EDUCATION PRACTICE

PRACTICE POINTER
Assessment and management of facial nerve palsy
• Link to this article online
for CPD/CME credits Liam Masterson,1 Martin Vallis,2 Ros Quinlivan,3 Peter Prinsley4
1
Ear, Nose, and Throat Department, The facial nerve is important for both communication and When an upper motor neurone lesion is suspected, it
Cambridge University Hospitals expression, and impairment of its function can severely may help to determine whether this is localised to the
NHS Trust, Cambridge CB2 0QQ, UK
2
Rosedale Surgery, NHS Great
affect quality of life.1 The main concern at first presenta- brainstem or cerebral cortex. Brainstem disease may
Yarmouth and Waveney Clinical tion of a facial nerve lesion is to exclude the possibility present with vertigo, ataxia, or crossed neurology signs
Commissioning Group, Lowestoft, of a stroke or other serious cause.2 The figure outlines (ipsilateral cranial nerve involvement and contralateral
UK
3
possible causes. Correct management within the first few hemiplegia). A cortical lesion often affects the contralat-
MRC Centre for Neuromuscular
Disease, National Hospital for days may prevent long term complications. eral limbs and involuntary movements of the face, such
Neurology and Neurosurgery, as spontaneous smiling, may be spared.6 Urgent referral
London, UK How is it assessed? to secondary care (neurology or acute medical unit) is
4
Ear, Nose, and Throat Department,
The facial nerve is responsible for motor supply to the needed at this stage to assess the need for thrombolysis.
Norfolk and Norwich University
Hospital NHS Trust, Norwich, UK muscles of facial expression (frontalis, orbicularis oculi,
Correspondence to: L Masterson buccinators, and orbicularis oris) and stapedius, para- Lower motor neurone
[email protected] sympathetic supply to the lacrimal and submandibular Once a central cause for facial palsy has been excluded,
Cite this as: BMJ 2015;351:h3725
glands, and sensory input from the anterior two thirds of perform a focused examination of the ears, mastoid
doi: 10.1136/bmj.h3725
the tongue. Thus, as well as a facial droop, patients may region, oral cavity, eyes, scalp, and parotid glands to
present with a dry eye, reduced corneal reflex, drooling, look for the specific signs in the table. Bell’s palsy is
hyperacusis, altered taste, otalgia, and speech articula- an idiopathic lower motor neurone (LMN) facial nerve
tion problems.5 paralysis that accounts for most new cases (incidence
10-40/100 000 population each year). 3  7 However,
Upper motor neurone 30-41% of patients with LMN facial nerve weakness will
After identifying the affected side, it is important to estab- have another cause that requires specific management
lish whether an upper motor neurone lesion is respon- and is often associated with a poorer prognosis.2‑4
sible for the facial weakness. Although not an infallible Bell’s palsy is a diagnosis of exclusion, made only
sign,3 classic neurology describes a bilateral innervation after excluding features in the table. Epidemiological
of that part of the facial nuclei supplying the forehead, studies suggest that it normally develops fully within
and thus preserving forehead movement in upper motor 24-48 hours.3  4 Most cases (60%) are associated with
lesions. Lower motor neurone disorders of the main nerve mild post-auricular pain. Incidence does not differ sig-
trunk result in a weakness of the entire side of the face. nificantly with ethnicity or sex, but diabetes is associated
Patients may have risk factors for stroke, which include with as many as 10% of cases, and it occurs more often
older age (>60 years), hypertension, previous stroke or in the last trimester of pregnancy (three times baseline
transient ischaemic attack, diabetes, high cholesterol, risk).8 Incomplete facial nerve paralysis at presentation
smoking, and atrial fibrillation.6 Corroborative evidence (some residual muscle movement and partial closure of
may also be found by examining for abnormalities in the eyelid) is a good prognostic sign, indicating a 94%
other cranial nerves and the peripheral nervous system— chance of full recovery, as opposed to 61% in those with
increased tone, limb weakness, hyper-reflexia, upgoing complete paralysis.3
plantars, and sensory loss.4 The next most common cause of facial nerve paraly-
sis is trauma (accidental or surgical). Accidental trauma
includes any sharp or blunt mechanism of injury, such as
HOW PATIENTS WERE INVOLVED IN THE CREATION OF THIS ARTICLE
facial laceration, stab injury, or temporal bone fracture.
We sought feedback on the paper from patient and medical representatives of the charity
Facial Palsy UK. We incorporated their comments into the paper and developed a patient Detection of a temporal bone fracture is essential because
consultation guide for management and prognosis of Bell’s palsy (see box below) of the 90% risk of associated intracranial disease.9 A post-
mortem correlation study indicates that periorbital bruis-
ing (racoon sign), mastoid bruising (Battle’s sign), and
THE BOTTOM LINE blood in the ear canal have a positive predictive value of
85%, 66%, and 46%, respectively, for detecting a tempo-
• In patients presenting with facial weakness, the first priority is to exclude
an upper motor neurone lesion; important associated signs may include ral bone fracture.10 Cerebellopontine angle and middle
concurrent limb weakness, hyper-reflexia, upgoing plantars, or ataxia ear surgical procedures are the main causes of iatrogenic
injury, which may also be seen after procedures carried
• Check for causes of a lower motor neurone lesion by examining the ears,
mastoid region, oral cavity, eyes, scalp, and parotid glands out on the parotid gland or any other region along the
facial nerve.4
• Bell’s palsy is a diagnosis of exclusion, and oral steroids are needed within
After infection by herpes zoster virus, a geniculate
72 hours to increase the chance of complete recovery. Prognosis is usually
ganglionitis causes a prodrome of otalgia and vesicular
good compared with other causes of lower motor neurone weakness, such as
tumours and Ramsay Hunt syndrome eruption within the ear canal, with or without spread to
the oral cavity. Facial paralysis (Ramsay Hunt syndrome)
• Eye protection is crucial if lid closure is impaired normally follows this and is associated with sensorineu-

