Ophthalmic Management of Facial Nerve Paralysis

by Steven C. Dresner, M.D., June 2000 (Illustrations by Christine Gralapp)

Introduction

Patients with facial nerve paralysis may present to the ophthalmologist primarily with symptoms of corneal exposure related to poor eyelid closure, or may be referred by a colleague for the management of these symptoms.  An understanding of the anatomy of the facial nerve and the etiology of the facial nerve paralysis is essential in managing the patient’s symptoms with medical treatment or surgical rehabilitation.

Anatomy

The facial nerve, cranial nerve VII, is divided into four anatomic segments: supranuclear, nuclear, fascicular, and peripheral nerve.  The supranuclear neurons that innervate the facial nerve nucleus lie in the precentral gyrus of the frontal lobe (see Figure 1).

Figure 1. Topographic anatomy of the facial nerve.

Discharges from the motor face area are carried through fascicles of the corticobulbar tract to the internal capsule, descending through the upper mid-brain to the lower brain stem, where they synapse in the facial nerve nucleusFacial nerve paralysis diagram. located in the pons.  The corticobulbar tracts for the upper face cross and recross in reaching the facial nerve nucleus.  The tracts for the lower face are crossed only (see Figure 2a).

The facial motor nucleus is in the lower third of the pons, beneath the fourth ventricle.  In this area, the facial nerve is proximal with cranial nerves VI and VIII.  The facial nerve emerges from the brain stem with the vestibular acoustic nerve at the cerebellopontine angle.  The nervus intermedius (responsible for tearing, salivation, and taste) is between these two nerves and carries facial nerve sensory and parasympathetic information.  The anteroinferior cerebellar artery courses between cranial nerves VII and VIII.  A tortuous anteroinferior cerebellar artery or posteroinferior cerebellar artery (PICA) or other vessels in this area may compress the facial nerve to produce hemifacial spasm.

The facial nerve traverses the temporal bone through the internal auditory canal with the nervus intermedius and the acoustic nerve.  Leaving the acoustic nerve, the facial nerve enters the fallopian canal, where it courses serpiginously for approximately 30 mm through the labyrinthine tympanic and mastoid segments.  The labyrinthine segment of the facial nerve includes the geniculate ganglion, which yields the first branch of the facial nerve, the greater petrosal nerve.  This branch carries secretory motor fibrils to the lacrimal gland.  The motor branches of the facial nerve leave the fallopian canal at the skull base through the stylomastoid foramen.  The facial nerve immediately enters the parotid gland, within which the main trunk of

the nerve usually divides into superior (temporofacial) and inferior (cervicofacial) divisions.  Branching patterns in the temporal, zygomatic, buccal, mandibular, and cervical branches, vary among individuals (see Figure 2b ).  Illustration of facial nerve branches.The numerous interconnections among these branches correlate with the clinical picture seen with aberrant regeneration following facial nerve paralysis.  The temporal branch of the facial nerve exits the parotid gland and runs within the superficial muscular aponeurotic system over the zygomatic arch and temple to enter the frontalis muscle.  The nerve is particularly vulnerable to damage over the zygomatic arch and to a lesser extent in the lateral brow, and may be injured in facial rhytidectomy or with coronal or endoscopic brow lifting.

Workup for Diagnosis of Facial Nerve Paralysis Signs and Symptoms of Facial Nerve Paralysis

Patients may present to the ophthalmologist with a variety of symptoms associated with facial nerve paralysis that may suggest an etiology.  Pain behind the ear or in the mastoid region may accompany facial nerve paralysis.  Although this pain is usually associated with the Ramsay Hunt syndrome, or herpes zoster, it may also be seen in approximately 50% of patients with Bell’s palsy.  If numbness of the face is present, a lesion within the temporal bone or a compressive disorder at the brain stem or cerebellopontine angle should be suspected.

Dryness of the eye, a common symptom, may be secondary to diminished tear production resulting from a lesion at or proximal to the geniculate ganglion affecting sympathetic innervation.  More often, however, dryness is linked to ectropion, lid retraction, a poor blink mechanism, and lagophthalmos.  The patient may also have conjunctival injection, corneal drying changes, or frank corneal ulceration.

Presentations of eyelid and eyebrow malposition in facial nerve paralysis will differ according to the age of the injury and the etiology.  Most commonly, the patient presenting with the combination of eyebrow ptosis, lower eyelid retraction, and ectropion has acute facial nerve paralysis.  This patient also has a poor blink mechanism and lagophthalmos.  Patients with an early paresis or a permanent paralysis may also have upper eyelid retraction.

