Facial Nerve Palsy
Facial nerve palsy includes both paralysis and weakness of the seventh cranial nerve. There are multiple etiologies of facial nerve palsy, and Bell’s palsy (idiopathic, acute onset unilateral facial nerve palsy) is the most common cause. Ocular signs and symptoms of facial nerve palsy include inability to close the eye, dry eye syndrome, as well as eye redness, tearing, burning, and foreign body sensation. Conservative management of ophthalmic complications of facial nerve palsy include instilling artificial tears, applying lubricating ointment, and taping the eyelids closed, while surgery is reserved for refractory cases with limited potential for recovery. Overall, the prognosis of facial nerve palsy depends on the cause of the palsy, and ophthalmologists have an important role in managing the symptoms and limiting the sequelae of this condition.
Facial Nerve Palsy: ICD-10 Codes
- G51 Facial nerve disorders
- G51.0 Bell's palsy
- G51.1 Geniculate ganglionitis
- G51.2 Melkersson's syndrome
- G51.3 Clonic hemifacial spasm
- G51.4 Facial myokymia
- G51.8 Other disorders of facial nerve
- G51.9 Disorder of facial nerve, unspecified
Facial nerve palsy includes both paralysis (complete loss of function) and paresis (weakness) of the seventh cranial nerve (CN 7). CN 7 is a mixed nerve providing both sensory afferents and motor efferent fibers.
Of significance to ophthalmologists, CN 7 has both a visceral motor branch that responds to parasympathetic stimuli and a somatic motor branch. The visceral motor fibers of CN 7 innervates the lacrimal gland, stimulating reflexive tearing of the ipsilateral eye. The somatic motor fibers of CN 7 innervates all three parts of the obicularis oculi muscle (palpebral, orbital, and lacrimal) that functions to close the ipsilateral eyelid and draw tears towards the lacrimal punctum. As a result, facial nerve palsy can result in loss in any of these functions. Additionally, patients may present with unilateral or bilateral facial nerve palsy.
Three nuclei make up the facial nerve including the facial nerve nucleus (somatic motor fibers), the superficial salivary nucleus (parasympathetic fibers), and the nucleus tractus solitarius (special sensory fibers). The facial nerve originates from these nuclei at the ponto-meduallary junction of the brain stem. CN7 then follows a complex course that is both intra- and extra-cranial in location.
The intracranial portion of the nerve consists of both a motor and sensory root and travels through the internal acoustic meatus through the temporal bone and becomes the geniculate ganglion. The geniculate ganglion is responsible for parasympathetic innervation of the lacrimal gland. It also gives rise to the greater petrosal nerve that travels through the stylomastoid foramen and is responsible for the sensory functions of CN 7.
Upon exiting the stylomastoid foramen, the facial nerve becomes extra-cranial, and travels through the parotid gland, giving off five terminal branches that provide the somatic motor functions of CN7 responsible for facial expression. Of note, two of the terminal branches of CN 7 (temporal and zygomatic branches) innervate the obicularis oculi muscle.
Facial nerve lesions can occur at any point during the course of the facial nerve and localization of the lesion is initially guided by the patient’s presenting history and physical examination findings. Typically, the combination of sensory and motor symptoms correlate to intra-cranial CN 7 pathology, while isolated motor symptoms are associated with extra-cranial CN 7 lesions.
There are numerous possible etiologies of facial nerve palsy that can be broadly classified into the following areas: idiopathic, congenital, infectious, traumatic, inflammatory, neoplastic, and an iatrogenic.
For a complete list of such etiologies, see Jackson C, von Doersten. The Facial Nerve: Current Trends in Diagnosis, Treatment, and Rehabilitation. Otolaryngology for the Internist. 1999; 83(1):179-195.
Epidemiology and Risk Factors
The overall prevalence of facial nerve palsy has been estimated at 2-3 cases per 10,000 people in the general population. Facial nerve palsy affects individuals regardless of sex, age, or race. Currently, there is no clear consensus on whether males or females are affected more frequently. However, facial nerve palsy most commonly affects individuals aged 15-45 years. 
Of note, the most common cause of facial palsy is idiopathic facial nerve palsy, representing 51% of all CN 7 palsy cases. While sometimes considered to be synonymous with idiopathic facial nerve palsy, Bell’s palsy is specifically defined as acute onset (<72 hours) idiopathic, unilateral facial nerve palsy that resolves spontaneously.
A thorough history is essential to establishing the etiology of facial nerve palsy.
