42 Facial Nerve

Question 1

What types of nerve fibers are carried by the facial nerve?

Answer 1

What types of nerve fibers are carried by the facial nerve?

The facial nerve carries both motor and sensory nerve fibers (Figure). These include:

• Special visceral efferent: Motor innervation of the muscles of facial expression, stylohyoid, stapedius, platysma, and posterior belly of the digastric muscle
• General visceral efferent: Parasympathetic innervation of the lacrimal, submandibular, sublingual, minor salivary, mucosal glands of the nose, and palate
• Special sensory afferent: Taste from the anterior two thirds of the tongue, palate, and tonsillar fossa
• Somatic sensory afferent: Sensation from the external ear canal and skin of the concha portion of the auricle
• General visceral afferent sensory: Sensation from the nasal mucosa, palate, and pharynx

Question 2

What branchial arch is associated with the facial nerve during development?

Answer 2

What branchial arch is associated with the facial nerve during development?

Second branchial arch. All muscles innervated by the facial nerve are second arch derivatives, as well as the stapes suprastructure, styloid process, stylohyoid ligament, and the lesser cornu of the hyoid.

Question 3

Name the three anatomic segments of the fallopian canal, their course, and their length.

Answer 3

Name the three anatomic segments of the fallopian canal, their course, and their length.

• Labyrinthine segment: From fundus of IAC (meatal foramen) to the geniculate ganglion; 3 to 5 mm. The labyrinthine segment represents the narrowest portion of the fallopian canal at 1 mm.
• Tympanic segment: From geniculate ganglion to pyramidal process; 8 to 11 mm. Begins at the second genu (the first genu is intrapontine). The bony covering of the facial nerve is often dehiscent in this segment. This is the most common site of iatrogenic injury during ear surgery
• Mastoid segment: From pyramidal process to stylomastoid foramen; 10 to 14 mm

Question 4

What is the nervus intermedius?

Answer 4

What is the nervus intermedius?

The nervus intermedius is a division of the facial nerve that carries its nonbranchial motor components. It is anatomically adjacent to but separate from the main trunk of the facial nerve as it exits the brainstem and then fuses with the facial nerve within the internal auditory canal. The chorda tympani is the terminal extension of the nervus intermedius.

Question 5

What is the chorda tympani?

Answer 5

What is the chorda tympani?

The chorda tympani carries parasympathetic innervation to both the submandibular and sublingual glands and special sensory afferents from the anterior two thirds of the tongue. It branches off from the mastoid segment of the facial nerve and traverses the middle ear before exiting the tympanic cavity through the petrotympanic fissure to join the lingual branch of the trigeminal nerve. Stretching or cutting of this nerve during middle ear surgery produces transient taste alteration.

Question 6

What is the pes anserinis?

Answer 6

What is the pes anserinis?

The pes anserinus (“goose’s foot”) is the first major branching of the extratemporal facial nerve after it leaves the stylomastoid foramen. This branching usually splits the nerve into upper and lower divisions. More distally the branching is variable but normally forms five major branches (see Figure):

• Temporal: frontalis, corrugator supercilii, procerus, and upper orbicularis oculi
• Zygomatic: lower orbicularis oculi
• Buccal: zygomaticus major and minor, levator anguli oris, buccinator, and upper orbicularis oris
• Marginal mandibular: lower orbicularis oris, depressor anguli oris, depressor labii inferioris, and mentalis
• Cervical: platysma

Question 7

During parotid surgery, what are the landmarks for identifying the facial nerve?

Answer 7

During parotid surgery, what are the landmarks for identifying the facial nerve?
There are a number of methods to find the main trunk:

• Identify the tragal pointer, which is a triangular extension of the tragal cartilage. The main trunk of CN VII typically lies 10 mm inferior and 10 mm deep to this landmark.
• Follow the posterior belly of the digastric muscle to the styloid process. The stylomastoid foramen lies deep to this structure and is where the nerve exits the temporal bone. Typically it is 25 mm deep to the skin’s surface. NOTE: In children under the age of 2 the mastoid is not well developed, and the facial nerve lies much closer to the surface of the skin than would otherwise be expected.
• Find the tympanomastoid fissure. The nerve can be found 6 to 8 mm inferior to the end of the fissure.
• Identify a peripheral branch (e.g., marginal mandibular) and follow it proximally.
• Perform a mastoidectomy to find the mastoid portion of the nerve and follow it out of the stylomastoid foramen.