An upper eyelid mechanical ptosis is secondary to eyebrow ptosis.  In an old facial nerve paralysis with aberrant regeneration, the eyelid fissures may be narrowed.  Facial movement, such as smiling, or chewing may exacerbate the narrowing.  Chewing causes tearing, another common manifestation of aberrant regeneration.

Lower facial weakness can suggest supranuclear lesions involving the descending motor pathways; lower facial weakness associated with weakness of the arm, fingers, and hand on the same side as the facial weakness usually suggests a cortical lesion.  Peripheral facial nerve palsies associated with hearing loss and/or abducens palsies suggests a pontine lesion.  Hemifacial spasm suggests that a tortuous anteroinferior or posteroinferior cerebellar artery or other vessels in this area may be compressing the facial nerve.

Etiologies of Facial Nerve Paralysis

The etiology of facial paralysis will help determine whether the paralysis is permanent or whether the causes are treatable.  It is therefore important that the physician take a full medical history, the first step being to document the onset and duration of the facial paralysis.  Idiopathic paresis or paralysis of the facial nerve, or Bell’s palsy, is the most common cause of facial nerve weakness.  Nevertheless, other specific causes should be considered.  Consultation with an otolaryngologist is advisable, because early diagnosis and treatment can shorten the course of paralysis in some cases.  The possible causes for consideration follow.

A history of diabetes is important, because these patients may have a higher incidence of facial nerve weakness.

Sarcoidosis can cause either unilateral or bilateral facial nerve paralysis.

Because immunizations for polio or influenza have been associated with facial nerve weakness, an immunization history should be obtained.

A recent onset of a viral illness may also be related to a facial nerve palsy.  Some physicians use valacyclovir to treat Bell’s palsy, addressing the possibility that the paralysis may represent a viral neuronitis.

Lyme disease may lead to a facial paralysis.  The rash of Lyme disease, known as erythema chronicum migrans, consists of multiple expanding ring lesions with central clearing.  A history of this rash in a geographical area where tick bites are endemic may also be helpful in the diagnosis.

Herpes zoster cephalicus, or the Ramsay Hunt syndrome, is a frequent cause of facial nerve paralysis.  The varicella-zoster virus is the usual cause.  This syndrome consists of pain in the affected ear, facial nerve paralysis, and vesicles on the auricle or external auditory canal, and may also be associated with hearing loss, tinnitus, and dizziness.

Acute otitis media with or without mastoiditis in children or adults can lead to facial nerve paralysis.  Acute or chronic osteitis in the fallopian canal is also a possible cause.

A history of carcinoma in a patient with facial nerve paralysis should be investigated to rule out metastasis or local tumor involvement of the facial nerve anywhere along its course.  Appropriate radiologic imaging such as computerized tomography or magnetic resonance imaging is also indicated.

A schwannoma is the most common neoplasm of the facial nerve.  The slow, progressive onset of facial nerve paralysis from this tumor contrasts to the acute onset of paralysis in Bell’s palsy.

Malignancies of the parotid gland may also affect the facial nerve; a palpable or visible mass in the vicinity of this gland is usually apparent on exam.

Acoustic neuromas cause facial nerve paralysis by compression at the cerebellopontine angle.  The patient may also present with hearing loss, tinnitus, or other neurologic signs or symptoms.

Trauma to the facial nerve can occur with fractures to the temporal bone or the mandible or during surgery to the mandible.  The temporal branches of the facial nerve are particularly vulnerable to trauma over the zygomatic arch and over the temple superolateral to the brow.

Ocular Exam

The ocular exam gives the ophthalmologist an assessment of the condition of the patient’s eyes and can help confirm the etiology.  The ocular exam should include slit-lamp biomicroscopy and testing for acuity and for corneal sensation.  Extraocular motility should be evaluated and documented.  The tear film should be assessed and basic Schirmer testing performed.

The upper and lower eyelid positions should be examined.  The margin-reflex distance one (MRD1) and margin-reflex distance two (MRD2) –upper eyelid and lower eyelid to pupillary light reflex, respectively– should be documented.  The eyebrow position, blink mechanism, and amount of lagophthalmos with gentle closure should be examined.  The presence or absence of Bell’s phenomenon can be assessed by having the patient close the eyes while the examiner pulls the upper eyelids upward with moderate force.

