- The document provides guidance on assessing and managing facial nerve palsy, which can be caused by various upper or lower motor neuron lesions. - In patients presenting with facial weakness, the first priority is to determine if it is caused by an upper motor neuron lesion by checking for signs such as limb weakness or ataxia. - For lower motor neuron lesions, the causes include Bell's palsy (idiopathic), infections like Ramsay Hunt syndrome, and tumors. Bell's palsy is diagnosed after ruling out other causes. - Treatment depends on the cause but may include corticosteroids for Bell's palsy within 72 hours, antivirals for Ramsay Hunt syndrome

1. PRACTICE POINTER
Assessment and management of facial nerve palsy
Liam Masterson specialty registrar, ear, nose, and throat surgery
1
, Martin Vallis general practitioner
principal
2
, Ros Quinlivan consultant, neuromuscular disease
3
, Peter Prinsley consultant, ear, nose,
and throat surgeon
4
1
Ear, Nose, and Throat Department, Cambridge University Hospitals NHS Trust, Cambridge CB2 0QQ, UK; 2
Rosedale Surgery, NHS Great Yarmouth
and Waveney Clinical Commissioning Group, Lowestoft, UK; 3
MRC Centre for Neuromuscular Disease, National Hospital for Neurology and
Neurosurgery, London, UK; 4
Ear, Nose, and Throat Department, Norfolk and Norwich University Hospital NHS Trust, Norwich, UK
The facial nerve is important for both communication and
expression, and impairment of its function can severely affect
quality of life.1
The main concern at first presentation of a facial
nerve lesion is to exclude the possibility of a stroke or other
serious cause.2
The figure⇓ outlines possible causes. Correct
management within the first few days may prevent long term
complications.
How is it assessed?
The facial nerve is responsible for motor supply to the muscles
of facial expression (frontalis, orbicularis oculi, buccinators,
and orbicularis oris) and stapedius, parasympathetic supply to
the lacrimal and submandibular glands, and sensory input from
the anterior two thirds of the tongue. Thus, as well as a facial
droop, patients may present with a dry eye, reduced corneal
reflex, drooling, hyperacusis, altered taste, otalgia, and speech
articulation problems.5
Upper motor neurone
After identifying the affected side, it is important to establish
whether an upper motor neurone lesion is responsible for the
facial weakness. Although not an infallible sign,3
classic
neurology describes a bilateral innervation of that part of the
facial nuclei supplying the forehead, and thus preserving
forehead movement in upper motor lesions. Lower motor
neurone disorders of the main nerve trunk result in a weakness
of the entire side of the face.
Patients may have risk factors for stroke, which include older
age (>60 years), hypertension, previous stroke or transient
ischaemic attack, diabetes, high cholesterol, smoking, and atrial
fibrillation.6
Corroborative evidence may also be found by
examining for abnormalities in other cranial nerves and the
peripheral nervous system—increased tone, limb weakness,
hyper-reflexia, upgoing plantars, and sensory loss.4
When an upper motor neurone lesion is suspected, it may help
to determine whether this is localised to the brainstem or cerebral
cortex. Brainstem disease may present with vertigo, ataxia, or
crossed neurology signs (ipsilateral cranial nerve involvement
and contralateral hemiplegia). A cortical lesion often affects the
contralateral limbs and involuntary movements of the face, such
as spontaneous smiling, may be spared.6
Urgent referral to
secondary care (neurology or acute medical unit) is needed at
this stage to assess the need for thrombolysis.
