Bell's Palsy Flashcards
What is facial nerve palsy?
Damage to the facial nerve - either upper motor neurone (UMN) or lower motor neurone (LMN) - produces weak muscles of facial expression.
What is the neuroanatomy of facial nerve palsy?
The VIIth cranial (facial) nerve is largely motor in function (some sensory fibres from external acoustic meatus, fibres controlling salivation and taste fibres from the anterior tongue in the chorda tympani branch).
It also supplies the stapedius (so a complete nerve lesion will alter auditory acuity on the affected side).
From the facial nerve nucleus in the brainstem, fibres loop around the VI nucleus before leaving the pons medial to VIII and passing through the internal acoustic meatus.
It passes through the petrous temporal bone in the facial canal, widens to form the geniculate ganglion (taste and salivation) on the medial side of the middle ear, whence it turns sharply (and the chorda tympani leaves), to emerge through the stylomastoid foramen to supply all the muscles of facial expression, including the platysma.
What is the presentation of facial nerve palsy?
Weakness of the muscles of facial expression and eye closure. The face sags and is drawn across to the opposite side on smiling. Voluntary eye closure may not be possible and can produce damage to the conjunctiva and cornea.
In partial paralysis, the lower face is generally more affected.
In severe cases, there is often demonstrable loss of taste over the anterior two thirds of the tongue and intolerance to high-pitched or loud noises. It may cause mild dysarthria and difficulty with eating.
If bilateral, particularly consider immunosuppression (HIV), Guillain-Barré syndrome or Lyme disease.
If recurrent, particularly consider lymphoma, sarcoidosis and Lyme disease.
In children, particularly consider Lyme disease and middle ear disease.
What is the most used system to describe paralysis of the facial nerve?
The most common system used for describing the degree of paralysis is the House-Brackmann scale, where 1 is normal power and 6 is total paralysis.
How do you differentiate between UMN and LMN lesion of the facial nerve?
In an LMN lesion, the patient can’t wrinkle their forehead - the final common pathway to the muscles is destroyed. The lesion must be either in the pons, or outside the brainstem (posterior fossa, bony canal, middle ear or outside skull).
In a UMN lesion, the upper facial muscles are partially spared because of alternative pathways in the brainstem, ie the patient can wrinkle their forehead (unless there is bilateral lesion) and the sagging of the face seen with LMN palsies is not as prominent. There appear to be different pathways for voluntary and emotional movement.
Cerebrovascular accidents usually weaken voluntary movement, often sparing involuntary movements (e.g., spontaneous smiling).
The much rarer selective loss of emotional movement is called mimic paralysis and is usually due to a frontal or thalamic lesion.
What is the aetiology of LMN lesion of CN VII?
o Idiopathic (Bell’s palsy):
Pregnancy - 3x more common.
Diabetes mellitus.
o Iatrogenic:
Local anaesthetic for dental treatment.
Linezolid.
o Infective: Herpesvirus (type 1). Herpes zoster (Ramsay Hunt syndrome) HIV. Epstein-Barr virus. Cytomegalovirus. Lyme disease (more likely if bilateral when responsible for 36% of cases). Otitis media or cholesteatoma.
oTrauma:
Fractures of the skull base.
Forceps delivery.
Haematoma after acupuncture.
o Neurological:
Guillain-Barré syndrome.
Mononeuropathy - eg, due to diabetes mellitus, sarcoidosis or amyloidosis.
o Neoplastic:
Posterior fossa tumours, primary and secondary.
Parotid gland tumours.
o Hypertension in pregnancy and eclampsia.
o Sarcoidosis.
o Sjögren’s syndrome and rheumatoid arthritis.
o Melkersson-Rosenthal syndrome (recurrent facial palsy, chronic facial oedema of the face and lips, and hypertrophy/fissuring of the tongue).
What is the aetiology of UMN lesion of CN VII?
o Cerebrovascular disease. o Intracranial tumours, primary and secondary. o Multiple sclerosis. o Syphilis. o HIV. o Vasculitides.
How do you assess for acute LMN palsy?
Acute LMN palsy can present at any age but is most frequently seen at age 15-60 years, affecting both sexes equally.
There is a rapid onset of unilateral facial paralysis:
o Ask the patient to give a big grin showing their teeth.
o Ask them to blow out their cheeks.
o Ask them to screw up their eyes.
o Ask them to raise their eyebrows (preserved in UMN lesion).
Aching pain below the ear or in the mastoid area is also common and may suggest middle ear or herpetic cause.
There may be hyperacusis.
Patients with lesions proximal to the geniculate ganglion may be unable to produce tears and have loss of taste.
What is Bell’s palsy?
This, the most common cause of acute LMN facial palsy, was originally described by Sir Charles Bell in 1821.