32 19 September 2015 | the bmj

 EDUCATION PRACTICE

Facial nerve palsy

Lower motor neurone (forehead muscles affected) Upper motor neurone (forehead muscles not affected)
for example, cortical or brainstem infarct, intracranial tumour

Idiopathic (59-70%) Traumatic (10-23%) Viral (4.5-7%) Neoplastic (2.2-5%) Other (3-5%)
Bell’s palsy Temporal bone fracture Herpes zoster virus Acoustic neuroma Acute or chronic
latrogenic (post-surgical) (Ramsay Hunt syndrome) Parotid malignancy otitis media
Sharp/blunt facial trauma Malignant otitis externa
Birth canal trauma Lyme disease*
Misdiagnosed†

Differential diagnosis of a unilateral facial palsy. Percentages are based on combined epidemiological data from 6024 patients
with lower motor neurone facial palsy (rarer conditions including mumps, syphilis, HIV, Guillain-Barré syndrome, otitic
barotrauma, myasthenia gravis, systemic lupus erythematosus, sarcoidosis, and multiple sclerosis have been excluded).3  4
*Endemic in forested regions; †misdiagnosed cerebrovascular disease evident in about 1.5% of all patients3

ral hearing loss and vertigo in 40% of cases owing to Red flags for urgent referral
involvement of cranial nerve VIII.6 Patients with Ramsay These include potential upper motor neurone causes
Hunt syndrome generally have a poorer prognosis than (such as limb paresis, paraesthesia of the face or limbs,
those with Bell’s palsy, with only 21% showing full recov- involvement of other cranial nerves, postural imbal-
ery at 12 months.3 ance), trauma, features suggesting cancer (such as
A slowly progressive onset of facial weakness is sug- gradual onset, persistent facial paralysis >6/12, pain
gestive of cancer.3  5 In addition, cancer may be asso- within the facial nerve distribution, ipsilateral hearing
ciated with pain or paralysis of select branches of the loss, suspicious head or neck lesion, previous regional
nerve, such as zygomatic (eyelid) or marginal mandib- cancer), and acute systemic or severe local infection.
ular (angle of mouth) branches.7 There may be a his- Urgent paediatric referral is warranted in children, for
tory of regional cancer. A thorough examination of the whom Bell’s palsy is less likely to be a cause of facial
head and neck region will be needed to look for cervical weakness (<50% of cases).5
lymphadenopathy, a parotid mass, or a scalp lesion in
particular. Acoustic neuromas account for about 80% Treatments applicable to all patients
of cerebellopontine angle lesions and most cases of Eye care is paramount for those with corneal exposure.
tumour related LMN facial nerve paralysis; they can be To prevent ulceration or dehydration of the cornea,
differentiated from other causes by ipsilateral sensori- apply artificial tears (such as hypromellose drops) every
neural hearing loss (95% of cases) and absence of the one or two hours during the day. At night, keep the eye
corneal reflex (60%).4  11 moist by using a thin strip of paraffin based ointment
Bacterial infections are responsible for 1-4% of new (such as Lacrilube) and secure the upper eyelid in the
cases of LMN facial palsy.3  4 Acute otitis media accounts closed position by applying permeable synthetic tape
for most and is associated with systemic sepsis, a bulg- (http://www.facialpalsy.org.uk/advice/guides/how-
ing tympanic membrane, conductive hearing loss, and to-tape-eyes-shut/433). All cases of incomplete eyelid
pinna lateralisation. Malignant otitis externa (or, more closure require urgent ophthalmology consultation at
accurately, skull base osteomyelitis) is characterised by presentation.
lack of sleep due to otalgia. More than 95% of cases are Some cases of LMN facial palsy will need to be referred
seen in older people (>65 years), immunocompromised to the ear, nose, and throat department or another hos-
people, and those with poorly controlled diabetes.12 The pital specialty. Such cases include all patients with
condition is associated with Pseudomonas aeruginosa atypical symptoms (see table) and those with suspected
