Facial Weakness

Paediatric Clinical Guideline
Neurosciences 4.11 Facial Weakness
Short Title:
Facial Weakness
Full Title:
Date of production/Last revision:
Guideline for the management of facial weakness in children and young
May 2008
Explicit definition of patient group
to which it applies:
This guideline applies to all children and young people under the age of 19
Name of contact author
Dr Damian Wood, Consultant Paediatrician
Ext: 64041
May 2011
Revision Date
This guideline has been registered with the Trust. However, clinical guidelines are 'guidelines' only. The interpretation
and application of clinical guidelines will remain the responsibility of the individual clinician. If in doubt contact a
senior colleague or expert. Caution is advised when using guidelines after the review date.
Facial Weakness
Acute lower motor neurone facial palsy is a common presentation in childhood
In most cases a cause is not identified and the vast majority of these cases resolve
Upper Motor Neurone vs. Lower Motor Neurone
Complete facial paralysis is only seen with lower motor neurone lesions. In upper motor
neuron lesions there is sparing of the upper face due to bilateral cortical innervation of the
orbicularis oculi and frontalis muscles.
Causes of Acquired Facial Nerve Palsy
Bell’s palsy
The term Bell’s palsy refers to an acute unilateral facial nerve palsy of rapid onset related to a
lesion of the nerve within the facial canal. It is sometimes used to describe idiopathic facial
palsy, although this is not universal. The aetiology of Bell's palsy remains unclear, but many
consider it to be a reactivation to viral inflammation rather than ischaemia. Other causes of
acquired facial weakness are listed in Table 1.
The upper and lower portions of the face are weak, and the corner of the mouth droops. The
child may be unable to close the eye on the affected side and may develop an exposure
keratitis at night. Taste is lost on the anterior thirds of the tongue in about 50% of cases.
Numbness and parasthesia do not occur in Bell’s palsy.
Damian Wood
Page 1 of 5
May 2008
Paediatric Clinical Guideline
Neurosciences 4.11 Facial Weakness
Table 1 - Other Causes of Acquired Facial Weakness
Otitis media
Herpes Zoster (Ramsay-Hunt
Temporal lobe abscess
Varicella zoster
Bacterial meningitis
Viral meninigoencephalitis
Cat scratch disease
Lyme disease
Kawasaki disease
Guillan Barre syndrome
Basal skull fracture
Blunt or penetrating
Facial surgery
Facial burns
 Leukaemia
 Cerebellar astrocytoma
 Rhabdomyosarcoma
Intracerebral AVM
Melkersson-Rosenthal syndrome
Hearing loss, otalgia and discharge from the ear
Headache, neck stiffness and photophobia
Clumsiness, falls and visual disturbance
Change in behaviour or academic performance
Weakness, parasthesia and abnormal movements
Bruising, pallor and lumps
Systemic symptoms (malaise, fatigue and lethargy)
History of trauma
Bruising, rashes and mucosal changes
Cervical, inguinal and axillary lymphadenopathy
Mastoid swelling and tenderness
Parotid swelling or tenderness
Cranial nerves
o Complete or partial facial weakness
o Can they close their eye (bury their eye lashes)
o Papilloedema and visual field defects
o Other cranial nerve lesions
Irritability, neck stiffness, extensor posturing
Abnormal movements
Ataxia, nystagmus and cerebellar signs
Focal neurological signs
Abnormality on otoscopy
Damian Wood
Page 2 of 5
May 2008
Paediatric Clinical Guideline
Neurosciences 4.11 Facial Weakness
All children with facial weakness must have an ENT and neurological examination and
their blood pressure checked.
The use of further investigation in the absence of other physical signs and symptoms is
controversial. Investigation should be reserved for those with “red flag” symptoms or signs.
Symptoms and signs indicative of underlying pathology
 Ear ache and ear discharge
 Hearing loss
 Pain or parasthesia
 Abnormality on otoscopy
 Associated cranial nerve lesions or other neurological signs
 Hypertension
 Lymphadenopathy, pallor or bruising
 Vesicles in external auditory meatus or on palate (see below)
 Single branch involvement
 Progression of weakness beyond 3 weeks
 Recurrence
 Mastoid swelling
Consider – if no red flag symptoms or atypical features no investigations are indicated
 FBC and Film – required if considering corticosteroid treatment
 CRP and ESR
 Swabs of vesicular lesions for HSV and VZV PCR
 Serology for viruses, bartonella or borrelia (if history/examination findings suggestive)
 Audiological assessment for those complaining of hearing loss (refer to ENT)
 Cranial imaging (discuss with neuroradiologist as appropriate modality may depend
on likely site of the lesion)
The treatment of idiopathic facial palsy is controversial. A high proportion of children with
idiopathic facial palsy recover spontaneously without treatment. The use of corticosteroids
early in the course of the disease has been suggested as a way of reducing the duration of
paralysis and the risk of long term impairment.
