Facial nerve palsy

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Original article contributed
Sohani Amarasekera, Raymond Clifford, MD
by:
All contributors: Cat Nguyen Burkat, MD FACS and Raymond Clifford, MD
Assigned editor: Cat Nguyen Burkat, MD FACS
Assigned status Up to Date by Cat Nguyen Burkat, MD FACS on January 31,
Review:
2017.

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.

Contents
[hide]

 1 Disease Entity
o 1.1 Disease
o 1.2 Anatomy
o 1.3 Etiology
o 1.4 Epidemiology and Risk Factors
 2 Diagnosis
o 2.1 History
o 2.2 Physical examination
o 2.3 Clinical diagnosis
o 2.4 Diagnostic procedures
 3 Management
o 3.1 General treatment
o 3.2 Medical therapy
o 3.3 Surgery therapy
o 3.4 Complications
o 3.5 Prognosis
 4 Additional Resources
 5 References
 Disease Entity
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
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
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
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

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
History
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
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
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
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
General treatment
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
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
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
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
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
 American Academy of Ophthalmology. Oculoplastics/Orbit: Facial nerve palsy Practicing
Ophthalmologists Learning System, 2017 - 2019 San Francisco: American Academy of
Ophthalmology, 2017.

References
1. ↑ Jump up to:1.0 1.1 1.2 1.3 Patestas M, Gartner L. A Textbook of Neuroanatomy. Malden, MA: Blackwell
Publishing; 2006.
2. ↑ Jump up to: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. Jump up↑ Lorch M, Teach S. Facial Nerve Palsy: Etiology and Apporach to Diagnosis and
Treatment. Pediatric Emergency Care. 2010;26: 763Y772).
4. ↑ Jump up to: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. Jump up↑ 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. ↑ Jump up to: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. ↑ Jump up to: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;31:140–144.
8. ↑ Jump up to: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. ↑ Jump up to: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. ↑ Jump up to: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. ↑ Jump up to:11.0 11.1 Valls-Sole J. Handbook of Clinical Neurology: Chapter 20- Facial Nerve Palsy and
Hemifacial Spasm. 2013: 367-380.
12. Jump up↑ 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. Jump up↑ 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.

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