Non-ophthalmic complaints may include: facial asymmetry, synkinetic movement of the eye and mouth, overall facial muscle weakness or spasticity, difficulty chewing, difficulty enunciating certain words or sounds, increased sensitivity to sound, altered taste sensation, and decreased salivation.
Ophthalmologists should characterize the onset, duration, and severity of symptoms, as well as whether symptoms are present at rest or only upon voluntary movement. Given the myriad causes of facial nerve palsy, it is also important to document any associated symptoms (such as fever, rash, other neurologic deficits, tick exposure, weight loss), systemic medical conditions (diabetes mellitus, pregnancy, hyperthyroidism, neoplasia), medications, toxic exposures, prior facial surgeries, and history of trauma to the face.
Patients should also be asked about history of prior skin cancers of the face since squamous cell carcinoma that becomes recurrent or deeply invasive can result in facial pain and eventually progress to facial nerve palsy.
Gross physical examination of the face should note any facial asymmetry and whether the patient presents with unilateral or bilateral involvement of CN 7. Also, involvement of the forehead and periocular region indicates whether the lesion is at the level of the upper motor neuron (no involvement of the forehead) or the lower motor neuron (forehead involvement).
- Lids/Adnexa: eyebrow position, eyebrow movement, frontalis function, incomplete or delayed blink, orbicularis oculi function, ocular synkinesis (with opening the mouth or puckering the lips), palpebral fissure width, location of lower punctum, ectropion, lid retraction, lagophthalmos, and epiphora
- Cornea: tear lake height, punctate epithelial erosions/epithelial defects/ulcers, corneal thinning/neovascularization/pannus formation, corneal reflex
- Conjunctiva: chemosis, hyperemia
Thorough examination of patients with CN 7 palsy warrants assessment of other cranial nerve functions. CN 2, 3, 4, and 6 are assessed as part of the ophthalmic exam as above. Sensory components of CN 5 can be evaluated by assessing sensation on the forehead and upper eyelid (ophthalmic division) as well as along the lower eyelid (maxillary division). CN 8 travels with CN 7 through the internal acoustic meatus, so referral to otolaryngology should be considered.
Facial nerve palsy is a clinical diagnosis based on history and physical examination. Further workup of facial nerve palsy is dictated by clinical suspicion of the underlying cause of facial weakness. Bell’s Palsy is a diagnosis of exclusion.
Complete assessment of facial nerve palsy should address the chronicity, severity, and laterality of the palsy, and comment on whether the palsy is either primary or secondary, and if lesion is likely a proximal or distal lesion.
Importantly, objective grading of the severity of facial nerve palsy remains difficult. Overall, the most widely used scale of facial nerve palsy is the House-Brackmann scale. However, the only ophthalmic manifestation of facial nerve palsy assessed in this scale is eye closure. Therefore, currently, there is no universal scale available to document and assess the complete spectrum of ophthalmic presentations of facial nerve palsy.
Given that facial nerve palsy is a clinical diagnosis, and that the most common cause of facial nerve palsy is idiopathic, routine imaging, serology, or other testing is not necessary.
However, features suggestive of facial nerve palsy secondary to an underlying cause may require additional workup. As a result, Clinical Practice Guidelines state that the following tests may be ordered to aid in diagnosis or prognosis of facial nerve lesions:
- Imaging—Computed tomography (CT) or magnetic resonance imaging (MRI)—to identify potential infection, tumor, fractures, or other potential causes for facial nerve involvement
- Electrodiagnostic testing to stimulate the facial nerve to assess the level of facial nerve insult
- Serologic studies to test for infectious causes
- Hearing testing to determine if the cochlear nerve or inner ear has been affected
- Vestibular testing to determine if the vestibular nerve is involved
The overall goal of treating facial nerve palsy is to maintain quality of life by protecting vision and improving morbidity and disfigurement. A framework for approaching the management of facial nerve palsy was developed by Seiff and Chang and specifies how interventions target the complications of facial nerve palsy at several stages after the initial insult.
To achieve these goals, both medical and surgical options for management of facial nerve palsy are available. Typically, conservative and medical management strategies are used in patients whether there is potential for facial nerve recovery, while surgical options are typically reserved for cases in which these is no potential for recovery from facial paralysis.
Medical management is recommended for patients with low risk of corneal changes and a good prognosis for recovery.
Initial conservative management aims to protect and lubricate the cornea to prevent exposure keratopathy. Patients are instructed to use artificial tears and can use an artificial tear gel at bedtime for lagophthalmos. Additionally, patients can tape their eyelids closed and apply petroleum-jelly based lubricating ointment if there is significant lagophthalmos. Punctal plugs may be useful for persistent dry eyes. Lower lid ectropion can be managed by applying tape to the lower lid. Patching and padding of the affected eye should be avoided to prevent accidental corneal abrasion.