infection.12 Lyme disease is a bacterial infection caused Bell’s palsy who do not respond to a trial of oral pred-
by a tick bite that results in facial nerve paralysis in one nisolone (observe for maximum of two to three weeks).
in 10 seropositive patients.13 Post referral tests may include computed tomography
or magnetic resonance imaging to visualise the skull
How is it managed? base, stylomastoid foramen, and parotid gland; blood
Management is influenced strongly by the initial clinical tests (full blood count, urea, and electrolytes); pure
review and provisional working diagnosis. With an LMN tone audiography; and topographical studies (such as
lesion, the main priority is to treat the underlying cause, Schirmer’s test, taste sensation, and stapedial reflex).
to improve symptoms, and to reduce associated morbid- Electroneuronography can guide prognosis in cases of
ity, such as contracture of the facial muscles, synkinesis complete paralysis, but this test is expensive, time con-
(involuntary movement of one part of the face due to aber- suming, and it has a short window of opportunity after
rant re-innervation), and autonomic dysfunction (croco- onset of symptoms (less than three weeks). In the case
dile tears or hemi-facial spasm). In Bell’s palsy, routine of longstanding facial palsy, impairment of eye closure
investigations in the primary care setting are no longer may require insertion of a gold weight into the upper
recommended.2 eyelid or lateral tarsorrhaphy.14

the bmj | 19 September 2015 33

 EDUCATION PRACTICE

Clinical signs to check in lower motor neurone facial nerve palsy

Are the ears clear on otoscopy? Assess the tympanic membrane and ear canal; acute or chronic otitis media (±cholesteatoma) and malignant otitis externa can all cause lower motor neurone
facial palsy and will require further urgent assessment in secondary care (ear, nose, and throat)
•Is there
Link ipsilateral hearing loss?
to this article online Perform Weber’s and Rinne’s tuning fork tests; although Ramsay Hunt syndrome will be associated with sensorineural hearing loss (SNHL), it is important to
for CPD/CME credits exclude a cerebellopontine angle lesion (normally presents with gradual onset unilateral SNHL); acute otitis media or cholesteatoma may be associated with
conductive hearing loss, whereas patients with Bell’s palsy normally have abnormal sensitivity to loud sounds
Is there a rash? Small vesicular eruptions that affect the tympanic membrane, ear canal, external pinna, or oral cavity may indicate Ramsay Hunt syndrome; Lyme disease is
restricted to heavily forested regions and presents with a characteristic erythematous “bullseye” lesion on the limbs or trunk (70% of cases), arthralgia, and facial
swelling; it is caused by a bite from a tick carrying Borrelia burgdorferi (US) or B afzalii/garinii (Europe), and an antibody test may help confirm the diagnosis13
Are there any bruises or scars in The palsy may be secondary to a skull base fracture (common associated signs include periorbital or mastoid bruising, blood in the ear canal, and
the head and neck region? haemotympanum)9 or recent mastoid, parotid, or submandibular gland surgery
Is the corneal reflex intact on both In addition to facial muscle weakness, a cerebellopontine angle lesion (such as an acoustic neuroma) may cause a reduced or absent corneal reflex on the affected
sides side ± aural fullness (owing to trigeminal nerve deficit)
Is the mastoid region tender or A tender swelling of the mastoid with associated middle ear inflammation or pinna lateralisation (or both) may suggest acute mastoiditis
swollen?
Is the parotid gland enlarged? Palpation of a parotid lump may suggest cancer (particularly if associated with a history of regional skin cancer, delayed onset facial palsy, or pain); if cancer
is suspected, thoroughly examine the rest of the head and neck and refer urgently (for example, through the “two week wait suspected head and neck cancer
pathway” in the UK)