The facial musculature should be assessed to differentiate a partial paresis from a complete facial nerve paralysis.  Having the patient forcefully close the eyes against the examiner’s resistance approximates the orbicularis force.  Both sides of the face are examined and compared.  Aberrant regeneration is elicited by having the patient open the mouth wide or by smiling or chewing.  If aberrant regeneration is present, the upper eyelid will often come down, and the lower eyelid may ride up as well.

The head, neck, and hearing should also be examined.  The auricle and pinna should be examined to evaluate for the vesicles of herpes zoster.  Hearing can be roughly assessed by whispering in each ear or by rubbing fingers and thumb together next to each ear, with the patient comparing the difference on each side.  The parotid gland should be palpated, since infiltrative tumors may produce a facial nerve paralysis.  Head and neck adenopathy should be evaluated because the presence of nodes may indicate an infectious or neoplastic process.

Medical Management

If recovery from a paresis is expected, medical management alone should suffice for the duration.  All patients with facial nerve paralysis are at risk for punctate keratopathy, corneal ulceration, and/or perforation.  Artificial tears and lubricating ointments are the mainstays of the medical management of facial nerve paralysis.  Artificial tears should be liberally applied every hour, or every half hour if necessary.  If lagophthalmos is evident or is suggested by the corneal exam, then lubricating ointment should be used at night.  Patients with more severe symptoms may need ointment during the day and/or more viscous artificial tear supplements.

Taping of the eyelids at night can be helpful in selected patients.  If upper eyelid retraction is prominent, the upper eyelid can be taped down to the cheek after ointment is applied.  Usually, lower eyelid retraction and ectropion are more prominent, requiring, in addition to ointment, that the cheek be taped up to the brow.  Patients for whom this method is uncomfortable may be better served with commercially available moist chambers or swimming goggles in addition to ointment.  Patching by the patient or family is often incomplete and can allow the cornea to be exposed under the patch.

Surgical Management

When medical management by itself will not prevent corneal complications or when recovery from facial paralysis is not expected, surgical rehabilitation should be considered.  The specific anatomic abnormalities presenting and the patient’s symptoms should dictate the choice of surgical method for managing problems caused by the facial nerve paralysis.  A temporary lateral canthoplasty, or tarsorrhaphy, can be performed in emergent situations to promote corneal healing. However, permanent tarsorrhaphy should be avoided if possible.  Newer procedures, including gold weight implantation and elevation of the lower eyelid with grafts, are better options for less urgent cases because they preserve peripheral vision and compromise cosmetic appearance less.  A medial canthoplasty is a useful addition to these procedures in patients who continue to have corneal exposure.

Lateral Canthoplasty

The most common eyelid malposition seen with facial nerve paralysis is ectropion (see Figure 3a).  Lateral canthoplasty is the mainstay of surgical rehabilitation; it is the most efficient and anatomic approach to lower eyelid shortening.  Shortening the lower eyelid at the lateral canthus avoids vertical blepharotomy or wedge resection.  An incision is made at the lateral canthus with a 15 blade.  The canthoplasty is completed with a Stevens scissors.  The inferior crus of the lateral canthal tendon is cut with the needle tip of the monopolar cautery.  The eyelid is pulled laterally and marked for shortening.

With a facial nerve paralysis, it is prudent to tighten the lowerIllustration: Tarsal strip is sewn to the inner lateral orbital rim. eyelid as much as possible, since there is usually
poor orbicularis tone and recurrences of ectropion are common.  The tarsus is separated from the orbicularis and skin, and a new lateral canthal tendon is fashioned out of the lateral tarsus.  The mucocutaneous margin is trimmed.  The lower eyelid retractors are detached from the lower margin of the tarsal strip.  The strip is shortened appropriately and reinserted on the inner lateral orbital rim through the periosteum with a 4-0 polypropylene suture and tied temporarily (see Figure 3b).  The patient can then be examined for tone and contour.  An overcorrection is desirable, with the lateral canthus residing at least 2 mm or more above the level of the medial canthus.  A second 4-0 polypropylene suture is passed on the lower portion of the tarsal strip, and both are tied.  Remnants of the anterior lamella are laterally trimmed, and the wound is closed with 6-0 or 5-0 plain sutures (see Figure 3c).

Medial Canthoplasty

Medial canthoplasty is a useful adjunct to lateral canthoplasty in patients with facial nerve paralysis.  The addition of a medial canthoplasty will improve closure and minimize lagophthalmos.  Local anesthetic with epinephrine and hyaluronidase is injected in the lower and upper eyelids medially.  The upper and lower puncta are dilated, and a 00 Bowman probe is passed into the upper and lower canaliculi.  A V-shaped incision is made medial to the punctum in both upper and lower eyelids (see Figure 4a).  The anterior and posterior lamella are separated by making a small skin and muscle flap.  The posterior lamella from the lower lid is sewn to the posterior lamella of the upper lid with a series of 6-0 polygalactic sutures (see Figure 4b).  Care must be taken to avoid injury to the canaliculi.  The anterior lamella is sewn together with vertical mattress sutures of 6-0 plain (see Figure 4c).