Question 8

What are the three types of nerve injury?

Answer 8

What are the three types of nerve injury?

• Neuropraxia results when a lesion stops the axoplasm flow within an axon, blocking electrical conduction. Examples would include traumatic swelling or pharmacologic blockade. The nerve is viable and returns to normal function when the blockade is corrected. Electrophysiologic testing reveals normal function, except that the electromyogram fails to show voluntary motor action potentials because they are not conducted across the blockade.
• Axonotmesis is a state of Wallerian degeneration distal to the lesion with preservation of the motor axon endoneural sheaths. Examples would include mild crush or stretch injuries. Electrically, the nerve shows rapid and complete degeneration, with loss of voluntary motor units. Regeneration to the motor end plates will occur, as long as the endoneural tubules are intact.
• Neurotmesis is characterized by both Wallerian degeneration and loss of endoneural tubules. Electrophysiologic studies yield evidence of complete nerve degeneration. Regeneration is dependent on many factors, including the integrity of the endoneurium, perineurium, and epineurium and the extent of ischemia and scarring around the lesion.

Question 9

What is synkinesis?

Answer 9

What is synkinesis?

If a facial nerve lesion results in Wallerian degeneration, subsequent axon regeneration may result in “cross-wiring” in which voluntary movement of one facial muscle group induces involuntary movement of another. For example, after recovering from a facial palsy a patient may have squinting whenever he or she smiles. Although this is usually thought to occur from aberrant routing of regenerating axons, it is also proposed to be the result of ephaptic transmission (abnormal connections between axons) and postsynaptic hyperexcitability.

Question 10

What is the House-Brackmann Facial Nerve Grading System?

Answer 10

What is the House-Brackmann Facial Nerve Grading System?

This grading system is used to classify the degree of function of the facial nerve following its recovery after injury (Table 42-1).

Question 11

What is Bell’s palsy?

Answer 11

What is Bell’s palsy?

Bell’s palsy is the most commonly diagnosed cause of facial paralysis. The etiology is thought to be a viral neuropathy caused by the herpes simplex virus. Most importantly, it is a diagnosis of exclusion with the following minimum diagnostic criteria:

• Paralysis or paresis of all facial muscle groups on one side of the face
• Sudden onset
• Absence of signs of central nervous system (CNS) disease, ear disease, or a parotid mass

It often follows a viral prodrome with a typical 3- to 5-day duration and a peak in symptoms at 48 hours. The patient may have a widened palpebral fissure, diminished taste, difficulty chewing, hyperesthesia in one or more branches of the fifth cranial nerve, facial pain, and hyperacusis. In 14% of patients with Bell’s palsy, family history will be positive. Some 12% of patients may have recurrent facial paralysis, either ipsilateral or contralateral.

HSV has been shown to be present within the geniculate ganglion of affected individuals, in contrast to the normal population in which this is rare. It has been proposed that reactivation of this virus in the geniculate ganglion causes swelling and subsequent paralysis. Bell’s palsy accounts for roughly 70% of acute facial palsies. However, it is important to remember that this is a diagnosis of exclusion.

Question 12

List the common etiology categories of facial paralysis.

Answer 12

List the common etiology categories of facial paralysis.

• Congenital: Möbius syndrome, congenital unilateral lower lip paralysis, Melkersson-Rosenthal syndrome, dystrophic myotonia
• Traumatic: Temporal bone fractures, intrauterine compression, birth trauma/forceps delivery, facial contusions or lacerations, penetrating wounds to face or ear, iatrogenic injury (parotid/ear/cranial surgery, embolization for epistaxis, mandibular block anesthesia)
• Infection: Bell’s palsy, herpes zoster oticus, otitis media with effusion, acute mastoiditis, malignant otitis externa, tuberculosis, Lyme disease, acquired immunodeficiency syndrome, mononucleosis, influenza, encephalitis, malaria, syphilis, botulism
• Idiopathic: Recurrent facial palsy
• Neoplasia: Cholesteatoma, carcinoma, acoustic neuroma, meningioma, facial neuroma, glomus jugulare or tympanicum, leukemia, hemangioblastoma, osteopetrosis, histiocytosis, rhabdomyosarcoma
• Metabolic/systemic: Diabetes, hyperthyroidism, pregnancy, autoimmune disorders, sarcoidosis, hypertension
• Neurologic: Guillain-Barré syndrome, multiple sclerosis, Millard-Gubler syndrome

Question 13

What elements of the history and physical examination are important in evaluating a facial paralysis?

