NEUROLOGY,  NEUROPATHY

Bells palsy

  • Lower motor neuron weakness of the facial nerve in the absence of an identifiable cause
  • Viral etiology suspected – ?inflammation from reactivation HSV or VZV  
  • Facial nerve innervates lacrimal glands, salivary glands, stapedius muscle, taste fibres from anterior tongue, sensory fibres posterior ear canal and tympanic membrane
  • Risk factors
    • Pregnancy, pre-eclampsia, obesity, hypertension, diabetes, URTI
  • Symptoms
    • the eyebrow droops
      • forehead wrinkles of the brow are smoothed out
      • frowning and raising the eyebrows are impossible
      • if there is an UMN lesion affecting the facial nerve then the ability to wrinkle the brow is preserved; in Bell’s palsy this ability is lost
    • Unilateral facial weakness
    • Eye
      • corneal reflex
        • intact sensory component – trigeminal nerve
        • motor component is lost – facial innervation of orbicularis oculi.
      • Dryness of eye
        • Eye irritation often occurs due to lack of lubrication and constant exposure.
      • Loss of eye lid control
        • tear excessively 🡪 tears to spill freely from the eye
    • Hyperacusis
      • if the lesion of the facial nerve extends to above the point at which the branch to the stapedius muscle is given off
    • Mouth
      • mouth sags
      • Taste disturbance
      • lips cannot be pursed and whistling is impossible
      • Saliva drooling
    • unable to blow out the cheeks
  • Onset/timing – Sudden but not stroke like – evolves minutes to hours
  • Red flags
    • Gradual progression – suggests infectious or neoplastic
    • Underlying medical problems – previous stroke, brain tumour, cutaenous cancers face and neck, parotid tumour, head or facial trauma, recent infection
    • Diplopia, dysphagia, numbness of the face, dizziness
  • Differential diagnosis
    • Bell’s palsy must be distinguished from other causes of facial palsy 
    • PERIPHERAL – nuclear – causes
      • lyme disease
        • this is more likely if the facial weakness is bilateral
        • history of tick exposure, and arthralgias
        • look for a rash 
      • otitis media
        • suppurative otitis is excluded by examining the ear
        • there is gradual onset ear pain, fever, and conductive hearing loss
      • Ramsay Hunt syndrome
        • herpes zoster may produce an acute facial weakness but is accompanied by a rash within the auricle – geniculate herpes – or on the palate, pharynx, face, neck or trunk
      • there may be a pronounced prodrome of pain
      • sarcoidosis
        • sarcoidosis affecting the parotid gland is suggested by recurrent facial palsy
        • facial weekness is often bilateral 
      • Guillain-Barré syndrome
        • facial weekness is often bilateral
      • HIV infection
        • more likely if the facial weakness is bilateral
        • look for lymphadenopathy 
      • tumours
        • cholesteatoma, parotid gland tumours 
    • CENTRAL – supranuclear causes
      • multiple sclerosis
        • multiple sclerosis should be considered if the palsy is
          • unilateral, in a young adult
          • painless
          • resolves in 2-3 weeks
        • stroke
        • tumours
          • metastases or primary brain tumours
          • history of cancer
          • look for mental status changes
        • Horner’s syndrome and IIIrd nerve palsies
          • produce a ptosis
  • Examination
    • 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 
    • Insepct ear and TM for herpes zoter infection – suggests Ramsay hunt syndrome
    • Head and neck – cancer/masses
    • Assess all cranial nerves
    • Sparing of forehead suggests central pathology – but could also be seen in a peripheral lesion of one nerve branch
    • Usually resolve spontaneously, 70% notice improvement within 3 weeks, complete recovery 3 months
  • Treatment
    • Corticosteroids
      • Initiate within 72 hours of symptom onset
      • eTG – prednisone 1mg/kg up to 75mg orally for 5 days, could continue 10 days and taper down
    • Antiviral therapy
      • may have a small benefit but not clear in studies
      • Definitely needed if Ramsay hunt – consider IV antibirals
        • valacyclovir (1000 mg three times daily).S/E: nausea, vomiting and diarrhoea
    • Incomplete eye closure
      • Risk
        • foreign body
        • exposure keratitis
        • corneal ulceration
        • loss of vision
      • Wear sunglasses, lubricating eye drops/ointment
      • Tape eyelid at night
      • Immediately report any eye symptoms
    • Psychological help
      • patients with facial dysfunction suffer from depression and a reduced quality of life as a result of their appearance
      • support and counselling to cope
  • Refer
    • worsening neurological findings
    • facial diplegia
    • ocular symptoms or complications
    • incomplete facial nerve recovery three months after initial symptom onset
    • Consider investigations for neoplasms for brainstem, cerebellopontine angle, parotid gland – MRI
    • Refer to opthal if incomplete eye closure, other complications If persistent could consider cosmetic

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