Lower Eyelid Retraction

Many patients with facial nerve paralysis have some degree of lower eyelid retraction and mid-facial ptosis that lateral and medial canthoplasty will not completely address.  These patients can be helped with grafts of either hard palate (Figure 5a) or ear cartilage to the posterior lamella with lateral canthoplasties.  Hard palate grafts are preferable in most cases because they are stiff but pliable and give the best cosmetic results.  Ear cartilage grafts, however, can be used when very large grafts are desirable or the patient refuses hard palate surgery.

The hard palate is harvested from the lateral aspect of the palate 3-4 mm from the adjacent molars and incisors.  The submucosal tissues are infiltrated with local anesthetic with epinephrine.  The graft is harvested freehand with a 15 blade.  Absorbent gelatin sponge (Gelfoamâ) can be placed in the palatal defect, and a hard palate stent can be fabricated by a dentist.  If the patient wears dentures, these will serve as a stent.

The canthoplasty begins with a lateral canthal incision using a 15 blade.  The canthoplasty is completed with Stevens scissors.  A 4-0 silk traction suture is placed through the lid margin.  With the needle point of the cautery, an incision is made through the conjunctiva and lower lid retractors at the lower tarsal border.  A pocket is developed in which to place the graft, which recesses the lower eyelid retractors and helps support the lid at a higher position.  Usually, a 2:1 graft-to-retraction ratio is desired; thus, 2 mm of lower eyelid retraction requires a 4 mm graft.  The graft is cut into a pennant shape and sewn into the lower tarsal plate with 6-0 plain suture, and the lower portion of the graft is sewn to the conjunctiva and lower lid retractors in a similar fashion (see Figure 5a).  The lateral canthus is tightened with a tarsal strip as previously described.  Figure 5b shows a patient after medial canthoplasty and Figure 5c showsthe patient after both medial and lateral canthoplasties with lower lid elevation (see Figures 5b & 5c).Photograph of hard palate graft set in eyelid.

Another useful adjunct in patients with significant mid-facial ptosis is to perform a subperiosteal cheek lift in conjunction with a posterior lamella graft and canthoplasty.  This procedure elevates the cheek and midface and may prevent recurrent lid retraction and/or ectropion.

Upper Eyelid Retraction

Patients with lagophthalmos may benefit from gold weight implantation.  Patients with upper eyelid retraction should be considered for levator aponeurosis recession with or without a gold weight.  Gold weights are available in sizes ranging from 0.6-1.6 g in 0.2-g increments.  These implants are placed in the upper lids to correct retraction and to assist in closure.  Before hard palate graft and lateral canthoplasty.The size of the weight is determined preoperatively in the office with the patient seated.  Fitting weights can be purchased, or a few weights can be kept in stock and tried in the office.  A trial weight is applied to the upper pretarsal eyelid with double-stick tape or benzoin, and the patient is examined (see Figures 6a & 6b). The goal is improved or complete closure with 1 mm of induced ptosis or less.  Usually, 1.2-1.4 g are adequate for implantation.

The gold weight can be autoclaved.  It is surgically implanted with a central 1.0-1.5 cm lid crease incision.  Dissection is taken down through the orbicularis to the tarsal plate.  The weight is inserted and sewn to the upper tarsus with three 6-0 braided nylon sutures (see Figure 6c).  The orbicularis is closed with a series of 6-0 polygalactic sutures and the wound closed with running 6-0 polypropylene sutures.After hard palate graft and lateral canthoplasty.

The advantages of gold weight implantation include simplicity of insertion and a low extrusion rate; the disadvantages include its occasional visibility through the dermis and the need for gravity assistance in its effectiveness.  The use of a stainless steel spring to help reanimate the upper eyelid presents neither disadvantage: the spring’s thinness makes it invisible in the upper eyelid, and it does not need gravity assistance.  Its disadvantages include the technical difficulty of the operation, the need for postoperative adjustment, and a fairly high extrusion rate.  It is, however, useful in patients with profound facial nerve paralysis after tumor surgery where no return in function is expected.  Successful implantation of springs requires a surgeon experienced in the technique.