Answer 13

What elements of the history and physical examination are important in evaluating a facial paralysis?

With a good history, the wide differential diagnosis listed above can be narrowed significantly. Identifying factors for systemic and/or infectious causes is mandatory. Any palsy with slow progression or without improvement after 3 months should be considered a neoplasm until proven otherwise. Additional signs of possible tumor involvement include facial twitching, other cranial nerve involvement, hearing loss, recurrent episodes of facial paralysis, a mass behind the tympanic membrane or in the parotid gland, unilateral eustachian tube dysfunction, skin lesions suggesting skin cancer, and/or prolonged ear pain.

Bell’s palsy and herpes zoster oticus may also have associated numbness in the middle and lower face, otalgia, hyperacusis, decreased tearing, or altered taste sensation.

Question 14

How can you distinguish whether the lesion causing facial paralysis is peripheral or central?

Answer 14

How can you distinguish whether the lesion causing facial paralysis is peripheral or central?

A unilateral central lesion (supranuclear) will spare the upper face, since these muscles receive both crossed and uncrossed fibers. Lesions of the peripheral system involve both the upper and the lower face. A central lesion is also suggested by the lack of emotional facial movement as well as decreased lacrimation, taste, and salivation on the ipsilateral side. Cortical lesions are also frequently associated with tongue or hand dysfunction.

Question 15

Which radiologic studies should be part of the diagnostic workup for a patient with a facial paralysis?

Answer 15

Which radiologic studies should be part of the diagnostic workup for a patient with a facial paralysis?

Routine radiologic tests are not indicated for the assessment of every patient presenting with a facial nerve paralysis. The need for such studies is based on both the clinical history and the course of the paralysis (i.e., if a neoplasm is suspected). If radiologic imaging is deemed necessary, high-resolution computed tomography (CT) or magnetic resonance imaging (MRI) are the studies of choice. MRI scans are superior to CT in imaging the nerve at the cerebellopontine angle and internal auditory canal. Gadolinium-enhanced MRI is the test of choice for facial nerve paralysis secondary to inflammatory, neoplastic, and other nontraumatic etiologies. CT, on the other hand, is preferred for the evaluation of traumatic seventh nerve paralysis and other etiologies involving the temporal bone such as cholesteatoma.

Question 16

What is Schirmer’s test?

Answer 16

What is Schirmer’s test?

Schirmer’s test is a method to assess parasympathetic innervation to the lacrimal gland via the greater superficial petrosal nerve. The procedure entails placing small filter paper strips in the conjunctival fornix of each eye and measuring lacrimation by comparing the length of paper moistened by tear flow over a 5-minute period. An abnormal Schirmer’s test occurs with <15 mm lacrimation or a 25% reduction as compared to the contralateral eye.

Question 17

Describe the electrophysiologic tests that are important in evaluating a patient with a facial paralysis?

Answer 17

Describe the electrophysiologic tests that are important in evaluating a patient with a facial paralysis?