Lower motor neurone
Once a central cause for facial palsy has been excluded, perform
a focused examination of the ears, mastoid region, oral cavity,
eyes, scalp, and parotid glands to look for the specific signs in
the table⇓. Bell’s palsy is an idiopathic lower motor neurone
(LMN) facial nerve paralysis that accounts for most new cases
(incidence 10-40/100 000 population each year).3 7
However,
30-41% of patients with LMN facial nerve weakness will have
another cause that requires specific management and is often
associated with a poorer prognosis.2-4
Bell’s palsy is a diagnosis of exclusion, made only after
excluding features in the table. Epidemiological studies suggest
that it normally develops fully within 24-48 hours.3 4
Most cases
(60%) are associated with mild post-auricular pain. Incidence
does not differ significantly with ethnicity or sex, but diabetes
is associated with as many as 10% of cases, and it occurs more
often in the last trimester of pregnancy (three times baseline
risk).8
Incomplete facial nerve paralysis at presentation (some
residual muscle movement and partial closure of the eyelid) is
a good prognostic sign, indicating a 94% chance of full recovery,
as opposed to 61% in those with complete paralysis.3
The next most common cause of facial nerve paralysis is trauma
(accidental or surgical). Accidental trauma includes any sharp
or blunt mechanism of injury, such as facial laceration, stab
injury, or temporal bone fracture. Detection of a temporal bone
Correspondence to: L Masterson lmm398@doctors.org.uk
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Practice
PRACTICE

2. The bottom line
• In patients presenting with facial weakness, the first priority is to exclude an upper motor neurone lesion; important associated signs
may include concurrent limb weakness, hyper-reflexia, upgoing plantars, or ataxia
• Check for causes of a lower motor neurone lesion by examining the ears, mastoid region, oral cavity, eyes, scalp, and parotid glands
• Bell’s palsy is a diagnosis of exclusion, and oral steroids are needed within 72 hours to increase the chance of complete recovery.
Prognosis is usually good compared with other causes of lower motor neurone weakness, such as tumours and Ramsay Hunt syndrome
• Eye protection is crucial if lid closure is impaired
How patients were involved in the creation of this article
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 consultation guide for management and prognosis of Bell’s palsy (see box below)
fracture is essential because of the 90% risk of associated
intracranial disease.9
A postmortem correlation study indicates
that periorbital bruising (racoon sign), mastoid bruising (Battle’s
sign), and blood in the ear canal have a positive predictive value
of 85%, 66%, and 46%, respectively, for detecting a temporal
bone fracture.10
Cerebellopontine angle and middle ear surgical
procedures are the main causes of iatrogenic injury, which may
also be seen after procedures carried out on the parotid gland
or any other region along the facial nerve.4
After infection by herpes zoster virus, a geniculate ganglionitis
causes a prodrome of otalgia and vesicular eruption within the
ear canal, with or without spread to the oral cavity. Facial
paralysis (Ramsay Hunt syndrome) normally follows this and
is associated with sensorineural hearing loss and vertigo in 40%
of cases owing to involvement of cranial nerve VIII.6
Patients
with Ramsay Hunt syndrome generally have a poorer prognosis
than those with Bell’s palsy, with only 21% showing full
recovery at 12 months.3
A slowly progressive onset of facial weakness is suggestive of
cancer.3 5
In addition, cancer may be associated with pain or
paralysis of select branches of the nerve, such as zygomatic
(eyelid) or marginal mandibular (angle of mouth) branches.7
There may be a history of regional cancer. A thorough
examination of the head and neck region will be needed to look
for cervical lymphadenopathy, a parotid mass, or a scalp lesion
in particular. Acoustic neuromas account for about 80% of
cerebellopontine angle lesions and most cases of tumour related
LMN facial nerve paralysis; they can be differentiated from
other causes by ipsilateral sensorineural hearing loss (95% of
cases) and absence of the corneal reflex (60%).4 11
Bacterial infections are responsible for 1-4% of new cases of
LMN facial palsy.3 4
Acute otitis media accounts for most and
is associated with systemic sepsis, a bulging tympanic
membrane, conductive hearing loss, and pinna lateralisation.
Malignant otitis externa (or, more accurately, skull base
osteomyelitis) is characterised by lack of sleep due to otalgia.
More than 95% of cases are seen in older people (>65 years),
immunocompromised people, and those with poorly controlled
diabetes.12
. The condition s associated with Pseudomonas
aeruginosa infection.12
Lyme disease is a bacterial infection
caused by a tick bite that results in facial nerve paralysis in one
in 10 seropositive patients.13
How is it managed?