Incidence is 11-40 per 100,000 with a lifetime risk of 1 in 60.
Probably caused by ischaemic compression of the facial nerve within the facial canal, as a result of inflammation, most likely due to a viral infection.
In the past no cause was found in the majority of cases of LMN facial nerve palsy and these were labelled as idiopathic (i.e. Bell’s palsy). Increasingly, various viral causes are being identified, particularly herpes simplex type 1 or varicella (herpes) zoster.
Approximately 7% of patients have a recurrence.
There may be a familial component in recurrent cases, possibly due to anatomical abnormality of the facial canal.
The incidence is higher in people with diabetes than in those without diabetes.
What is Ramsay Hunt syndrome?
LMN facial nerve palsy due specifically to varicella (herpes) zoster is Ramsay Hunt syndrome.
Pain is often a prominent feature and vesicles are seen in the ipsilateral ear, on the hard palate and/or on the anterior two thirds of the tongue.
What are the investigations for facial nerve palsy?
Serology - Lyme, herpes and zoster (paired samples 4-6 weeks apart). It may not influence management but may reveal aetiology.
Check blood pressure in children with Bell’s palsy (two case reports of aortic coarctation presenting with facial nerve palsy and hypertension).
The following tests are rarely done but, combined with a good understanding of the neuroanatomy, can determine the level of the palsy:
o Schirmer’s tear test (reveals a reduced flow of tears on the side of a palsy affecting the greater palatine nerve).
o Stapedial reflex (an audiological test, absent if the stapedius muscle is affected).
o Electrodiagnostic studies (generally a research tool) reveal no changes in involved facial muscles for the first three days but a steady decline of electrical activity often occurs over the next week and will identify the 15% with axonal degeneration.
When should you refer a patient with Bell’s palsy?
Do not routinely refer adults with an uncomplicated episode of Bell’s palsy (unilateral lower motor neurone pattern facial weakness affecting all parts of the face and including weakness of eye closure) and no evidence of another medical condition such as middle ear disease.
Advise adults with Bell’s palsy about eye care, and explain that Bell’s palsy improves at different rates and maximum recovery can take several months.
Consider referring adults with Bell’s palsy who have developed symptoms of aberrant re-innervation (including gustatory sweating or jaw-winking) five months or more after the onset of Bell’s palsy for neurological assessment and possible treatment.
When should you refer patients with facial nerve palsy?
Refer urgently to an appropriate specialist people with facial nerve palsy and:
- Worsening or new neurological findings.
- Features suggestive of an upper motor neurone cause - eg, limb weakness, facial paraesthesia, other cranial nerve involvement, postural imbalance.
- Features suggestive of cancer - eg, gradual onset of symptoms, persistent facial paralysis for more than six months, pain in the distribution of the facial nerve, head or neck lesion suggestive of cancer, history of head and neck cancer, hearing loss on the affected side.
- Systemic or severe local infection.
- Trauma.
What are the general measures in the management of facial nerve palsy?
Reassurance - the majority of cases resolve spontaneously.
Eye care:
- Ophthalmologists play an important role in preventing irreversible loss of sight from corneal exposure. This may be successfully achieved by using lubricating drops hourly and eye ointment at night ± an eye patch.
- Botulinum toxin or surgery (upper lid weighting or tarsorrhaphy) may also be required temporarily.
- After the cornea has been protected but recovery is thought to be unlikely, longer-term management of eyelid and facial re-animation may be arranged.
What is the management of Bell’s palsy?
Steroids are effective in the treatment of facial nerve palsy. Of the 29% that wouldn’t be expected to recover fully, a third to a half will do so if given steroids.
Prednisolone should be given to patients over the age of 16 presenting within 72 hours. The optimum dosing regime is not known but the following are suggested:
o 25 mg bd for 10 days.
o 60 mg od for 5 days then reducing by 10 mg each day.
o There is no evidence to support the use of steroids after 72 hours.
o It is not known whether steroids in children are effective.
There is moderate-quality evidence of benefit from adding antivirals to steroid therapy, with no significant increase in adverse events. This remains controversial. It is currently not recommended as treatment in the UK.
Physiotherapy may be beneficial but there is no high-quality evidence to support significant benefit or harm.
Surgery:
o Surgical options for patients with facial palsy not responding to medical treatment include facial nerve decompression.
o If there is residual paralysis after 6-9 months, consider referral to a plastic surgeon with a special interest in facial reconstructive surgery. The muscle targets remain viable for cross-facial nerve grafting for about 12-18 months.
o Where the nerve fails to regenerate, cosmetic surgery to elevate the mouth or anastomosis of the hypoglossal nerve to the facial nerve may help.