• Nerve Excitability Test (NET): In this study, a 1/sec2 wave pulse, which is 1 msec in duration, is applied over both the affected and the unaffected facial nerves. Thresholds for minimal facial muscle response are recorded and compared. A 3- to 4-mA or greater difference is considered significant, suggesting denervation. This test is not accurate during the first 72 hours after onset of paralysis, since it takes 3 days for Wallerian degeneration to occur.
• Maximal Stimulation Test (MST): A variation of the NET, the MST stimulates the ipsilateral and contralateral facial muscles at a level sufficient to depolarize all motor axons underlying the stimulator. Therefore, it utilizes maximal as opposed to minimal stimulation to evaluate muscular response. The results of the test are recorded as a subjective account of the difference in facial muscle movement between the normal and involved sides. Generally, it is thought that the MST becomes abnormal before the NET and is therefore a better prognostic indicator. However, the MST is limited by its lack of objectivity.
• Electroneuronography (ENoG): ENoG measures and compares the amplitudes of the muscle summation potentials that are elicited when a supramaximal level of current is applied over the main trunk of the facial nerve on the affected and unaffected sides. The peak-to-peak amplitude is directly proportional to the number of intact motor axons, thus providing a gauge to assess neuronal degeneration. For example, an evoked summation potential of 5% to 10% indicates 90% degeneration. This test is commonly used to predict who may benefit from a surgical facial nerve decompression. Just like the MST, it is only accurate after Wallerian degeneration has occurred so it must be performed more than 72 hours after onset of symptoms. To accurately predict which patients may benefit from surgical decompression, ENoG must be performed within 2 weeks of the onset of symptoms.
• Electromyography (EMG): EMG is complementary in the evaluation of acute facial paralysis, helping to eliminate false positive results obtained by NET, MST, and ENoG. The EMG determines the activity of the muscle rather than the activity of the nerve. This test can (1) provide information regarding intact motor units in the acute phase and (2) confirm the integrity of intact axons in the recovery phase, detecting reinnervation potentials 6 to 12 weeks before the return of facial muscle function is clinically evident. However, unlike NET, MST, and ENoG, an EMG cannot assess the degree of degeneration or prognosis for recovery.
• Audiometry: Audiometry should be performed to evaluate for conductive and sensorineural hearing losses. Conductive hearing losses are most consistent with middle ear tumors, cholesteatomas, and other middle ear processes involving the tympanic segment of the facial nerve. Sensorineural hearing losses may indicate neoplastic conditions such as acoustic neuroma, meningioma, and facial nerve neuromas, which affect the nerve in the cerebellopontine angle or internal auditory canal.

Question 18

What is the most important complication following the onset of facial paralysis?

Answer 18

What is the most important complication following the onset of facial paralysis?

Exposure keratitis in the eye of the affected side can lead to vision loss. It is caused by (1) paralysis with inability to close the eyelid completely, (2) diminished tearing, and (3) loss of corneal sensitivity if there is coexistent trigeminal nerve dysfunction. Evidence for corneal irritation includes redness, itching, foreign-body sensation, and visual blurring. Avoidance of this complication involves using artificial tears 4 to 5 times/day. While sleeping, ophthalmic lubricant should be instilled along with taping the eyelid shut. The eye should be protected from wind, foreign bodies, and drying with glasses and/or moisture chambers. Surgical placement of a gold weight within the eyelid can facilitate full closure in complete paralysis. An ophthalmology consult should be obtained for these patients.

Question 19

What are crocodile tears?

Answer 19

What are crocodile tears?

Injuries to the facial nerve may be associated with aberrant nerve regeneration. Fibers that normally innervate the salivary glands may regenerate to innervate the lacrimal gland. This leads to “crying” when the patient eats (gustatory tearing). Similarly, these fibers can regenerate to innervate sweat glands in the skin, leading to gustatory sweating (Frey’s syndrome).

Question 20

How do you treat facial nerve paralysis medically?

Answer 20

How do you treat facial nerve paralysis medically?

• If infectious processes are involved, appropriate treatment with antimicrobial and/or antiviral agents, in addition to eradication of the infectious nidus (i.e., mastoidectomy/ myringotomy) should be instituted.
• A course of oral steroids, if initiated within the first 72 hours after onset of symptoms, may improve recovery via decreased inflammation.
• Electrophysiologic assessment of the extent of nerve damage provides valuable information, particularly in cases in which surgical decompression may be a treatment option.
• Prophylactic eye care to protect against exposure keratitis should be initiated in all patients with a facial nerve paralysis.
• For Bell’s palsy, specifically, the current recommendation for treatment is (1) oral steroids to begin within 72 hours of onset of symptoms, (2) optional oral acyclovir in addition to steroids if started within 72 hours of onset of symptoms, and (3) eye care.

Question 21

When is surgical treatment for the facial nerve indicated?

Answer 21

When is surgical treatment indicated?

Surgical intervention may take multiple forms depending on the etiology of the facial nerve lesion. Bony decompression of the facial nerve may improve recovery in certain cases where total paralysis is present with evidence of rapid severe nerve degeneration. Serial studies with ENoG have shown that when the number of motor fibers falls to less than 10% of normal (tested prior to day 14 post-onset), the recovery rate of normal function is substantially decreased. It is therefore at this level that surgical exploration/decompression is most likely to be considered. In Bell’s palsy, swelling in the labyrinthine segment causes an entrapment neuropathy, which is decompressed via a middle fossa craniotomy.

