Facial nerve palsy

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Facial nerve palsy
Classification and external resources
ICD-10 [1]51


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. 

Disease Entity[edit | edit source]

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

Disease[edit | edit source]

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.[1]  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.

Anatomy[edit | edit source]

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).[1] 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.[2]

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. [2]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.[2]  Of note, two of the terminal branches of CN 7 (temporalis and zygomatic branches) innervate the obicularis oculi muscle.[3]

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.[1]

Etiology[edit | edit source]

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.[4]

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[edit | edit source]

The overall prevalence of facial nerve palsy has been estimated at 2-3 cases per 10 000 people in the general population.[5] 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.[2] However, facial nerve palsy most commonly affects individuals aged 15-45 years. [2]

Of note, the most common cause of facial palsy is idiopathic facial nerve palsy, representing 51% of all CN 7 palsy cases.[2] 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.[6]

Diagnosis[edit | edit source]

History[edit | edit source]

A thorough history is essential to establishing the etiology of facial nerve palsy.

Patients may seek ophthalmologic attention because of eye redness, tearing, burning, and foreign body sensation.[7] Patients may also report dry eyes, excess tearing and inability to completely close their eyes. [7]

Non-ophthalmic complaints may include: facial asymmetry, overall facial muscle weakness, difficulty chewing, increased sensitivity to sound, altered taste sensation, and decreased salivation.[4]

Ophthalmologists should characterize the onset, duration, and severity of symptoms, as well as whether symptoms are present at rest or only upon voluntary movement.[2][4] 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 and history of trauma to the face.[4][2]

Physical examination[edit | edit source]

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 at the level of the upper motor neuron (no involvement of the forehead) or the lower motor neuron (forehead involvement).[1]

As part of a complete ophthalmic exam, assess visual acuity, extra-ocular movements, and pupillary movements.[2] Baseline optic disc evaluation is also recommended.[2]

The slit lamp examination of suspected facial nerve palsy focuses on the lids/adnexa, cornea, and conjunctiva. Make note of the following physical examination findings as part of the exam:[2][7][8]

  • Lids/Adnexa: eyebrow position, eyebrow movement, frontalis function, incomplete blink movement, palpebral fissure width, location of lower punctum, ectropion, lid retraction, lagophthalmos, and epiphora
  • Cornea: tear lake height and epithelial abrasion, laceration, or ulceration, results of Schirmer's test, corneal reflex
  • Conjunctiva: chemosis, hyperemia


Thorough examination of patients with CN 7 palsy warrants assessment of involvement of other cranial nerves. 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.[6]

Clinical diagnosis[edit | edit source]

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.[6]

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.[2]

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.[4] 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.[9]

Diagnostic procedures[edit | edit source]

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.[6]

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:[6]

  • 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    

Management[edit | edit source]

General treatment[edit | edit source]

The overall goal of treating facial nerve palsy is to maintain quality of life by protecting vision and retaining cosmesis.[8] 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.[2]

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.[7]

Medical therapy[edit | edit source]

Medical management is recommended for patients with low risk of corneal changes and a good prognosis for recovery.[2]

Initial conservative management aims to protect the cornea as facial nerve function recovers.[7] Patients should be instructed to lubricate the eye with methylcellulose based, preservative-free artificial tears three to four times per day. Additionally, overnight, patients should tape their eyelids closed and apply petroleum-jelly based lubricating ointment.[7] Punctal plugs may be useful in patients with reduced tear production unresponsive to the above measures.[2] 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.[2]

If conservative management fails, medical management should be pursued. Transcutaneous or subconjuncitval injection of botulinum toxin can paralyze the levator palpebrae superioris, thus inducing ptosis of the upper lid for approximately 6 weeks to protect the cornea.[2] [7][8]

The role of steroids and oral acyclovir in managing Bell’s Palsy remains debated. Current practice guidelines recommend starting oral steroids with 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.[6]

Surgery therapy[edit | edit source]

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 lag ophthalmos and its sequelae, implantation of a gold weight in the upper eyelid can be performed. The gold weight of typically 1.6-1.8 gm can be placed in either the pretarsal or prelevator aponeurosis space and aids in more complete closure of the eyelids. Alternatives to this procedure include palpebral springs, periocular silicon slings, and facial slings.[8][10]

Surgical treatment of upper lid retraction includes Muller’s myomectomy for 1-3 mm of retraction, and levator recession or retractor recession for retraction > 3 mm.[10]

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.[8] Alternatively, a fascia lata lower lid sling can be performed.[8][10]

Tarsorraphy, which partially sews upper and lower eyelids together, can provide either temporary or permanent corneal protection. Tarsorraphy can be performed at either the medial or lateral canthus via canthoplasty or tarsal strip. Alternatives include lateral canthal sling.[10]