The routine use of corticosteroids to treat acute unilateral facial palsy in children is not
recommended; however, in children presenting within 72 hours of onset consideration
should be given to the use of oral prednisolone and oral aciclovir. The relative benefits
and risks of treatment including the need for blood tests and steroid treatment should
be discussed with parents.
A recent trial in adult patients showed early treatment (within 72 hours of onset) with oral
prednisolone and oral acyclovir significantly improves the chances of complete recovery. A
meta-analysis of RCTs in adults showed that a large proportion of patients treated with
steroids recovered completely and the mean time to recovery was shorter. Treatment appears
to be more effective when started earlier.
Damian Wood
Page 3 of 5
May 2008
Paediatric Clinical Guideline
Neurosciences 4.11 Facial Weakness
A recent systematic review found no positive evidence for the beneficial effects of
corticosteroids in Bell's palsy in children. The authors concluded that the routine use of
corticosteroids for the treatment of paediatric Bell's palsy is not recommended.
Prednisolone Dose
Child <50 kg Prednisolone 1mg/kg po od for 10 days and then stop with no taper of dose
Child >50kg Prednisolone 25mg po bd for 10 days and then stop with no taper of dose
Patients with facial weakness should have a FBC and film checked prior to
commencing corticosteroid treatment.
Prevention of Corneal Damage
Protection of the cornea with:
1. Viscotears Liquid Gel 0.2% four times/day to eye on affected side
2. Overnight eye patching on the affected side
Patients with acute idiopathic unilateral facial weakness should be discharged home with:
 Verbal and written information regarding Bell’s palsy
 Advice to return if vesicles develop in ear or mouth
 Follow-up with paediatrician in 6 weeks time if fails to resolve completely within 3
95% of children with idiopathic acute unilateral facial palsy will recover full function, most
within 3 weeks.
Ramsay-Hunt Syndrome
Ramsay-Hunt syndrome is the second most common cause of acquired unilateral facial palsy
and is caused by varicella zoster reactivation in the geniculate ganglion.
There is unilateral facial weakness and herpetic lesions in the external auditory canal or on
the soft palate. There may be associated hearing loss, tinnitus and vertigo.
In a small number the facial weakness may precede the onset of the appearance of the
The prognosis for complete recovery in patients with Ramsay-Hunt syndrome is not as good
and current recommendations are for treatment with:
1. Oral Prednisolone 2mg/kg po for 4 days with tapering over 4 days
2. Intravenous Aciclovir (see dosing guideline in BNFC) for 7 days
1-3 months
3 months – 12 years
12-18 years
Intravenous Aciclovir Dose
8 hourly
8 hourly
8 hourly
Between 50-75% of children with Ramsay-Hunt syndrome will show complete recovery.
Damian Wood
Page 4 of 5
May 2008
Paediatric Clinical Guideline
Neurosciences 4.11 Facial Weakness
Melkersson-Rosenthal syndrome
Melkersson-Rosenthal syndrome is a rare neurological disorder characterized by recurring
facial paralysis, swelling of the face and lips (usually the upper lip), and the development of
folds and furrows in the tongue. Onset is in childhood or early adolescence. After recurrent
attacks (ranging from days to years in between), swelling may persist and increase,
eventually becoming permanent. The lip may become hard, cracked, and fissured with a
reddish-brown discoloration. The cause of Melkersson-Rosenthal syndrome is unknown, but
there may be a genetic predisposition. It can be symptomatic of Crohn's disease or
Salinas RA, Alvarez G, Ferreira J. Corticosteroids for Bell’s Palsy (idiopathic facial paralysis)
Cochrane Database of Systematic Reviews 2004.
Riordan M. Investigation and treatment of facial paralysis. Arch Dis Child 2001;84:286-287
Sweeney CJ, Gilden DH. Ramsay Hunt Syndrome. J Neurol, Neurosurg and Psychiatry
Ashtekar CS, Joishy M, Joshi R. Do we need to give steroids in children with Bell’s palsy?
Emerg Med J. 2005; 22:505-507
Royal Children’s Hospital Melbourne, Clinical Practice Guideline
Damian Wood
Page 5 of 5
May 2008
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