Clinical features

The clinical features of Bell's palsy are varied:

• usually of sudden onset and complete within 24 hours; less frequently, the condition is progressive developing over a course of less than 4 days
• almost always unilateral
• onset may be preceded by post-auricular pain which develops over a 48 hour period
• there is paralysis of the upper and lower facial muscles
  • the eyebrow droops and the wrinkles of the brow are smoothed out; frowning and raising the eyebrows are impossible
    • if there is an upper motor neurone lesion affecting the facial nerve then the ability to wrinkle the brow is preserved; in Bell's palsy this ability is lost
  • the eye cannot be closed. When asked to close the eyes and show the teeth, the eyeball rotates upwards and outwards - Bell's phenomenon.
• the lower lid is everted. Tear production (lachrymation) is decreased. Eye irritation often occurs due to lack of lubrication and constant exposure. The eye may appear to tear excessively due to loss of lid control, which may cause tears to spill freely from the eye (3)
• the mouth sags and the patient dribbles. The patient is unable to blow out the cheeks. The lips cannot be pursed and whistling is impossible. The effects tend to be more pronounced in the elderly.
• sensory component of the corneal reflex is intact - trigeminal nerve - but motor component is lost - facial innervation of orbicularis oculi.
• involvement of the chorda tympani nerve results in loss of taste
• hyperacusis develops if the lesion of the facial nerve extends to above the point at which the branch to the stapedius muscle is given off

Notes (1,2):

• a central upper motor neurone deficit causes weakness of the lower face only. More complex segmental deficits may be caused by peripheral facial nerve lesions. Therefore patients with facial palsy require careful examination of the other cranial nerve and cerebellar function
  • a prospective study revealed that a small percentage (approximately 8%) of patients with otherwise typical Bell's palsy may harbour additional cranial neuropathies (2):
    • additional cranial neuropathies identified were trigeminal, glossopharyngeal, hypoglossal and vagal motor weakness (1)
• points in the history include: (4)
  • associated symptoms
  • aetiological factors
  • incidence of age
• points to note on examination include: (4)
  • differentiate between an upper and lower motor neurone lesion
    
  • check that other cranial nerves are not involved
    
  • exclude masses in the head and neck
    • a deep lobe parotid tumour may only be identified clinically by careful examination of the oropharynx and ipsilateral tonsil to rule out asymmetry
    • erythema migrans on the limbs or trunk with a history of tick bite suggests possible Lyme disease, which may cause facial palsy
  • look for pointers to serious underlying causes such as:
    • bilateral Bell's palsy
    • recurrent Bell's palsy
    • association with a rash elsewhere or looking ill (may indicate sarcoid or Lyme disease)
    • space occupying lesion (rare)
      
• assessment of the ear should include pneumatic otoscopy and tuning fork tests
  • polyposis or granulations in the ear canal may imply cholesteatoma or malignant otitis externa. Vesicles in the soft palate, or tongue implies Ramsay Hunt syndrome

Reference:

• (1) Holland NJ et al. Recent developments in Bell's palsy. BMJ, 2004;329:553-557
• (2) Benatar M, Edlow J. The spectrum of cranial neuropathy in patients with Bell's palsy. Arch Intern Med. 2004 Nov 22;164(21):2383-5.
• (3) Effrey D. Tiemstra, et al, Bell's Palsy: Diagnosis and Management, Am Fam Physician 2007;76:997-1002, 1004.
• (4) Piercy J.Bell's palsy. BMJ, 2005, June 11;330:1374