Procedures to further improve a patient’s aesthetic appearance following facial nerve paralysis include surgical correction of brow ptosis (via direct, internal or endoscopic aprroach) and suborbicularis oculi fatpad lift.[8][10]

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.[4][6]

Complications[edit | edit source]

There are multiple complications of facial nerve palsy. Conservative management aims to limit the ophthalmic complications such as exposure keratitis and corneal drying.[2]

However, preventative measures cannot be taken against other hyperkinetic complications of facial nerve palsy including 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).[9] 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 secondary to axonal degeneration of the nerve.[11]

Lastly, patients may also find the facial asymmetry associated with seventh nerve palsy to be disfiguring.

Management of each of these hyperkinesias is similar, and involves a combination of facial physical therapy and use of botulinum toxin. Facial physical therapy can be used to compensate for synkinesis and to strengthen the muscles on the weaker side of the face in hemifacial spasm. By contrast, botulinum toxin is used to paralyze muscles, and is used in the management of synkinesis, hemifacial spasm, and in weakening the stronger side of the face in hemifacial spasm.[4][11][12]

Prognosis[edit | edit source]

The prognosis of facial nerve palsy depends on multiple factors. Prognosis of secondary facial facials depends on the success and management of the primary disease process. Idiopathic facial nerve palsy, such as Bell’s Palsy, resolves spontaneously in approximately 70% of patients within 6 weeks.[6]

Additionally, even if the palsy itself cannot be corrected, ophthalmologists can help manage symptoms and sequale 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.[13]

Additional Resources[edit | edit source]

References[edit | edit source]

  1. 1.0 1.1 1.2 1.3 Patestas M, Gartner L. A Textbook of Neuroanatomy. Malden, MA: Blackwell Publishing; 2006.
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 2.16 2.17 Rahman I, Sadiq S. Ophthalmic Management of Facial Nerve Palsy: A Review. Survey of a Ophthalmology. 2007; 52(2):121-144.
  3. Lorch M, Teach S. Facial Nerve Palsy: Etiology and Apporach to Diagnosis and Treatment. Pediatric Emergency Care. 2010;26: 763Y772).
  4. 4.0 4.1 4.2 4.3 4.4 4.5 4.6 Jackson C, von Doersten. The Facial Nerve: Current Trends in Diagnosis, TReatment, and Rehabilitation. Otolaryngology for the Internist. 1999; 83(1):179-195.
  5. Pieterson E. Bell's Palsy: The Spontaneous Course of 2,500 Peripheral Facial Nerve Palsies of Different Etiologies. Acta Otolaryngology Supplement. 2002;549: 4-30.
  6. 6.0 6.1 6.2 6.3 6.4 6.5 6.6 6.7 Baugh et al. Clinical Practice Guideline: Bell's Palsy. Otolaryngology- Head and Neck Surgery. 2013; 149(3S); S1-S27.
  7. 7.0 7.1 7.2 7.3 7.4 7.5 7.6 Sohrab M, Abugo U, Grant M, Merbs S. Management of the Eye in Facial Paralysis. Facial Plastic Surgery. 2015;31:140144.
  8. 8.0 8.1 8.2 8.3 8.4 8.5 8.6 Harrison A, Lee E. Management of the Facial Nerve Palsy Patient: Update and Pearls. American Academy of Ophthalmology. http://www.aao.org/current-insight/management-of-facial-nerve-palsy-patient-update-pe. Accessed [8/11/15].
  9. 9.0 9.1 Ziahosseini, Nduka Cm Malhotra R. Ophthalmic Grading of Facial Paralysis: Need for a Closer Look. British Journal of Opthalmology. 2015; 0: 1-5.
  10. 10.0 10.1 10.2 10.3 10.4 Lee V, Currie Z, Collin JRO. Ophthalmic Management of Facial Nerve Palsy. Eye. 2004; 18: 1225-1234.
  11. 11.0 11.1 Valls-Sole J. Handbook of Clinical Neurology: Chapter 20- Facial Nerve Palsy and Hemifacial Spasm. 2013: 367-380. 
  12. Borodic G, Bartley M, Slattery W, et al. Botulinum toxin for aberrant facial nerve regeneration: doubleblind, placebo controlled trial using subjective endpoints. Plast Reconstr Surg. 2005;116(1):3643.
  13. Henstrom D, Lindsar R, Cheney M, Hadlock, T. Surgical Treatment of the Periocular Complex and Improvement of Quality of Life in Patients with Facial Paralysis. Archives of Facial Plastic Surgery. 2011;13(2):125-128.