Management is influenced strongly by the initial clinical review
and provisional working diagnosis. With an LMN lesion, the
main priority is to treat the underlying cause, to improve
symptoms, and to reduce associated morbidity, such as
contracture of the facial muscles, synkinesis (involuntary
movement of one part of the face due to aberrant re-innervation),
and autonomic dysfunction (crocodile tears or hemi-facial
spasm). In Bell’s palsy, routine investigations in the primary
care setting are no longer recommended.2
Red flags for urgent referral
These include potential upper motor neurone causes (such as
limb paresis, paraesthesia of the face or limbs, involvement of
other cranial nerves, postural imbalance), trauma, features
suggesting cancer (such as gradual onset, persistent facial
paralysis >6/12, pain within the facial nerve distribution,
ipsilateral hearing loss, suspicious head or neck lesion, previous
regional cancer), and acute systemic or severe local infection.
Urgent paediatric referral is warranted in children, for whom
Bell’s palsy is less likely to be a cause of facial weakness (<50%
of cases).5
Treatments applicable to all patients
Eye care is paramount for those with corneal exposure. To
prevent ulceration or dehydration of the cornea, apply artificial
tears (such as hypromellose drops) every one or two hours
during the day. At night, keep the eye moist by using a thin strip
of paraffin based ointment (such as Lacrilube) and secure the
upper eyelid in the closed position by applying of permeable
synthetic tape (http://www.facialpalsy.org.uk/advice/guides/
how-to-tape-eyes-shut/433). All cases of incomplete eyelid
closure require urgent ophthalmology consultation at
presentation.
Some cases of LMN facial palsy will need to be referred to the
ear, nose, and throat department or another hospital specialty.
Such cases include all patients with atypical symptoms (see
table) and those with suspected Bell’s palsy who do not respond
to a trial of oral prednisolone (observe for maximum of two to
three weeks). Post referral tests may include computed
tomography or magnetic resonance imaging to visualise the
skull base, stylomastoid foramen, and parotid gland; blood tests
(full blood count, urea, and electrolytes); pure tone audiography;
and topographical studies (such as Schirmer’s test, taste
sensation, and stapedial reflex). Electroneuronography can guide
prognosis in cases of complete paralysis, but this test is
expensive, time consuming, and it has a short window of
opportunity after onset of symptoms (less than three weeks). In
the case of longstanding facial palsy, impairment of eye closure
may require insertion of a gold weight into the upper eyelid or
lateral tarsorrhaphy.14
Alternative rehabilitation methods include physical therapy
(facial retraining exercises, transcutaneous electrical stimulation,
acupuncture), botulinum toxin injections (to reduce facial muscle
contractures, synkinesis, and hemifacial spasm), dynamic facial
reanimation surgery, or counselling. Of these interventions,
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PRACTICE

3. only physical therapy has been subjected to controlled trials,15
and no overall benefit over placebo was found. Tailored facial
retraining exercises show limited evidence of earlier recovery
of nerve function but this result needs to be confirmed by future
trials that are adequately powered with low risk of bias.
Treatments in primary care for Bell’s palsy
and Ramsay Hunt syndrome
Corticosteroids in Bell’s palsy
A Cochrane review (1569 patients, eight randomised trials)
found that significantly more patients taking oral steroids
recovered complete motor function, compared with those taking
placebo, if started less than 72 hours after symptom onset (77%
v 67%; relative risk 0.71, 95% confidence interval 0.61 to
0.83).16
They also had significantly fewer motor synkinesis
symptoms (0.60, 0.44 to 0.81).16
The results of one randomised
trial that recruited patients to oral steroids 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 regimens to be of similar, significant
benefit—prednisolone 25 mg twice daily for 10 days or 60 mg
once daily for five days (the last dose should be tapered by 10
mg/day over the subsequent five days).18 19
A systematic review
of 10 randomised controlled trials found no significant difference
in adverse event rates between oral steroids and placebo,20
although most studies excluded patients with specific
contraindications (such as poorly controlled diabetes, immune
compromise, hypertension, peptic ulcer disease, glaucoma,
active tuberculosis, first and second trimester of pregnancy,
sepsis, renal or hepatic impairment, and psychosis).2 5 21
It is
important to discuss specific risks versus benefits of treatment
with patients (box).
