Bell palsy, also known as idiopathic peripheral facial paralysis, is characterized by rapid onset facial nerve paralysis, often with resolution in 6-8 weeks. As there are numerous causes of facial nerve palsy, many acute in onset, it is currently a diagnosis of exclusion supported by a typical presentation.
The peak age of presentation is between 15-50 years with ~25 cases per 100,000 per year. There is no gender predominance 10.
The classical presentation is rapid onset unilateral facial paralysis; both upper and lower facial muscles are affected (cf. central cause e.g. brainstem stroke where unilateral facial paralysis only affects the lower facial muscles). Onset can be as quick as over a few hours.
Up to 70% of patients will describe altered taste sensation in the week preceding paralysis, due to nervus intermedius compression. It should be remembered that sensory nerves have thinner myelin and are more susceptible to dysfunction than motor nerves.
Recurrent Bell palsy is reported to occur in 6.5% of patients (range 0.8-19.4%), with multiple recurrences rare. Recurrence can be ipsilateral or contralateral to the original episode. The mean time to recurrence is ~10 years (range 7.8-11.2 years), although ~50% experience recurrence within 5 years 12.
Bell palsy was long thought to be idiopathic; strong evidence is now present to implicate reactivation of herpes simplex virus or varicella zoster virus with latent infection in the geniculate ganglion.
There is a limited role for imaging of patients with Bell palsy. MRI should be considered for the following patients:
- decompressive surgery is being contemplated
- atypical signs and symptoms suggest another diagnosis may be possible:
- slow progressive palsy
- spasm preceding palsy
- multiple cranial nerves involved
- recurrent palsy
- no recovery after 6-8 weeks
Enhancement of the nerve is not seen in all patients with Bell palsy, reported variably between 57-100%. It is also essential to appreciate the normal pattern of facial nerve enhancement, that include the geniculate ganglion and mastoid segments.
In Bell palsy, long segments of the facial nerve enhance in a uniformly linear fashion, more intensely than the contralateral non-affected side. A prominent focus of enhancement may also be seen laterally with the acoustic canal, known as the fundal tuft sign 11.
The facial nerve on either side of the geniculate ganglion is most frequently involved, from the distal internal auditory canal to the distal tympanic segment. The mastoid and extratemporal segments are less frequently involved.
Importantly, nodularity should raise suspicion of a neoplastic cause and a careful search for remote areas of leptomeningeal enhancement performed.
Treatment and prognosis
- 80-90% full recovery
- rest chronic facial paralysis
- corneal drying is the most problematic complication
Risk factors for incomplete recovery include:
- older age of onset
- complete paralysis
History and etymology
It is named after Sir Charles Bell (1774-1842), a Scottish anatomist, surgeon, and physiologist, who described it in 1821 3.
- care should be taken not to mistake normal facial nerve enhancement on MRI for that seen in Bell palsy; focal enhancement in the most lateral aspect of the internal auditory meatus is probably the most useful feature and has been proposed as a marker of severity and prognosis.
- hemangioma of facial nerve
- perineural spread of tumor
- enhancement may persist by up to one year beyond clinical improvement
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