in the disease process, the orbicularis spasm predominates, and botulinum toxin reduces the spasm. If apraxia develops, the patient may perceive that the injections are no longer working. If this is the case when you ask the patient to close the eyes, you can see that the orbicularis muscle is still weak, and spasm is not the main cause of the inability to open the eyes. I am not a big believer that patients develop immunity to the botulinum. In all cases where the injections “fail” there seems to be a strong element of apraxia. Some relief of the apraxia of eyelid opening has been reported using frontalis sling surgery. I have found that this procedure can be helpful but is not entirely effective. Some injectors recommend a 1- to 2-unit injection into the central pretarsal orbicularis muscle for apraxia.
Surgical myectomy was popularized in the 1980s before the use of botulinum toxin became widespread. In this procedure, the orbital orbicularis, corrugator, and procerus muscles and portions of the preseptal and pretarsal orbicularis muscles are resected from the upper eyelid. Anatomic problems related to the constant spasm, such as dermatochalasis, eyelid ptosis, and brow ptosis, can be corrected at the same time. Surgical myectomy has been refined over recent years and remains a possible option for patients who do not get a satisfactory effect from botulinum toxin injections. Reports indicate approximately half of all patients undergoing myectomy continue to require botulinum toxin injections postoperatively, often at a reduced dose or frequency. Myectomy does not eliminate the apraxia of lid opening. For these reasons, I am not a strong advocate of myectomy. Although the role for surgical myectomy is limited, it seems that some patients with essential blepharospasm benefit from this procedure.
At this point you should:
Understand the mechanism and presentation of orbicularis myokymia, facial tics, hemifacial spasm, and essential blepharospasm.
Imagine a patient in your office with some facial spasm; while you listen to and watch the patient, use this information to make the diagnosis; remind yourself of the facial quadrant scheme.
Know that botulinum toxin injections are the mainstay of treatment for hemifacial spasm and essential blepharospasm; you should know how to treat these disorders. What are the main side effects of botulinum toxin?
Weakness of the Facial Muscles
Medical Conditions Associated With Facial Weakness
If you study the facial movements of your patients, you soon see abnormalities of decreased facial movement. The most common medical condition that you see is the masklike facies of the patient suffering from Parkinson disease. Many of these patients are seeing you for unrelated problems. Some are seeing you for watery eyes or corneal exposure symptoms related to a decreased rate and force of blinking.
The other patients you may see with decreased facial expression are those with myopathic ptosis. As you recall, these patients include those with oculopharyngeal dystrophy, chronic progressive external ophthalmoplegia (CPEO), and myotonic dystrophy. Often the patient is unaware that the facial movements are decreased, but the patient may develop corneal exposure after ptosis surgery.
Facial Nerve Palsy: History
The most common cause of decreased facial movement is facial nerve palsy. The most common form of unilateral facial weakness is Bell palsy. Other causes include local trauma and facial tumor or acoustic neuroma resection. You should pay particular attention to the corneal sensation if the facial palsy is the result of an acoustic neuroma resection. Because the fifth, seventh, and eighth nerves leave the brainstem in close proximity, resection may compromise fifth nerve function. A facial nerve palsy patient with a neurotrophic cornea may have corneal exposure that is difficult to manage. Tarsorrhaphy and serum drops may help with the usual lubrication schedule. A relatively new corneal reinnervation procedure has been recently developed for patients with unilateral loss of sensation. The contralateral supratrochlear nerve is dissected free, and an end-to-side coaptation of a sural nerve graft is made. The graft is tunneled across to the ipsilateral eye and sewn under the conjunctiva around the limbus. Variations in the technique are found. Reports indicate successful reinnervation of the cornea after this procedure. The procedure is new and not yet in widespread use.
Bell palsy is idiopathic by definition. It is a diagnosis of exclusion, so before making it be sure that the history and physical examination are consistent with this diagnosis. Bell palsy is presumed to result from a viral infection, most commonly, herpes. The associated swelling of the nerve within the bony canal causes compression and loss of function. The onset of the palsy is abrupt . Imaging is not indicated in patients with a typical presentation. If the diagnosis of Bell palsy is made, steroids given early in the course are worthwhile. Antiviral treatment does not seem to help these patients.
However, any gradual onset of, progression of, or associated cranial nerve deficit or parotid mass signals a different diagnosis, and imaging should be performed. In these cases, referral to an otolaryngologist is appropriate ( Figure 9.12 ). Similarly, if the typical case does not show improvement in 6 to 8 weeks the patient should be referred and imaging should be performed. There are no specific diagnostic laboratory tests to identify the cause of the facial palsy. Diabetic patients have a higher incidence of facial nerve palsy, so ordering hemoglobin A 1c and blood glucose levels is reasonable. Recurrent episodes are rare (<10%) and should be investigated thoroughly for tumor, hypertension, diabetes, or any familial predisposition to facial nerve palsy.
The role of the oculoplastic surgeon in managing facial nerve patients is to identify the atypical cases, make appropriate referrals, and manage early and late complications related to corneal exposure, tearing, and loss of peripheral vision. Most of the patients that we see have had the diagnosis already sorted out and are being referred for evaluation and treatment of the related ocular and periocular issues. Complaints of irritation, red eye, discharge, and tearing are common. Brow ptosis may interfere with the peripheral vision. The treatment that you offer depends, in part, on how permanent the palsy is likely to be. Talk with colleagues who are taking care of the patient with you and find out the likelihood of recovery. If, perhaps, a tumor resection required cutting the facial nerve, there is no chance of recovery. Surgical repair offering a long-term solution is needed. Alternatively, the nerve may have been contused, and full recovery is anticipated. Lubrication alone may be appropriate. Remember, most Bell palsy patients recover significant function over several weeks.
Facial Nerve Palsy: Physical Examination
The deficit in function ranges from mild paresis to complete paralysis ( Figure 9.13 ). After accidental or surgical trauma, the weakness may be confined to one or more branches. The loss of function to the frontalis muscle is particularly common after operations involving the temporal scalp because the innervation to the frontalis muscle is provided by a single nerve, the frontal nerve. Bell palsy patients lose function in all branches of the facial nerve.