Bell palsy

Last revised by Dr Yuranga Weerakkody on 06 Jul 2022

Bell palsy, also known as idiopathic peripheral facial paralysis, is characterized by rapid onset facial nerve paralysis, often with resolution in 6-8 weeks, without an identifiable etiology. 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 in a lower motor neuron pattern whereby both upper and lower facial muscles are affected (cf. central cause e.g. brainstem stroke where unilateral facial paralysis is in an upper motor neuron pattern and classically only affects the lower facial muscles) 12. Onset can be as quick as over a few hours, and generally paralysis reaches its peak within 72 hours 12

Associated symptoms include 12:

  • ipsilateral hyperacusis
  • ipsilateral dysguesia, particularly the anterior two-thirds
  • pain behind the ipsilateral ear or neck
  • ipsilateral altered facial sensation

Recurrent Bell palsy is reported to occur in 4-7% of patients 14, 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 11

The etiology of Bell palsy is yet to be elucidated, and thus the diagnosis remains one of exclusion after other etiologies for facial palsy have been considered 12,13. Prominent theories include reactivation of a virus with herpes simplex virus type 1 (HSV-1) being the strongest pathogenic candidate, an immune-mediated phenomenon, or a microvascular issue 12,13. Anatomical predisposing factors, such as narrowing of the path of the facial nerve through the internal auditory canal, have also been suggested as contributory 13.

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

In Bell palsy, long segments of the facial nerve enhance in a uniformly linear fashion, more intensely than the contralateral non-affected side. However, enhancement of the nerve is not seen in all patients, 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.

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.  

Corticosteroids are the mainstay of treatment, to be started within 72 hours of symptom onset 12. Additionally, eye care should also be sought, with use of eye drops (artificial tears) and ointments, and taping down eyes shut, to protect the cornea 12. There is no role for empiric antiviral treatment 12.

Prognosis is generally good, with 70-90% of patients making a full recovery, especially if corticosteroids were used 12.

Complications of incomplete recovery from Bell palsy include 12:

  • cosmetic, psychological, and social sequelae
  • facial synkinesis
  • risk of corneal ulceration (without eye care)

It is named after Sir Charles Bell (1774-1842), a Scottish anatomist, surgeon, and physiologist, who described it in 1821 3.

  • facial nerve enhancement may persist by up to one year beyond clinical improvement

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Cases and figures

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  • Case 5: annotated image
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  • Case 6
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