If conservative management fails, medical management should be pursued. Transconjunctival injection of botulinum toxin into the upper lid can weaken the levator palpebrae superioris and induce ptosis of the upper lid for approximately 4-6 weeks to protect the cornea.  It is important to make sure to inject the levator muscle and not inject too superficially, as injecting into the orbicularis oculi muscle will further worsen lagophthalmos.
The role of steroids and oral acyclovir in managing Bell’s Palsy remains debated. Current practice guidelines recommend starting oral steroids within 72 hours of symptom onset in patients older than 16 years of age diagnosed with Bell's palsy. However, these guidelines strongly recommend against the use of oral acyclovir as monotherapy for facial nerve palsy attributed to Bell’s palsy.
For facial symmetrization, botulinum toxin can be injected to improve brow position or asymmetric frontalis action, to address ocular synkinesis, to address smile asymmetry of the upper or lower lips, to improve spasticity of the mentalis and platysma muscle, or to reduce lacrimation and tearing either due to synkinesis or inadequate tear drainage.
When clinical judgment suggests that there is limited likelihood of functional improvement in facial nerve function, surgery can be performed to limit corneal complications of facial nerve palsy.
To reduce lagophthalmos and its sequelae, implantation of a gold or platinum weight in the upper eyelid can be performed. The weight typically is 1.0-1.8 gm and can be placed in either the pretarsal or prelevator aponeurosis planes to assist with more complete eyelid closure. 
Surgical treatment of upper lid retraction includes Mullerectomy surgery for 1-3 mm of retraction, and levator recession or legator-mueller's muscle recession for retraction > 3 mm.
Paralytic ectropion secondary to lower lid laxity can be addressed using lateral tarsal strip procedure with an additional posterior lamellar spacer graft for more severe cases. Alternatively, a fascia lata lower lid sling can be performed.
A tarsorrhaphy, which partially sews the upper and lower eyelids together, can provide either temporary or permanent corneal protection. It can be performed laterally and/or medially depending on the extent of lagophthalmos and exposure keratopathy.
Conjunctivodacryocystorhinostomy (cDCR) surgery with Jones tube can be used to address tearing due to an impaired lacrimal pump function and weakened orbicularis oculi.
Procedures to further improve a patient’s aesthetic appearance following facial nerve paralysis include surgical correction of paralytic brow ptosis and face lift or facial sling to address the facial droop and increased jowling on the paralytic side.
Surgical decompression of the seventh cranial nerve is a procedure performed by otolaryngologists and is limited to only a subset of Bell’s palsy patients. Facial reanimation surgery is mainly geared toward allowing patients to smile again on the paralytic side and is typically performed by an ENT facial plastic surgeon.
There are multiple complications of facial nerve palsy. Conservative management aims to limit the ophthalmic complications such as exposure keratopathy.
However, there are no preventative measures that can be taken to prevent synkinesis, hemifacial spasm, and facial asymmetry.
A disabling complication of facial nerve palsy is synkinesis, in which involuntary movements accompany voluntary facial movements. The most common synkinesis is movement of the mouth with voluntary eye closure (ocular-oral synkinesis). However, many other examples of synkinesis secondary to facial nerve palsy have been reported, including gustatory lacrimation (or crocodile tear syndrome). The mechanism underlying such synkinesis remains unclear.
Hemifacial spasm, or involuntary muscle contractions of one side of the face, can occur as part of the post-facial paralytic syndrome.
Lastly, patients may also find the facial asymmetry associated with seventh nerve palsy to be disfiguring. Botulinum toxin injection and working with a facial therapist can help with facial function, symmetry. A facial therapist can help patients compensate for synkinesis and strengthen the muscles on the weaker side of the face. By contrast, botulinum toxin can weaken spastic or synkinetic muscles, reduce hemifacial spasm, and weaken the stronger side of the face to improve facial symmetry.
The prognosis of facial nerve palsy depends on multiple factors. Prognosis of secondary facial nerve palsy depends on the success and management of the primary disease process. Idiopathic facial nerve palsy, such as Bell’s Palsy, improves spontaneously in approximately 70% of patients within 6 weeks.
Additionally, even if the palsy itself cannot be corrected, the ophthalmologist can help manage symptoms and sequelae of this condition. Thus, treatments such as those listed above (medical, surgical, and physical therapy), have been found to greatly improve the quality of life of facial nerve palsy patients.
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