Antivirals
A meta-analysis of combination therapy (anti-viral (aciclovir
or valaciclovir) plus oral steroid (prednisolone)) for Bell’s palsy,
suggested a marginal benefit only when small poorer quality
trials are included.24
The conclusion suggested that combined
therapy should be reserved for patients with suspected Ramsay
Hunt syndrome (herpes zoster virus infection). In these patients,
primary care physicians may wish to start a trial of oral steroids
(dose as described above) if there are no contraindications,
together with an antiviral agent (such as 1 g valaciclovir three
times daily for one week.5 25
Because of the relatively poor
functional outcome in this group and the high rate of coexistent
sensorineural hearing loss, it is advisable (where appropriate)
to consider referral to ear, nose, and throat specialists for repeat
assessment and imaging of the cerebellopontine angle.
Thanks to Fiona Walter (general practitioner principal and senior lecturer,
primary care unit, University of Cambridge, UK), Chaudhary Riaz (GP
specialty registrar, The Pennine Acute Hospitals NHS Trust, UK),
Anthony Males (GP principal and senior partner, York Street Medical
Practice, Cambridge), and Martin Roland (primary care unit, University
of Cambridge) for their expert review and constructive feedback. The
patient consultation guide (box) for Bell’s palsy was produced in
conjunction with the charity Facial Palsy UK.
Competing interests: We have read and understood BMJ policy on
declaration of interests and declare the following interests: none.
Provenance and peer review: Not commissioned; externally peer
reviewed.
1 Coulson SE, O’Dwyer NJ, Adams RD, et al. Expression of emotion and quality of life after
facial nerve paralysis. Otol Neurotol 2004;25:1014-9.
2 Baugh RF, Basura GJ, Ishii LE, et al. Clinical practice guideline: Bell’s palsy executive
summary. Otolaryngol Head Neck Surg 2013;149:656-63.
3 Peitersen E. Bell’s palsy: the spontaneous course of 2500 peripheral facial nerve palsies
of different etiologies. Acta Otolaryngol Suppl 2002;549:4-30.
4 May M, Schaitkin B, Shapiro A. The facial nerve. Thieme, 2001.
5 Holland NJ, Bernstein JM. Bell’s palsy. BMJ Clin Evid 2014;2014. pii:1204.
6 Donnan GA, Fisher M, Macleod M, et al. Stroke. Lancet Neurol 2008;371:1612-23.
7 De Diego-Sastre JI, Prim-Espada MP, Fernández-García F. The epidemiology of Bell’s
palsy. Rev Neurol 2005;41:287-90.
8 Kosins AM, Hurvitz KA, Evans GR, et al. Facial paralysis for the plastic surgeon. Can J
Plast Surg 2007;15:77-82.
9 Kamerer DB, Thompson SW. Middle ear and temporal bone trauma. In: Bailey BJ, ed.
Head and neck surgery—otolaryngology. 3rd ed. Lippincott Williams & Wilkins,
2001:1108-14.
10 Pretto Flores L, De Almeida CS, Casulari LA. Positive predictive values of selected clinical
signs associated with skull base fractures. J Neurosurg Sci 2000;44:77-82.
11 Sharp MC, MacfArlane R, Hardy DG et al. Team working to improve outcome in vestibular
schwannoma surgery. Br J Neurosurg 2005;19:122-7.
12 Hobson CE, Moy JD, Byers KE, et al. Malignant otitis externa: evolving pathogens and
implications for diagnosis and treatment. Otolaryngol Head Neck Surg 2014;151:112-6.
13 Smith RP, Schoen RT, Rahn DW, et al. Clinical characteristics and treatment outcome
of early Lyme disease in patients with microbiologically confirmed erythema migrans. Ann
Intern Med 2002;136:421-8.
14 Buchanan M, Lyons M. Clinical review: Bell’s palsy GPonline 2010. www.gponline.com/
clinical-review-bells-palsy/neurology/article/1000464.
15 Teixeira LJ, Valbuza JS, Prado GF. Physical therapy for Bell’s palsy (idiopathic facial
paralysis). Cochrane Database Syst Rev 2011;12:CD006283.