Ptosis and Brow Ptosis Surgery

Many patients with facial nerve paralysis will have brow ptosis that can cause mechanical ptosis of the upper eyelid.  For patients with severe exposure and lagophthalmos, it is better to rehabilitate the upper and lower eyelids to improve closure and attend to the eyebrow position at a later date if necessary.  However, for those who do not have severe exposure or for those with partial recovery, eyebrow surgery can be performed at the same time as eyelid surgery to reposition the eyebrow to a more anatomic position.

To most effectively raise and stabilize the eyebrow position in the patient with facial nerve paralysis, eyebrow surgery is best performed either directly over the brow or in the midforehead. A trial weight is applied to the eyelid. Endoscopic brow surgery is not useful for unilateral brow ptosis and usually does not significantly elevate the brow in such a patient.  Trans-eyelid browpexy is also not as effective as direct browplasty, and may further weaken the eyelid protractors or orbicularis force.

The amount of brow ptosis is assessed preoperatively with the patient seated.  An elliptical incision is marked over the brow.  The subcutaneous tissues are infiltrated with local anesthetic with epinephrine.  The incision is begun with a 15 blade.  The brow tissue is excised with a scissors or with the cutting cautery.  The incision is deeper laterally, but does not need to extend down to the periosteum (see Figure 7a).  As the excision proceeds medially, a shallower dissection is made to avoid injury to the supraorbital neurovascular bundle.
The subcutaneous tissues inferiorly in theGold weight is sewn to the upper tarsus. incision are fixed to the deeper tissues and periosteum superiorly with a series of 4-0 polypropylene sutures tied firmly but not tight.  The wound can be closed with vertical mattress sutures of 4-0 polypropylene (see Figure 7b). Usually, a slight undercorrection is desirable to avoid further lagophthalmos.

Patients who have recovered from a Bell’s palsy may have varying amounts of aberrant regeneration.  This may be manifested as minimal ptosis in the upper eyelid.  But the ptosis is often exacerbated with eating, chewing, or smiling.  In sympomatic patients, botox can be used to lessen the effect of aberrant regeneration, although care must be taken to avoid further weakening of the facial and eyelid musculature.

The Müller’s muscle conjunctival resection procedure is an excellent operation, in the setting of post-Bell’s palsy with aberrant regeneration, to elevate the ptotic eyelid and yet avoid lagophthalmos with corneal exposure.  The Muller’s muscle conjunctival resection procedure can correct from 1-3 mm of ptosis in patients with a positive phenylephrine test.  This technique plicates Muller’s muscle via an internal approach.  Since no skin incision is required, the protractors are not weakened further in a condition in which they are already compromised.  The increase in ptosis with facial animation remains undiminished, but the procedure does allow the lid fissures to be better normalized, and it lessens the tendency for the lid to encompass the pupillary axis with facial movement.

Facial Reanimation Surgery

The temporalis muscle can be used to reanimate the face in long-standing facial paralysis where the fifth cranial nerve is intact.  The temporalis muscle can function as a motor activator to the cheeks, upper lip, and nasolabial fold.  Although strips from the temporalis muscle with attached fascia can also be placed into the upper and lower eyelid as slings, this method is much less satisfactory than mid- and lower facial reanimation.  Through an extended facelift incision, the temporalis muscle and deep temporalis fascia can be harvested (see Figure 8a).  The central portion of the muscle is mobilized from the bony temporalis fossa, reflected over the zygomatic arch, and then sewn to the nasolabial fold and the corner of the mouth.  Fascial extensions are used if necessary.

Overcorrection at the time of surgery is necessary to better establish facial tone.  The defect in the tempIe can be replaced by a temporalis fossa implant if desired.  The postoperative patient can initiate movement of the face or smiling by chewing or biting the teeth together.  Mid- and lower facial reanimation in conjunction with lower eyelid resuspension and either gold weight or eyelid spring can give very gratifying results, as Figures 8b and 8c show; patients’ general appearance and psychological well-being are greatly improved, and their vision is preserved and protected as well.

Conclusion

The ocular signs and symptoms of facial nerve weakness include ectropion, lid retraction, lagophthalmos, Patient before reanimation surgery.brow ptosis, and impaired blinking resulting in dryness of the eye.  The patient’s medical history and ocular exam determine whether medical treatment alone will suffice or whether the condition requires surgical correction.  If surgery is required, the patient’s specific anatomic abnormalities and symptoms dictate the choice of surgical method.  Although the patient’s comfort and cosmetic appearance are important considerations, preserving or restoring corneal health is the chief goal of surgery.