Alternative rehabilitation methods include physical Treatments in primary care for Bell’s palsy and Ramsay
therapy (facial retraining exercises, transcutaneous Hunt syndrome
electrical stimulation, acupuncture), botulinum toxin Corticosteroids in Bell’s palsy
injections (to reduce facial muscle contractures, synki- A Cochrane review (1569 patients, eight randomised trials)
nesis, and hemifacial spasm), dynamic facial reanima- found that significantly more patients taking oral steroids
tion surgery, or counselling. Of these interventions, only recovered complete motor function, compared with those
physical therapy has been subjected to controlled trials,15 taking placebo, if started less than 72 hours after symptom
and no overall benefit over placebo was found. Tailored onset (77% v 67%; relative risk 0.71, 95% confidence inter-
facial retraining exercises show limited evidence of ear- val 0.61 to 0.83).16 They also had significantly fewer motor
lier recovery of nerve function but this result needs to be synkinesis symptoms (0.60, 0.44 to 0.81).16 The results of
confirmed by future trials that are adequately powered one randomised trial that recruited patients to oral ster-
with low risk of bias. oids versus placebo up to one week after symptoms began
were significantly inferior to those of trials that recruited
within 48 hours.17  18 Randomised trials showed two steroid
Patient consultation guide for management and prognosis of Bell’s palsy
regimens to be of similar, significant benefit—prednisolone
What is Bell’s palsy? 25 mg twice daily for 10 days or 60 mg once daily for five
This condition involves swelling adjacent to the facial nerve as it passes through the days (the last dose should be tapered by 10 mg/day over
skull base into the ear. Compression of this nerve can stop the muscles that it supplies the subsequent five days).18  19 A systematic review of 10
from working. The cause of the swelling is currently unknown.22 randomised controlled trials found no significant difference
in adverse event rates between oral steroids and placebo,20
How is it managed?
although most studies excluded patients with specific contra-
Steroid tablets (usually prednisolone) help to reduce inflammation and are normally indications (such as poorly controlled diabetes, immune
taken for 10 days.18  19 This short course of drugs is unlikely to have notable side effects compromise, hypertension, peptic ulcer disease, glaucoma,
if you have no history of high blood sugar levels (diabetes), hypertension, gastric ulcer, active tuberculosis, first and second trimester of pregnancy,
or glaucoma.22 To ensure maximum benefit, the steroid tablets should be started within
sepsis, renal or hepatic impairment, and psychosis).2  5  21
three days of the facial weakness appearing.5
It is important to discuss specific risks versus benefits of
If the eyelid cannot shut completely, the surface of the eye may dry up and be harmed.
treatment with patients (box).
In addition, the tear ducts may not function temporarily, which could dry the eye
further.22 Treatment is needed to keep the eye moist. This normally involves frequent
lubricating eye drops during the day. At night, eye ointment can be applied before Antivirals
closing the eye shut with tape. A meta-analysis of combination therapy (anti-viral (aciclovir
or valaciclovir) plus oral steroid (prednisolone)) for Bell’s
What is the outcome? palsy, suggested a marginal benefit only when small poorer
Most studies indicate that if a steroid is not prescribed, seven of 10 patients will recover quality trials are included.24 The conclusion suggested that
completely. If a steroid is taken, eight of 10 patients will recover completely.16 Most combined therapy should be reserved for patients with sus-
patients will note an improvement in their facial weakness within three weeks, with the pected Ramsay Hunt syndrome (herpes zoster virus infec-
remainder resolving by three to five months.3 tion). In these patients, primary care physicians may wish to
In the 20-30% of cases where facial weakness does not recover fully, further start a trial of oral steroids (dose as described above) if there
interventions may be considered. These may include physiotherapy to undergo “facial are no contraindications, together with an antiviral agent
retraining exercises” or Botox injections to help with muscle spasms. It is important that (such as 1 g valaciclovir three times daily for one week.5  25
other potential causes of facial palsy are excluded by referral to a specialist if recovery
Because of the relatively poor functional outcome in this
fails to progress. A considerable proportion of patients are left with psychosocial
group and the high rate of coexistent sensorineural hearing
concerns because of their limited facial function and may need psychological support.23
loss, it is advisable (where appropriate) to consider referral
Surgical treatments also help improve the functional and cosmetic appearance of the
face. to ear, nose, and throat specialists for repeat assessment and
imaging of the cerebellopontine angle.

34 19 September 2015 | the bmj