16 Salinas RA, Alvarez G, Daly F, et al. Corticosteroids for Bell’s palsy (idiopathic facial
paralysis). Cochrane Database Syst Rev 2010:CD001942.
17 Taverner D. Cortisone treatment of Bell’s palsy. Lancet Neurol 1954;267:1052-4.
18 Engström M, Berg T, Stjernquist-Desatnik A. Prednisolone and valaciclovir in Bell’s palsy:
a randomised, double-blind, placebo-controlled, multicentre trial. Lancet Neurol
2008;7:993-1000.
19 Sullivan FM, Swan IR, Donnan PT. Early treatment with prednisolone or acyclovir in Bell’s
palsy. N Engl J Med 2007;357:1598-607.
20 De Almeida JR, Al Khabori M, Guyatt GH. Combined corticosteroid and antiviral treatment
for bell palsy: a systematic review and meta analysis. JAMA 2009;302:985-93.
21 Rafii B, Sridharan S, Taliercio S. Glucocorticoids in laryngology: a review. Laryngoscope
2014;124:1668-73.
22 Kenny T, Tidy C. Bell’s palsy. Cox J, series ed. 2013. www.patient.co.uk/health/bells-
palsy.
23 Walker D, Hallam M, Ni Mhurchadha S, et al. Our experience: the psychosocial impact
of facial palsy. Clin Otolaryngol 2012;37:474-7.
24 Browning GG. Bell’s palsy: a review of three systematic reviews of steroid and anti-viral
therapy. Clin Otolaryngol 2010;35:56-8.
25 Lockhart P, Daly F, Pitkethly M, et al. Antiviral treatment for Bell’s palsy (idiopathic facial
paralysis). Cochrane Database Syst Rev 2009;4:CD001869.
Accepted: 15 February 2015
Cite this as: BMJ 2015;351:h3725
© BMJ Publishing Group Ltd 2015
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4. Patient consultation guide for management and prognosis of Bell’s palsy
What is Bell’s palsy?
This condition involves swelling adjacent to the facial nerve as it passes through the skull base into the ear. Compression of this nerve can
stop the muscles that it supplies from working. The cause of the swelling is currently unknown.22
How is it managed?
Steroid tablets (usually prednisolone) help to reduce inflammation and are normally taken for 10 days.18 19
This short course of drugs is
unlikely to have notable side effects if you have no history of high blood sugar levels (diabetes), hypertension, gastric ulcer, or glaucoma.22
To ensure maximum benefit, the steroid tablets should be started within three days of the facial weakness appearing.5
If the eyelid cannot shut completely, the surface of the eye may dry up and be harmed. 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 closing the eye shut with tape.
What is the outcome?
Most studies indicate that if a steroid is not prescribed, seven of 10 patients will recover completely. If a steroid is taken, eight of 10 patients
will recover completely.16
Most patients will note an improvement in their facial weakness within three weeks, with the remainder resolving
by three to five months.3
In the 20-30% of cases where facial weakness does not recover fully, further interventions may be considered. These may include physiotherapy
to undergo “facial retraining exercises” or Botox injections to help with muscle spasms. It is important that other potential causes of facial
palsy are excluded by referral to a specialist if recovery fails to progress. A considerable proportion of patients are left with psychosocial
concerns because of their limited facial function and may need psychological support.23
Surgical treatments also help improve the functional
and cosmetic appearance of the face.
Table
Table 1| Clinical signs to check in lower motor neurone facial nerve palsy
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)
Are the ears clear on otoscopy?
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 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 ipsilateral hearing loss?
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
Is there a rash?
The palsy may be secondary to a skull base fracture (common associated signs include periorbital or mastoid bruising,
blood in the ear canal, and haemotympanum9
) or recent mastoid, parotid, or submandibular gland surgery
Are there any bruises or scars in the head
and neck region?
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 side ± aural fullness (owing to trigeminal nerve deficit)
Is the corneal reflex intact on both sides
A tender swelling of the mastoid with associated middle ear inflammation or pinna lateralisation (or both) may suggest
acute mastoiditis
Is the mastoid region tender or swollen?
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)
Is the parotid gland enlarged?
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5. Figure
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
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