Question 22

If the nerve is cut during surgery, can it be fixed?

Answer 22

If the nerve is cut during surgery, can it be fixed?

Yes. Several techniques may be employed for repairing a transected or partially transected nerve. A common clinical rule of thumb is that if greater than 50% of the nerve is transected, it should be repaired.

Direct anastomosis involves repair of the perineurium with exact end-to-end approximation. An 8-0 monofilament suture is used to approximate the nerve ends together without tension at the anastomosis. Grafting can also be utilized if there is loss of a segment of the nerve; great auricular or sural nerves can be used for interposition grafts. Jump grafts from other cranial nerves (such as CN XII) have also been used successfully to reanimate the facial muscles in cases in which the proximal facial nerve is not present. Cross nerve grafts connected to the contralateral facial nerve can also be used.

Question 23

What is the association between facial nerve paralysis and otitis media? Mastoiditis? Cholesteatoma?

Answer 23

What is the association between facial nerve paralysis and otitis media? Mastoiditis? Cholesteatoma?

In otitis media (OM), facial palsy can present as a complication of acute suppurative OM, OM with effusion, and chronic OM. The palsy results from an inflammatory reaction or bacterial toxins within the bony fallopian canal. In both mastoiditis and cholesteatoma, compression of the nerve and inflammatory response can result in facial nerve palsy.

The mainstay of treatment, particularly if the palsy is a complication of OM, is to eradicate the infection with a combination of aggressive antibiotic therapy and surgical drainage via myringotomy or tympanomastoid surgery. Facial palsy secondary to coalescent mastoiditis can be managed surgically with myringotomy followed by a mastoidectomy. The presence of cholesteatoma requires surgical management.

Question 24

Describe the most common traumatic injuries to the facial nerve.

Answer 24

Describe the most common traumatic injuries to the facial nerve.

Traumatic injuries to the facial nerve generally fall within two categories, penetrating wounds and temporal bone fractures.

Penetrating wounds of the cheek, face, or parotid gland may lacerate the facial nerve trunk or one of its branches. Nerve injuries such as these can often be repaired with direct anastomosis. Generally, the results of facial nerve repairs are good; however, repairs of the main trunk usually result in synkinesis during the regenerative process.

Temporal bone fractures involve the facial nerve via laceration or contusion injury within the bony fallopian canal. Eighty to ninety percent of temporal bone fractures are longitudinal (parallel to the petrous bone) and will have an associated facial nerve injury only 20% of the time. In contrast, transverse temporal bone fractures (perpendicular to the petrous bone) account for only 15% of cases but have an associated facial nerve injury about 50% of the time. A facial paralysis that occurs immediately following nonpenetrating head trauma is suggestive of laceration or impingement of the nerve within the bony fallopian canal. In these instances, surgical exploration with decompression or repair may be required. If, however, the paralysis develops in a delayed fashion, medical management with steroids and electrophysiologic monitoring to map the course of recovery are indicated.

Question 25

What are the most common facial nerve tumors?

Answer 25

What are the most common facial nerve tumors?

The two most common facial nerve tumors are facial schwannomas (facial neuromas) and geniculate ganglion hemangiomas. Facial schwannomas arise from the myelin-producing Schwann cells. Hemangiomas of the geniculate ganglion arise from the vascular plexus surrounding the ganglion. These tumors are often observed initially but many will require treatment due to growth and/or progressive facial nerve paralysis.

Question 26

What are herpes zoster oticus and Ramsay Hunt syndrome?

Answer 26

What are herpes zoster oticus and Ramsay Hunt syndrome?

Herpes zoster oticus is characterized by intense ear pain and vesicles on the external auditory canal and concha. It is caused by reactivation of the dormant herpes zoster (chickenpox) virus within the afferent sensory neurons of the facial nerve. If this progresses to involve the efferent motor axons of the facial nerve, a facial palsy can result. When both a facial palsy and painful vesicles are present, it is referred to as Ramsay Hunt syndrome. Hearing loss and vertigo may also occur. Treatment includes narcotic analgesics for pain relief, oral corticosteroids to decrease inflammation, and acyclovir to inhibit viral DNA replication. Topical antibiotic drops may also be used if there is concern for secondary bacterial otitis externa. Additionally, the facial paresis may affect eyelid closure and place the orbit at risk for dryness and excoriation and possible permanent damage.